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The British Journal of Psychiatry 2007; 190: 81-a [Full text] [PDF]

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Risperidone induced faecal incontinence: Gaurav Mehta (1 February 2007)

Methadone effects on Driving and the importance of notifying the Driver and Vehicle Licensing agency: Raafat S Labib Mishriky, Joseph Guirguis.Consultant addiction Psychiatrist, wolverhampton NHS trust (1 February 2007)

Annual Day of Remembrance for the Euthanized Mentally-Ill: Rael D Strous (1 February 2007)

Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria: ALBY ELIAS, FIJU CHACKO, MANOJ NARAYANAN, JASPREET SINGH, JAMES ANTONY (1 February 2007)

Early Intervention in Relapsing Schizophrenia: David, H Yates (6 February 2007)

A very long duration of untreated schizophrenia must be considered a risk factor for homicide.: Matthew M Large, DR OLAV NIELSSEN (6 February 2007)

Why don’t they just eat? The stigma of Eating disorders: Bethan Britt-compton (6 February 2007)

Escitalopram (cipralex) induced prolongation of QT interval: Howard Amital, Gustavo Goldenberg, Zamir Dovrish (7 February 2007)

Secondary Prevention of Psychoses and the Role of Crisis Resolution Services: Massimo Lanzaro (7 February 2007)

Causuality Relationship between ADHD and Depression: A Survey Results among Taiwan Young Soliders.: Yueh-Ming Tai, Hung-Wen Chiu (15 February 2007)

Social Phobia in Women: Treatment Trial with Mirtazapine: Marius Nickel (2 March 2007)

Change in Anger Symptoms in Female Borderline-Patients Treated With Lamotrigine: Marius Nickel (2 March 2007)

Re: Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria: Dallas P. Seitz (2 March 2007)

Smoking & Mental Health: Aadil Jan Shah, Ovais Wadoo,Sheffield Care Trust (9 March 2007)

Chess playing potentiates mental resources in schizophrenia: Caroline Demily, Laurence Jasse, Ghislaine Bailly, and Nicolas Franck (28 March 2007)

MTAS predated by 60 years?: T. C. Russ (11 April 2007)

Earliest evidence for malingering: There is no smoke without fire: Dr. Menachem Ben-Ezra, Yuval Palgi (2 May 2007)

Learned Helplessness: Doctor's in the MTAS experiment?: Asif M Bachlani (8 May 2007)

More about smoke-free mental health units: Vincenzo Villari, Giulio Barzega (29 May 2007)

Varenicline significantly reduced smoking in a mentally ill person: Enrique L.-M. Ochoa (29 May 2007)

Personality disorder managed in the general psychiatry setting: Rosemary Smyth (27 June 2007)

How Accessable are Website-Based Informational Resources for Disabled People?: Gavin J. Newby, Christine Groom (6 July 2007)

Deinstitutionalization of mental illness: At what cost?: Sahoo Saddichha (12 July 2007)

Reply to Peter Tyrer: Jesper Bent-Hansen (12 July 2007)

Reinstating clozapine after associated Diabetic ketoacidosis: John H M Crichton, Robert Brodick, Matthew Young, Fionnbar Lenihan (1 August 2007)

Smoking as a possible confounder in metabolic disease and cardiovascular risk with antipsychotics: Bo-Jian Wu, Tsuo-Hung Lan, Hsien-Jane Chiu, Tsung-Ming Hu, and Yung-Chang, Tuan (15 August 2007)

The heartland of psychiatry: Deborah A Mountain (6 September 2007)

Australian Firearms Data Requires a Cautious Approach: Samara McPhedran, Jeanine Baker (6 September 2007)

Comment on the efficacy and tolerability of sertindole (Serdolect®): Joseph C.J.R. Peuskens (7 September 2007)

High psychological distress among internally displaced women in West Darfur, Sudan: Marwan Khawaja, Mohammed D.A. Omer (7 September 2007)

Orthorexia Nervosa: who cares?: Arthur Kummer, Fernando M.V. Dias, Antonio L. Teixeira. (7 September 2007)

HIGH DOSES OF LONG-ACTING RISPERIDONE IN RESISTANT SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER: Sergio Ruiz-Doblado, Sánchez-Araña T, Rueda-Villar T, Baena-Baldomero A, Ruiz-Doblado S (7 September 2007)

The influence of the military institution on psychiatric practice in war zones: Emilio Bolla (7 September 2007)

Nicholas Rodney Drake (1948-1974): Oz Malkesman, Bethesda, MD, 20892 (7 September 2007)

Re: Australian Firearms Data Requires a Cautious Approach: Nestor D. Kapusta, Elmar Etzersdorfer, Gernot Sonneck (25 September 2007)

Firearms suicide in Queensland, 1990-2004: Professor Diego De Leo, Helen Klieve and Michael Barnes (25 September 2007)

Side-effects of Antipsychotics and frontal release signs among people with schizophrenia: Bo-Jian Wu, Tsuo-Hung Lan, M.D., Bo-Jian Wu, M.D., Hsien-Jane Chiu, Tsung-Ming Hu, M.D., Tsung-Yun Chuang, M.D. (26 September 2007)

Late-onset, recurrent and potentially progressive neutropenia in a patient receiving clozapine: Dr Sundararajan Rajagopal, Dr Tony Wong, Staff Grade Psychiatrist (26 September 2007)

Biological mechanisms and clinical psychiatry: Jonathan W Hill (4 October 2007)

The use of varenicline in mentally ill persons: Enrique L.M. Ochoa (31 October 2007)

Psychophysiological and behavioural characteristics in Comorbid ASPD/SSPD: Murali K Sekar, Ramanathan Ganapathy (28 November 2007)

Reclaiming the meaning of 'medical model': Tony B Benning (28 November 2007)

Smoke free: a plea to evaluate.: Catherine Pritchard, Ann McNeill and Irene Cormac (28 November 2007)

Why do we bother with evidence if we are only going to ignore them? Observations on psychosis EIS: Patapia M Tzotzoli (28 November 2007)

Diagnosis and management of non-organic paraplegia with Transcranial Magnetic Stimulation: SN Deftereos, G Panagopoulos, D Georgonikou and CE Karageorgiou (28 November 2007)

BRIEF TRAINING IN PSYCHOLOGICAL THERAPIES: Alasdair J Macdonald, Mark McKergow (28 November 2007)

Withdrawal symptoms after missing a single dose of Venlafaxine ER: Zoran M Pavlovic (3 December 2007)

Significant Weight Gain Occurring With Escitalopram: Daniel C White, MacDara McCauley, Consultant Psychiatrist (6 December 2007)

Author's Response: Robert A. Schug, Adrian Raine, Rand R. Wilcox (19 December 2007)

Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT): Markus Huber, Erwin Kirchler (30 January 2008)

One hundred and fifty years of evolutionary theory, psychology and psychiatry: Henry P O'Connell (30 January 2008)

Hot weather and suicide: not the same risk as other causes of mortality: Antonio Preti, Matteo Cella (30 January 2008)

Authors’ reply to: Mentalising impairment as a trait marker of schizophrenia? by Pousa et al: Mirjam Sprong, Patricia Schothorst, Ellen Vos, Joop Hox, Herman van Engeland (30 January 2008)

PSRHD versus PTSD: Chris H Cantor (30 January 2008)

Esomeprazole induced taste impairment associated with olfactory hallucinations: Adebusola A Akinmokun, Sabina Fahy, Consultant, Psychiatry of Later Life (6 February 2008)

Treatment-resistant depression as an onset of multiple sclerosis: Pierre LOULERGUE, Alexandre ORGIBET (8 February 2008)

PTSD's Future: Gerald M. Rosen, Robert L. Spitzer, Paul R. McHugh (21 February 2008)

Fall in the Rate of Usage of Electroconvulsive Therapy: Clinical and Research Implications: Allan I Scott, Tracy Fraser (21 February 2008)

Re: Goya Painting on BJP cover: Anne Weatherhead (27 February 2008)

Confidentiality: Robin Jacoby (17 March 2008)

Evolutionary Psychiatry on the 150th anniversary of Darwin's Origin: Riadh T Abed (9 April 2008)

Buspirone induced Hypomania: Nand Kumar, Jain Pramit (16 April 2008)

Salt Ingestion To Disguise Water Loading in a Patient With Anorexia Nervosa: Matthew O Cahill, Sean Lubbe, and Eric Johnson-Sabine (18 April 2008)

Clozapine-Induced Stammer and EEG abnormalities in a bipolar patient: Lena N Abreu, Cilly K. Issler, Beny Lafer (18 April 2008)

Mental Health related paintings of Vincent van Gogh: Arabinda Narayan Chowdhury (25 April 2008)

Cannabidiol and psychotic symptoms: Satish K Karunakaran (30 April 2008)

Mental Health related paintings of Vincent van Gogh: Arabinda Narayan Chowdhury (22 May 2008)

“TRUMAN” SIGNS AND VULNERABILITY TO PSYCHOSIS: Paolo Fusar-Poli, Oliver Howes, Lucia Valmaggia, Philip McGuire (30 May 2008)

Re: Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT): H Niederhofer (5 June 2008)

Exposure Therapy for Paranoid Anxiety: a Case Report: Dr Nir Essar, Menachem Ben-Ezra, Yuval Palgi, Merav Barkavi-Shani (5 June 2008)

Protecting Mental Health from Climate Change: Anne M. Doherty, Brendan D. Kelly, Consultant Psychiatrist Mater Misericordiae University Hospital; Senior Lecturer University College Dublin. (11 June 2008)

aripiprazole is not first choice in delusional parasitosis: Peter Lepping, Roland W Freudenmann (18 June 2008)

“Truman” signs: integrating qualitative psychopathology of Self and UHR criteria.: Andrea Raballo (2 July 2008)

A primary care view: Alan C Cohen, Andre Tylee, Chris Manning (13 July 2008)

Abortion Does Not Cause Mental Illness: Nada L Stotland, Gail Robinson, Donna Stewart, Carol Nadelson, Marta Rondon, Susan Kornfeld (17 July 2008)

Emergence of obsessive-compulsive symptoms during clozapine treatment in a pair of monozygotic twins: Kyung Sue Hong, Hee Jung Nam and Meerae Lim (17 July 2008)

Possible polyneuritis cranialis in a psychotic patient: diagnostic and therapeutic dilemmas: Konstantinos N. Fountoulakis, Eirini Tsirka, Maria Saiti, Melina Siamouli, Stamatia Magiria, Marina Paschalidou, Apostolos Iacovides, Nickolaos Iacovides, George S. Kaprinis (31 July 2008)

wake up call for british psychiatry: Kamini Vasudev (31 July 2008)

Ethnicity and mental health: precision required: Jonathan S Koffman (8 August 2008)

NWW: New Ways of What?: Mamdouh EL-Adl (8 August 2008)

Specificity of teachers and health professionals in referred pervasive developmental disorder childr: Sabrina Ribeiro, Cristiane S Paula, Associated Professor at the Mackenzie Presbyterian University, São Paulo-SP, Brazil and Marcos T Mercadante, Associate Professor of Psychiatry, Dept of Child & Adolescent Psychiatry at the Federal University of São Paulo-SP, Brazil (27 August 2008)

Neuropsychiatric systemic lupus erythematosus associated with neuroleptic malignant syndrome.: Philippe Verdoot, Eric L Constant, Arlette Seghers (27 August 2008)

Moving people to combat stigma and discrimination: the challenges ahead: Vanessa A Pinfold (8 September 2008)

DSM-V: Comorbidity studies suggest that PTSD belongs in its own class of traumatic-stress disorders: Mark W. Miller, Patricia A. Resick and Terence M. Keane (24 September 2008)

Mirtazapine induced akathisia: Ashish Aggarwal, Manish Jain, Ram C. Jiloha (1 October 2008)

AMISULPRIDE INDUCED GYNAECOMASTIA: Ashish Khandelwal, Ashish Aggarwal, Ram C Jiloha (25 October 2008)

Mentally Disorders Prisoners in Europe: Harald Dressing, Christine Kief and Hans-Joachim Salize (25 October 2008)

Challenges to binge drinking prevention: Napoleon Waszkiewicz, Agata Szulc (25 October 2008)

Is it time to start taking an internet history?: Gary M Cooney, Jane Morris (27 November 2008)

A Japanese survey on remission in schizophrenia.: Hirokazu Shida, Takefumi Suzuki, Fuminari Misawa, Koichiro Watanabe, Yasuo Fujii, Haruo Kashima (27 November 2008)

Dementia and Psychosis in Deaf and Mute Elderly Patients: Raafat Samir Labib Mishriky, S Bhattacharya, J Viswanathan, Consultants Psychiatrists, Wolverhampton City NHS Trust. (27 November 2008)

Ayahuasca and Psychosis: Rafael G. dos Santos, Rick J. Strassman, Department of Psychiatry, University of New Mexico School of Medicine (3 December 2008)

Dual Diagnosis Quandries: Patricia E. Hogan, St. Joseph, MO USA (10 December 2008)

The Cockcroft-Gault formula: an easy tool to assess renal function during lithium therapy: Roos van Westrhenen, Guido Nabarro, Jan. A. Swinkels (10 December 2008)

Depression and dementia: Ruoling Chen, Zhi Hu,Li Wei, Xia Qin, Cherie McCracken, John R Copeland (10 December 2008)

Geographical variation in use of the Mental Health Act: Andrew Donaldson, Remi Olaosun (SpR in Psychiatry), Peter Connelly (Consultant Psychiatrist) (24 January 2009)

The persistence of the "organic" problem: Jose-Alberto Palma (10 February 2009)

Renaming Schizophrenia?: AK Al-Sheikhli (10 February 2009)

From a patient's point of view: Bill E. George (10 February 2009)

Salience Dysregulation Syndrome: Reply to Bill George: Jim van Os (19 February 2009)

Suicide in dementia: Camilla M Haw (25 February 2009)

Risperidone for adolescent schizophrenia: double blind study: Ashok Kumar Jainer, Ahmad Mahmood, St Michael's Hospital, Coventry and Warwickshire Partnership Trust, CV34 5QW (25 February 2009)

Don't run NHS psychiatric services down: Sarah L Woolley (19 March 2009)

Re: Salience Dysregulation Syndrome: Reply to Jim van Os: Bill George, John Schillemans (19 March 2009)

CATARACTS AND CITALOPRAM: Armagan Yucel Samanci, Emre Cirakoglu (19 March 2009)

Public attitudes towards mental illness: John M. Eagles (19 March 2009)

Failure of NHS Information Technology systems and social change: William D Hall (7 April 2009)

Medical causal explanation and destigmatisation: Dusan Kecmanovic (17 April 2009)

A reply to Chua & McAlanon: Richard A Kanaan, Gareth Barker, Philip McGuire (28 April 2009)

IMPROVING OUTCOME FOLLOWING BRAIN INJURY: THE POTENTIAL ROLE OF CANNABINOIDS: Patrick O. Eghwrudjakpor, Amos A. Essien (27 May 2009)

MASS BEHAVIOR THERAPY FOR TREATING TERRORISM: Sumit K Gupta (27 May 2009)

Psychosis as dysregulated salience: affinities with phenomenological accounts of schizophrenia: Barnaby Nelson (18 June 2009)

Acute generalized exanthematous pustulosis induced after adding Lamotrigine to Divalproex: a case re: Ravi C Sharma, Ghanshyam Verma, Senior Resident, Dermatology, Indira Gandhi Medical College Shimla (3 July 2009)

still the heartland: David H Yates (2 September 2009)

Acute stress disorder in hospitalized victims of 26/11-terror attack on Mumbai, India: vanshree p. balasinorwala, nilesh shah (2 September 2009)

Schizophrenia, homicide and long-term follow up: George J Lodge (30 September 2009)

REMISSION OF DELUSIONAL PARASITOSIS IN SCHIZOPHRENIA AFTER TREATMENT WITH CLOZAPINE: JESUS RAMIREZ-BERMUDEZ, Mariana Espinola-Nadurille, Carlos Aviña-Cervantes (30 September 2009)

Trainee Forensic Psychiatrist: Suchitra Sabarigirivasan (30 September 2009)

Assertive Community Treatment teams need to implement key components if they are to survive: Helen T Killaspy (22 October 2009)

Empathic skills of authors: Martin P Lock (23 November 2009)

Letter to Professionals: Deborah J Padfield (2 December 2009)

A confusion over Odds Ratios: Zekria Ibrahimi (2 December 2009)

Is there a hope?: Devdutta Joardar, David Hague (2 December 2009)

Evolution at 150: Feargus F. O'Croinin, Centennial Centre for Mental Health and Brain Injury (7 December 2009)

The Importance of â€œCritical Communicative Actionâ€ for future of ICD & DSM: Kioumars Mackinejad, - (4 January 2010)

Oseltamivir-induced manic syndrome: Emmanuelle Corruble, Jean-Pierre Fidani, Samuel Rotenberg, Patrick Hardy, Florence Gressier (6 January 2010)

The Need for Championing the Cause of Elderly Mentally Ill in General Hospitals: Farooq Ahmed Khan, Birmingham and Solihull Mental Health NHS Foundation Trust (27 January 2010)

CLOZAPINE-INDUCED DOUBLE INCONTINENCE: Anurag Jhanjee, Dr Neeraj Gupta, Dr K.E.S Unni (27 January 2010)

A case of Religious Miracle: Tarun Sehgal, Partha Choudhury and Dawn Hodgson (29 January 2010)

Amendments to Mental health Act and Electroconvulsive Therapy, “'tis nobler in the mind to suffer?”: Dr Devdutta Joardar, Dr B K Rao, Dr Mohammad Mazharuddin, Felicity Baynes (1 February 2010)

Metrorrhagia during treatment with Risperdal consta: Cedo Miljevic, Dusica Lecic-Tosevski (15 February 2010)

A new treatment for stigmatizing scars after deliberate self-harm in borderline personality disorder: Matthias Aust, Andreas Gohritz, Marcel G. Sieberer, Karsten Knobloch, and Peter M. Vogt, (4 March 2010)

Adverse effect of escitalopram: severe receding hair attributed to escitalopram.: Panagiotis Bakaras, Maria Georgoussi (19 March 2010)

Olanzapine and clozapine associated weight loss: Varuni A de Silva, Raveen Hanwella (24 March 2010)

Jumping to conclusion (JTC) : a case with schizophrenia and obsessive-compulsive symptoms.: Alessandro Rossi, Francesca Struglia (14 April 2010)

A reply to van Os's "A salience dysregulation syndrome": Donald C Grant, Edwin Harari (14 April 2010)

Use of alcogels and alcometers: Alison R Rowe, Dr John Crichton PhD FRCPsych, Colin Mackintosh RMN, Amanda McFarlane RMN (16 April 2010)

PANSS scale - Are you disoriented?: Søren D Østergaard, Jimmi Nielsen MD, Psychiatric Research Unit, Aalborg Psychiatric Hospital, Aarhus University Hospital, Denmark (21 April 2010)

Suffrage or Suffering? Awareness of Voting Rights For Psychiatric Inpatients: Gareth Rees (12 May 2010)

CARE HOMES IN DEMENTIA CARE-NEED TO ACT: Farooq Ahmed Khan (24 May 2010)

AJWAIN (An Indian Spice): An unusual substance of dependence: Ashish Aggarwal, Ramesh Kumar, Ravi C. Sharma, Dinesh D. Sharma (2 June 2010)

Rabbit syndrome induced by risperidone & escitalopram: Sudhir Kumar, Shravani Sur, ashutosh singh, anil sisodia, pramit jain (2 June 2010)

Validity Issues with the Edinburgh Postnatal Depression Scale: Cynthia R. Ronzio (3 June 2010)

Early intervention in psychosis: A case of the emperor’s new clothes.: David J Castle (8 June 2010)

Clozapine induced eosinophil mediated hypersensitivity with cardiotoxicity and hepatotoxicity: Helen D Kenealy, Greg Winter (28 June 2010)

Diploma in Psychiatry? Everyone's a winner.: Will H W Squier (28 June 2010)

A case of Serotonin Syndrome and Manic switch following combined use of Tramadol and Fluoxetine: Agastya D Nayar, Chung Juliana (28 June 2010)

‘Gilahari’ (Lizard) syndrome: Is it a cultural manifestation of anxiety disorder?: Om Prakash (14 July 2010)

Risperidone induced faecal incontinence 1 February 2007

Gaurav Mehta,
Senior House Officer
-
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Re: Risperidone induced faecal incontinence

gmehta1975{at}hotmail.com Gaurav Mehta

Dear editor, I wish to highlight a rare untoward side effect of faecal incontinence following risperidone administration. Risperidone is commonly used as an atypical antipsychotic in the UK. It is licensed for both acute and chronic psychosis and mania. It acts predominantly by blocking D-2 and 5-HT2 receptors(1). Although urinary incontinence is a well known possible side effect of risperidone (2,3) not much evidence exists regarding its role in faecal incontinence and only one case of risperidone induced faecal incontinence has been reported so far (4).
A 24 year old Caucasian male was admitted in patient for treatment of an episode of paranoid schizophrenia. He showed initial remarkable improvement of symptoms on Olanzapine 20 milligrams per day and was transferred to rehabilitation services. However, he developed marked side effects (weight gain, sedation and high serum prolactin levels) whilst on Olanzapine. This was subsequently withdrawn gradually and Risperidone introduced as an alternative and eventually stabilised on 2 milligrams Risperidone twice daily. He had full control of his bowel and bladder at that time. Within a few days of risperidone prescription, the patient complained of fecal incontinence. Physical examination, including complete neurological examination, was unremarkable. All relevant blood investigations were within normal limits. Other possible causes of fecal incontinence were excluded.
Keeping the possibility of a drug-induced phenomenon, Risperidone was stopped, and the incontinence resolved within two weeks. The patient was then prescribed Aripiprazole 15 milligrams once daily. He is asymptomatic at the time of reporting this case.
The Adverse Event Report Form was filled and the drug safety manager of the manufacturer drug company was informed.
References 1. Horacek J,Bubenikova-Valesova V, Kopecek M et al .Mechanism of action of atypical antipsychotic drugs and the neurobiology of schizophrenia. CNS Drugs 2006;20 (5): 389-409 2. Vera PL,Miranda-Sousa A,Nadelhaft I .Effects of two atypical neuroleptics, olanzapine and risperidone, on the function of the urinary bladder and the external urethral sphincter in anesthetised rats .BMC Pharmacol. 2001;1:4. 3. Agarwal V. Urinary incontinence with risperidone. J Clin Psychiatry. 2000 Mar; 61(3): 219 4. Lundin F, Rousseau A, Kadowaki A. A case report. Risperidone induced fecal incontinence as a result of reduced anal sphincter tonus. Lakartidningen. 2004 Dec 2;101 (49): 4006-8

Methadone effects on Driving and the importance of notifying the Driver and Vehicle Licensing agency 1 February 2007

Raafat S Labib Mishriky,
SHO in Psychiatry
North Staffordshire combined NHS Trust,
Joseph Guirguis.Consultant addiction Psychiatrist, wolverhampton NHS trust
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Re: Methadone effects on Driving and the importance of notifying the Driver and Vehicle Licensing agency

raafatmishriky{at}hotmail.com Raafat S Labib Mishriky, et al.

Methadone is used for detoxification from heroin and other opioids, and in maintenance opioid detoxification programs. Driving is critical in maintaining independency in today’s society and is a complex task where the driver continuously receives information, analyses it and reacts. The common adverse effects of methadone that are relevant to driving include dizziness, sedation, insomnia, sleep irregularities, euphoria, agitation, seizures, syncope, hypotension and blurring of vision.
The opinion that there are few effects of methadone upon driving is shared by some experts in the field (Joo S 1994). Berghaus and Freidal (1998) reported that patients on methadone have more difficulty parking and drove at lower speeds in comparison to matched controls. Surprisingly this was interpreted as exercising more caution.
The effects on methadone on performance tasks related to driving such as tracking, vigilance and reaction time appears to be limited (Robinson and Moskowitz 1985). On the contrary an increase in the reaction time have been reported particularly during the initial weeks of treatment (Gordon 1970)
However it is reasonable to interpret the studies done carefully as comparable tests to detect drug levels in the body remains elusive. This is due to the differing effects of the drug on the body, the length of time remaining in the body and the diverse assortment and combination of drugs taken. This means that the level of the drug cannot be related to measurable and repeatable effects on driving performance.
Further research is still required as many factors are still needed to be examined closely for example the exact driving skills affected, the effects of different opioids, dose levels, interactions with other medications and the individual difference variables. Such research should allow robust guidelines to be given to health professionals and patients and result in reduced legal risk for both.
The British medical association (2003) in its report “driving under the influence of drugs” recognises the influence of drugs on driving. If a person is proven to be unfit to drive through the use of drugs (illicit and prescribed) they face the same penalty as those who drive under the influence of alcohol, “ At the very least disqualification from driving for a year and being heavily fined, with the opinion of imprisonment If death is caused by careless driving while under the influence of alcohol or drugs, spending up to ten years in prison and paying an unlimited fine” (DETR: Drinking and driving wrecks leaflet for Driver and Vehicle Licensing agency ; DVLA)
It is the duty of the license applicant, or holder to notify the DVLA of any medical condition, which might affect safe driving. The General Medical Council (GMC) guidelines regarding this issue included that the DVLA is legally responsible for deciding if a person is medically unfit to drive. The DVLA need to know when driving license holders have a condition, which may now or in the future affect their safety as drivers. Patients should understand that the condition might impair their ability to drive. If a patient is incapable of understanding this advice, for example because of dementia, the DVLA should be informed immediately. Patients should know that they have a legal duty to inform the DVLA about their condition. If a patient refuses to accept the effect of the condition on their ability to drive, it is suggested that they seek another doctor opinion, and they are advised not to drive until the second opinion is made. If the patients are not persuaded to stop driving, or there is evidence that a patient is continuing to drive contrary to advice, disclosure of relevant medical information should be done immediately with confidence to the medical advisor at the DVLA. Before giving information to the DVLA, you should inform the patient of your decision to do. Once the DVLA has been informed, you should also write to the patient, to confirm that a disclosure has been made.
It is worth knowing that applicants or drivers complying fully with a consultant supervised oral methadone program may be considered for an annual review license for group one entitlement (motor and motor cycles) subject to favourable assessments and normally annual medical review. They may be considered for group two entitlement (large lorries and buses) once a minimum three years period of stability on the maintenance program has been established with favourable random urine tests and assessments. (DVLA 2003)
Declaration of interest: None
References
1- British Medical Association (March 2003) Driving under the influence of drugs https://www.bma.org/ap.nsf/AttachmentsByTitle/PDFHubinternetresourcedrugsdriving/$FILE/DrugDrivingFeb2005.pdf
2- Berghaus G, Freidal B (1998) Methadone and driver fitness. Euro- Meshwork; A forum for methadone drivers in the European region 13:5-6
3- Driver and Vehicle Licensing agency (2003) For medical practitioners at a glance guide to the current medical standards of fitness to drive issued by drivers medical group, DVLA, Swansea
4- Gordon NB (1970) Reaction time to methadone treated ex heroin addicts. Psychopharmacologic J 16:337-334
5- Joo S (1994) Methadone substitution and driver ability: Research findings and conclusions from a discussion of experts. Journal of traffic medicine 22:101-103
6- Robinson Cd, Moskowitz H (1985) Methadone Maintenance treatment and aspects of skilled performance. In Kaye S, Meieir GW, Eds. Alcohol, drugs and traffic safety. Washington, US. Department of transportation: 1145-1157
For correspondence
Raafat S Labib Mishriky
SHO in psychiatry
North Staffordshire Combined NHS Trust
Lyme Brook Mental health Resource centre
New castle- under- lyme ST5 7TL
Phone 07725127013
Email; raafatmishriky@hotmail.com

Annual Day of Remembrance for the Euthanized Mentally-Ill 1 February 2007

Rael D Strous,
Psychiatrist, Director Chronic Inpatient Unit
Beer Yaakov Mental Health Center, Sackler Faculty of Medicine, Tel Aviv University
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Re: Annual Day of Remembrance for the Euthanized Mentally-Ill

raels{at}post.tau.ac.il Rael D Strous

Not too long ago, for the first time in history, members of the psychiatry profession during the Nazi era sought to methodically eradicate their patients. Many were profoundly involved in the atrocities consisting predominantly of sterilization and euthanasia with their function being essential to the success of Nazi policy and principles. It is believed that approximately 200 000 mentally-ill were put to death in the euthanasia program (Strous, 2006), much of which transpired before, and therefore came to inspire, the larger scale genocide of Jews, Gypsies and homosexuals now referred to as the Holocaust.
It remains an embarrassment for the field that so many senior internationally known members were so intimately involved, many of whom continued to practice and conduct research long after the war and were protected by colleagues. This is compounded by the fact that this period is not well documented in the international psychiatry literature and is minimally referred to, if at all, in the teaching of psychiatry trainees. The time has come to correct this oversight and to institute a “day of remembrance” for these murdered mentally-ill. An apt day would be September 1, the date of Hitler’s official letter in 1939 permitting (but not demanding) psychiatrists to carry out this process. More than a memorial for victims of euthanasia, this day would be devoted to education stressing the value of firm and unbending timeless ethics in psychiatric practice and the inherent dangers of dehumanizing the mentally-ill as well as not allowing political and environmental events to influence clinical practice.
Despite a refined ethics code, Nazi psychiatry provides a prime illustration of how ethics training and policy without a focus on history is of limited value. A "day of remembrance" for the mentally-ill perishing during this period would help address this void. The intent of such a day of remembrance for the mentally-ill would not aim to label psychiatric practice as unjust. Rather, it would address issues of general medical ethics in the field, the question of how psychiatrists were drawn into the euthanasia program and how to ensure it never reoccurs.
Strous R.D. (2006) Hitler’s Psychiatrists: Healers and Researchers Turned Executioners and its Relevance Today. Harvard Review of Psychiatry 14, 30-37.

Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria 1 February 2007

ALBY ELIAS,
Psychiatry Clinical Practice
Northern Sydeny and Central Coast Area Health Service NSW Australia,
FIJU CHACKO, MANOJ NARAYANAN, JASPREET SINGH, JAMES ANTONY
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Re: Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria

alby.elias{at}rediffmail.com ALBY ELIAS, et al.

Neuroleptic Malignant Syndrome (NMS) is a rare, but serious adverse effect of anti-psychotics. Published large-scale studies are seldom seen in the literature; case reports have formed the main source of information. Atypical presentation, as often the case is, has gained importance recently (Borovicka 2006, Nielsen 2005, Hall 2005, Peiris et al 2000, Ferioli 2000). Given that early detection and treatment is life saving atypical presentation should be given attention. We report the case of a 26-year-old gentleman who had disorganized schizophrenia. He received intravenous injection of haloperidole (10 mg) and oral risperidone (2 mg) on the day of admission at 6 p.m. Next day morning the patient developed protrusion of tongue suggesting acute dystonia. Intramuscular injection of promethazine (25 mg) was given. He improved, but developed slurring of speech towards the evening. Subsequent injections of promethazine (25 mg three times over a period of two hours) proved to be ineffective. He developed urinary incontinence, profuse sweating, dyspnoe, altered sensorium and mutism over the next 6-12 hours. The physical examination revealed hyperthermia (102 0 F), but blood pressure and pulse rate remained stable. There was no generalized or focal rigidity. Total leukocyte count was 10800/mm3. Cerebrospinal Fluid Analysis and renal and hepatic parameters did not show any abnormality. Creatinephosphokinase (CPK) level was 3720 U/L. A provisional diagnosis of NMS was considered. All antipsychotic medications were stopped and bromocriptine 2 mg three times daily, lorazepam 2 mg three times daily and supportive measures were administered. Following this he improved and his parameters became normal within 5 days. Although intramuscular injections may cause high CPK levels his symptoms in totality are difficult to explain with this factor. Central nervous system infections are likely to cause fever and altered sensorium, but normal CSF results and relatively fast improvement without any specific therapy does not support this possibility. Promethazine induced anti- cholinergic toxicity could be a potential cause for hyperthermia and altered sensorium, but absence of dilated pupil and presence of profuse sweating suggests that this complication is unlikely.
We report this case in order to highlight the probable occurrence of NMS without generalized muscular rigidity and disturbances in the cardiovascular parameters like blood pressure and heart rate. It is important to see that CPK level may rise in the absence of rigidity. This has been reported elsewhere (Borovicka 2006). It is speculated that NMS that develops without rigidity is most often associated with atypical antipsychotics. It is difficult to ascertain in this case because patient received haloperidole and risperidone. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV TR) requires two features-muscular rigidity and hyperthermia-essential for the diagnosis of NMS. Literature is replete with NMS occurring in the absence of these manifestations however (Borovicka 2006, Nielsen 2005, Hall 2005, Peiris et al 2000, Ferioli 2000). This suggests that the DSM diagnostic criteria for NMS may be revised.
References
1. Borovicka MC., Bond LC., Gaughan KM. (2006) Ziprasidone- and lithium-induced neuroleptic malignant syndrome. . Ann Pharmacother.40(1):139-42. 2. Ferioli V, Manes A, Melloni C, Nanni S, Boncompagni G (2000). Atypical Neuroleptic Malignant Syndrome Caused by Clozapine and Venlafaxine: Early Brief Treatment With Dantrolene. Can J Psychiatry, 49(7): 497-498 3. Hall RC, Appleby B, Hall RC. (2005) Atypical neuroleptic malignant syndrome presenting as fever of unknown origin in the elderly. South Med J. 98(1):114-7. 4. Nielsen J, Bruhn AM. Atypical neuroleptic malignant syndrome caused by olanzapine. (2005). Acta Psychiatr Scand.112(3):238-40. 5. Peiris D T S, Kuruppuarachchi K A L A, Weerasena L P et al. (2000) Neuroleptic malignant syndrome without fever: a report of three cases. J Neurol Neurosurg Psychiatry; 69:277-278

Early Intervention in Relapsing Schizophrenia 6 February 2007

David, H Yates
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Re: Early Intervention in Relapsing Schizophrenia

david{at}jidgey.e7even.com David, H Yates

Sir,
Early intervention in relapsing schizophrenia, where previous relapses have followed stopping previously efficacious medications, present difficulties for examiners in a one off examination in a psychiatric interview set in a structured context. It has been unusual for the psychiatric service to make use of the reports from lay observation of odd behaviour in the community.
The intervention can be crucial where a previous expression of active illness has led to violent behaviour to others or self, gaining a reputation in the community that irredeemably dooms the patient.
Comments in the Panel Report into the care and treatment of John Barrett, and in the findings in other patients suffering from continuing schizophrenia, point to how difficult it is for the psychiatric services that are supervising, to make a judgement that the degree of illness they determine is sufficient to make the grounds for, or invoke, Mental health Act compulsion, or recall under a Home Office restriction.
I suggest for consideration, where medication has been efficacious, that whether the medication is being taken or not will be a better trigger for intervention than the procedures presently adopted.
Whilst it is generally accepted that there is no particular blood level that can be applied generally as one which can be a standard of predictable efficacy for all, it is presently accepted that there is a level in a particular medication that below which it is not going to be efficacious.
I want to suggest that the profession can go further than this. It is likely that in any particular patient the level for them that is reliably efficacious for them, will be, in the future, the level that was previously found to be efficacious and acceptable, obtained during a period of care when the outcome of the effect on the illness in the particular patient over a sufficient time was observed to have been a successful one.
The trigger for intervention and the condition to be accepted before discharge into the community for those, whose illness behaviour has placed themselves and other people at risk of serious harm, will then be that the patients make themselves available, where there is an indication, for an unannounced recall for blood level examination.
There might then be an onus on Pharmaceutical Companies that supply to the NHS that they provide an effective test for the particular product and make that available under their contract.
The ability to lay down this condition would be helpful for appeal Tribunal decisions, for the conditions under release that the Home Office might expect. It will be to the benefit of those patients continuing with supervision in the community after discharge in that it will prevent them from being the victims of a return to a level of active illness that previously got them into trouble and that a return to it in the future would be an irredemiable loss their reputation in the community.
Dr D H Yates FRC Psych wintergreen St Jidgey Wadebridge, Cornwall PL27 7RE 01208 81 6035
Declaration of interest Family carer.

A very long duration of untreated schizophrenia must be considered a risk factor for homicide. 6 February 2007

Matthew M Large,
psychiatrist
Private Practice, 326 South Dowling Street Paddington 2025 NSW Australia,
DR OLAV NIELSSEN
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Re: A very long duration of untreated schizophrenia must be considered a risk factor for homicide.

mmbl{at}bigpond.com Matthew M Large, et al.

The recent ‘five year report of the national confidential inquiry into suicide and homicide by people with mental illness’ by Appleby and Shaw (1) revealed that 15 of the 49 (30.6%) schizophrenic patients who had committed homicide and had not received treatment had a been ill for in excess of five years. In the published distributions of the duration of untreated psychosis (DUP) more than 95% of patients were treated within four years (2). The high proportion of untreated schizophrenic patients who committed homicide who had been ill for several years demonstrates the association between delayed treatment and serious violence (3) and suggests that prolonged DUP is a significant risk factor for homicide.
Other important observations in the confidential inquiry report are that the first episode of psychotic illness and being from a less well integrated ethnic minority carry a particular risk of homicide (4).
The increased risk of homicide in both acute (5) and first onset psychosis with long DUP (1) relative to patients with established illness who have received treatment is probably because the experience of remission from symptoms after treatment reduces the likelihood of acting on delusional beliefs.
Although the association between prolonged untreated schizophrenia and homicide may be partially explained by an underestimation of the number of untreated patients in studies of first episode psychosis, clinicians should not be reassured about the safety of a patient merely because they have been unwell for a prolonged period. Reducing the duration of untreated psychosis would reduce the incidence of violence by patients with schizophrenia and should be a goal of all services.
1. Five year report of the national confidential inquiry into suicide and homicide by people with mental illness. Homicide enquiry. The University of Manchester. Appleby L. Shaw J. December 2006 Viewed at http:// www.medicine.manchester.ac.uk/suicideprevention/nci/Useful/ avoidable_deaths_full_report.pdf
2. Large MM , Nielssen O, Measures of the duration of untreated psychosis. Submitted for publication.
3. Milton J, Amin S, Singh SP, Harrison G, Jones P, Croudace T, Medley I, Brewin J. Aggressive incidents in first-episode psychosis. British Journal of Psychiatry. 2001; 178:433-40.
4. Erb M, Hodgins S, Freese R, Muller-Isberner R, Jockel D. Homicide and schizophrenia: maybe treatment does have a preventive effect. Crim Behav Ment Health. 2001;11(1):6-26.
5. Nielssen O, Westmore B, Large M, Hayes R. Homicide during psychotic illness in New South Wales from 1993 to 2002, Medical Journal of Australia in press, Jan 2007

Why don’t they just eat? The stigma of Eating disorders 6 February 2007

Bethan Britt-compton,
Scientist
Cardiff university
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Re: Why don’t they just eat? The stigma of Eating disorders

bethanbc{at}hotmail.com Bethan Britt-compton

What is an eating disorder? There are definite definitions and guide lines for the diagnosis of an eating disorder, but these guide lines are very black and white. Eating disorders come in may shapes, and can affect anybody. The only connection is some sort of difficulty with food, be it under eating, overeating, or any compensation method such as purging, drugs use, over exercise. Many suffers also have a plethora of other problems associated with their ED, such as depression, self harming, obsessive behaviour, or drug/alcohol dependency.
Celebrities have a lot to answer for, as we constant see the famous few, (who can barley stand on their stick insect legs), claming they eat like horses and are naturally thin. This heightened awareness has been a double edged sword, giving young venerable people not only ideas how to loose weight, but the need to loose weight to fit in. Today it is increasingly fashionable to be “Anorexic”. After all thin is in isn’t it? The generation waiting in the shadows is already tainted with the fashionable deadly waif look. If eve had anorexia then we wouldn’t be here today.
How are eating disorders perceived by the general public? People see the bones, not the twenty four hour consuming physiological battle, and they definitely don’t see the battle of the fleshier sufferers. A lot of people think to have an eating disorder you have to be thin. Some don’t even understand or believe you can be a normal weight and be an ED sufferer. Eating disorders are much more than the food complications, it’s a controlling internal sanctity created for many means. But we must remember eating disorders kill.
With such stigma generated around eating disorders is it really a surprise so many suffer alone, afraid to tell the world the dirty secret they carry. So how about the other eating disorder sub types? Bulimia is more prevalent in society than anorexia, yet there seems to be a great fog behind which an extremely taboo issue hides. Often bulimia’s curse is externally unnoticeable. This appears to leave society in a state where they cant really relate bulimia to an ED. Especially with the unfortunate lengths some sufferer go to hid their problem, even from themselves. Many such suffers are to ashamed to tell a soul their internal battles and external behaviours. If the pain of bulimic suffers is physically unnoticeable how can we reach out to these people?
What next? Awareness, without glamorising, is essential. Societies such as the eating disorder association- EDA are achieving huge leaps in this department, managing to reach out to many who are petrified. Such societies not only support suffers and carers, but also try to increase awareness to professionals, teachers and employers, to try and bridge the gap created by the stigma surrounding this disease. But further support is required from GP’s and the NHS for sufferers and carers.

Escitalopram (cipralex) induced prolongation of QT interval 7 February 2007

Howard Amital,
Head of Department of Medicine ’D’
Meir Medical Center, Tshernichovsky 59 Kfar-Saba, 4428, Israel,
Gustavo Goldenberg, Zamir Dovrish
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Re: Escitalopram (cipralex) induced prolongation of QT interval

hamital{at}netvision.net.il Howard Amital, et al.

Many studies comparing selective serotonin reuptake inhibitors (SSRIs) with other antidepressants have found that SSRIs rarely cause fatality or serious cardiac sequel. Escitalopram (cipralex) has not been associated with the prolongation of the QT interval. The following case however presents such an adverse event of escitalopram Therapy with Escitalopram 10 mg daily was commenced in an eighty-one year old patient with an ischemic heart disease and major depression who underwent a coronary artery bypass graft surgery two weeks earlier. Following two days of therapy he was admitted due to syncope, with no chest discomfort yet with a prolonged QT interval reaching 0.51 sec. No abnormal blood electrolyte tests were observed. Escitalopram therapy was stopped and two days afterwards the QT interval returned to normal range. Prolonged cardiac depolarization (long QT interval) may exert potentially life-threatening ventricular arrhythmias. Among the risk factors for prolonged QT intervals are congenital long QT interval syndrome, clinically significant bradycardia, organic cardiac disorders, hypokalaemia, hypomagnesaemia, impaired hepatic or renal function and medications.
The therapeutic dosages of escitalopram (10 to 20 mg/d) in humans have been associated with adverse effects similar to those associated with other SSRIs including nausea, diarrhea, insomnia, dry mouth, and ejaculatory disorders however prolonged QT interval has not been described (1). Eescitalopram, S-citalopram, is the pharmacologically active S-enantiomer of Citalopram, which is a racemic mixture of the R- and S- enantiomers. Dosages of less than 600 mg of citalopram usually do not cause significant cardiac toxicities which are encountered more often in higher dose intoxications (2). The metabolite S-didesmethylcitalopram (DDCT) is considered to cause ECG abnormalities, therefore such changes may have a delayed onset following drug ingestion (3). To the best of our knowledge this is the first report of clinically significant QT prolongation in a patient treated with a normal therapeutic dosage of escitalopram.
References 1. Barnett, A.K. Brush, DE, & Schroeder, W. (2003) The Pharmacology and Toxicology of Escitalopram. Internet Journal of Medical Toxicology, PharmD, http//www.ijmt.net/ijmt/pge.asp?PageID=178 2. Lindgren, K.N., Bangh, S.A, Ling, L. et al. (2003) Escitalopram, a review of adverse effects in overdose reported to select regional poison centers. J Toxicol Clin Toxicol 2003; 41:658 3. von Moltke. L.L. Greenblatt, D.J.Giancarlo, G.M et al. (2001) Escitalopram (S-citalopram) and its metabolites in vitro: cytochromes mediating biotransformation, inhibitory effects, and comparison to R- citalopram. Drug Metab Dispos 29:1102-9
Authors: Gustavo Glodenberg, Zamir Dovris, Howard Amital Department of Medicine "D", Affiliated to Sackler Faculty of Medicine, Tel -Aviv University, Tel-Aviv, Israel.

Secondary Prevention of Psychoses and the Role of Crisis Resolution Services 7 February 2007

Massimo Lanzaro,
Psychiatrist
Devon Partnership NHS Trust
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Re: Secondary Prevention of Psychoses and the Role of Crisis Resolution Services

maxlanzaro{at}btinternet.com Massimo Lanzaro

The work to improve the secondary prevention of psychoses has mainly two aims: to find strategies for earlier detection and to develop treatment methods and programs that are tailor-made for patients in the early phases of schizophrenia. Recent investigation of duration of untreated psychosis(DUP) has demonstrated that although individuals generally receive treatment within 6 months of symptom onset, others remain untreated in the community for 1-2 years (Birchwood et al, 2002). Understanding the service impediments to early detection may be an essential prerequisite for attempts to reduce these potentially deleterious treatment delays. In Devon, the Early Intervention Service (EIS) is only in its infancy within the County and we are tussling with issues (shared by others, according to the relevant literature) as to how to develop a network which meets the needs of a predominantly rural area, covering a large geographical patch with dispersed centres of population. EIS is unable to provide true secondary prevention, but only, at present, to treat people in the midst of their first major episode such that they have a decreased progression of the illness. However, we have noticed some encouraging preliminary results with the intensive home-treatment team (CRHT), and noticed unexpected potentials of this part of the Services for true secondary detection and intervention for people in the prodromal stages of psychosis. Of course, in this field, there are wide variations between regions and Trusts with different resource levels and different planning. Nonetheless an interesting, preliminary, recent study in the London boroughs of Camden (Gould et al, 2006) supports the hypothesis of crisis resolution teams as "earlier than early" intervention services, also highlighting the clinical implications in averting admissions and achieving a pragmatic balance of community and hospital care. In my opinion this is a new and challenging topic of research in the field of prevention and pathways to care.
References
Skeate, A., Jackson, C., Jones, C., Birchwood M. (2002) Duration of untreated psychosis and pathways to care in first-episode psychosis. British Journal of Psychiatry, 181: s73-s77.
Gould, M., Theodore, K., Pilling, S., Bebbington, P., Hinton, M., Johnson, S. (2006) Initial treatment phase in early psychosis: can intensive home treatment prevent admission? Psychiatric Bullettin, 30: 243 -246.
Massimo (aka Max) Lanzaro, Consultant Psychiatrist in IP and CRHT
Department of Psychiatry, Devon Partnership NHS Trust, Wonford House Hospital, Exeter, Devon, UK EX2 5AF
E-mail: maxlanzaro@btinternet.com

Causuality Relationship between ADHD and Depression: A Survey Results among Taiwan Young Soliders. 15 February 2007

Yueh-Ming Tai,
Psychiatrist
Department of Child and Adolescent Psychiatry Armed Forces Beituo Hospital,
Hung-Wen Chiu
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Re: Causuality Relationship between ADHD and Depression: A Survey Results among Taiwan Young Soliders.

ytai1123{at}ms24.hinet.net Yueh-Ming Tai, et al.

We recently make a survey of 216 Taiwan soliders and collected their self-administrated resultes of Chinese version depression scale(Zung Mental Health Scale for which Sport Depression Scale, SDS) and recalled ADHDscales ( Barkley Scales). We observed a strong correlations between them as the Pearson correlation coefficent between them was 0.604(p<0.01). In addition, among our samples, 50 soliders had been diagnosis of major depression or dysthymic disorder showed significant higher means of these two variables compared with others. Eyestone.L.L.,et al. published similar results among 102 prison male in 1994(Eyestone and Howell, 1994), and Fischer, M. et al. followed 147 hyperactivity children for 13years and diagnosed 26% major depression cases among them(Fischer et al, 2002). Thus we bravely susptectd the ADHD or hyperactivity sympotms might one of the causes of depression.
Since all the Taiwan males are arbitary to enter military serivce at age twenty, we are more confident to generalize this result to Taiwanese you man. However,we would appreciate any other mental health professionals sharing their exeriences in this area with us. If other studies confirm or support our finding, it could be extremely helpful in the prevention of young adult depression and treatment of ADHD.

Social Phobia in Women: Treatment Trial with Mirtazapine 2 March 2007

Marius Nickel,
Professor of Psychiatry
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Re: Social Phobia in Women: Treatment Trial with Mirtazapine

m.nickel{at}klinik-badaussee.at Marius Nickel

Social phobia is an anxiety disorder characterized by extreme fear and phobic avoidance of social and performance situations, as well as by a relatively poor health-related quality of life. We tested the antidepressant mirtazapine against placebo in the treatment of female patients suffering from social phobia in a randomized clinical trial (RCT) (Muehlbacher et al., 2005). After ten weeks, significant improvement on both the Social Phobia Inventory (SPIN) and the Liebowitz Social Anxiety Scale (LSAS) was observed in the group treated with mirtazapine. In addition, a statistically significant positive impact on the patients’ health-related quality of life was found in comparison to placebo, using the SF-36 Health Survey questionnaire (Muehlbacher et al., 2005).
In the subsequent 18-month follow-up it was our goal to assess whether mirtazapine treatment could produce sustained benefits in the long -term therapy of women suffering from social phobia.
After unblinding at the end of the RCT, all the patients (group treated with mirtazapine, n=33; former placebo group, n=33) were asked to participate in follow-up visits after 6, 12 and 18 months and patients from the mirtazapine group were invited to continue treatment at a fixed daily dose of 30 mg. The former placebo group was not permitted to take any psychotropic medication. A two-factor, repeated-measures analysis of variance was performed according to the intent-to-treat principle. The treatment condition was defined as the between-subject factor and the measurements in time as the within-subject factor. When the assumptions for repeated-measures analysis were not given, the results were adjusted using the Greenhouse-Geisser Epsilon. In order to assess whether there were differences at the initial and final points, multiple comparisons were performed by using contrasts for each treatment condition. The significance levels were corrected using the Bonferroni correction.
After 18 months, significant interaction of the group-by-time effect for the SPIN (p<0.01), the LSAS (p<0.01) with 6 out of 8 subscales of the SF-36 (General Health Perception, Vitality, Social Functioning, Role-Emotional, Mental Health, all p<0.01, and Bodily Pain, p=0.02) was observed. All of our subjects tolerated mirtazapine relatively well. In summary, we found that mirtazapine treatment produced sustained benefits in female patients suffering from social phobia during an observation period of 18 months, which confirmed the results of the previous short RCT. Taking both studies into consideration, mirtazapine appears to be an effective and relatively safe option in the long-term treatment of social phobia in women (Muehlbacher et al., 2005).
Muehlbacher, M., Nickel, M.K., Nickel, C. et al (2005) Mirtazapine treatment of social phobia in women: a randomized, double-blind, placebo- controlled study. J Clin Psychopharmacol 25, 580-583. Marius K. Nickel, MD Clinic for Psychosomatic Medicine and Psychotherapy, Medical University of Graz, Bad Aussee, Austria University Clinic for Psychiatry 1, PMU, Salzburg, Austria Clinic for Psychosomatic Medicine and Psychotherapy 8990 Bad Aussee, Austria Tel.: + 43 3622 521003203, m.nickel@klinik-badaussee.at Christoph Egger, MD University Clinic for Psychiatry 1, PMU, Salzburg, Austria Moritz Muehlbacher, MD University Clinic for Psychiatry 1, PMU, Salzburg, Austria

Change in Anger Symptoms in Female Borderline-Patients Treated With Lamotrigine 2 March 2007

Marius Nickel,
Professor of Psychiatry
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Re: Change in Anger Symptoms in Female Borderline-Patients Treated With Lamotrigine

m.nickel{at}klinik-badaussee.at Marius Nickel

In a double-blind placebo-controlled study with female borderline personality disorder (BPD) patients (Tritt et al., 2005) we found after eight weeks’ treatment with a daily dose of up to 200 mg lamotrigine, significant changes on most scales of the State-Trait Anger Expression Inventory (STAXI). In followed 18-month open-label observation (lamotrigine treated group continued taking 200 mg lamotrigine daily: n=18; former placebo group without psychopharmica: n=9; Tritt et al, 2005) patients were examined every six months.
The two-factor repeated measure analysis showed (Bonferroni correction) a significant interaction for the group-by-time effect for all STAXI scales according to the intend-to-treat principle: State-Anger, Trait-Anger, Anger Out and Anger Control scales (all p< 0.01), and Anger In Scale (p=0.02) . All patients tolerated lamotrigine relatively well. In the lamotrigine treated group, weight change was no significant than in the former placebo group (p=0.31).
Lamotrigine had a superior effect on the aggressive symptoms in female BPD patients, as indicated by the significantly greater changes in the STAXI scales when compared to the placebo/ex-placebo group for the total observation period. It seems that lamotrigine exerted an effect on the patients in the study on both the threshold for perceiving anger and the intensity of the anger perceived. Socially desirable anger control and the intra-psychological processing of aggression also appeared to be influenced. The follow-up study confirmed the results obtained in the previous short placebo-controlled investigation (Tritt et al, 2005).
Following a longer period of observation, lamotrigine appears to be a safe and effective agent for improving aggression in women with BPD.
Tritt, K., Nickel, C., Mitterlehner, F., et al (2005) Lamotrigine treatment of aggression in female Borderline Personality Disorder Patients: A double-blind, placebo-controlled study. J Psychopharmacol, 19, 287-291.
Marius K. Nickel, MD Clinic for Psychosomatic Medicine and Psychotherapy, Medical University of Graz, Bad Aussee, Austria University Clinic for Psychiatry 1, PMU, Salzburg, Austria 2 Clinic for Psychosomatic Medicine and Psychotherapy 8990 Bad Aussee, Austria Tel.: + 43 3622 521003203, m.nickel@klinik-badaussee.at

Re: Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria 2 March 2007

Dallas P. Seitz,
Resident
Department of Psychiatry, Queen's University Kingston, Ontario, Canada
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Re: Re: Neuroleptic Malignant Syndrome-Time For Revising DSM Criteria

seitzd{at}hdh.kari.net Dallas P. Seitz

To the editors:
Dr. Elias raises an important point regarding potential pitfalls in the diagnosis of neuroleptic malignant syndrome. Classically NMS is described in the literature as having all the signs of fever, muscle rigidity, rhabdomyolysis or elevated serum CK, and autonomic instability. As Dr. Elias' case illustrates, NMS may present without any of these individual features or these features may only be present in an attenuated form. A spectrum of illness concept in NMS has been suggested previously (Adityanjee, 1988) which we would also support.
We would also encourage the authors of the DSM V to exmanine future diagnostic criteria to reflect this heterogeneity in the presentation of NMS. At present, there are at least eight different published diagnostic criteria for NMS present in the literature each with different criterion requirements for diagnosis (Adityanjee, 1999; Nierenberg, 1991). Current criteria should also be examined in light the spectrum of illness apparent in NMS to facilitate earlier diagnosis and treatment of this serious condition.
References:
Andityanjee, Singh S, Singh G, Ong S. Spectrum Concenpt of Neuroleptic Malignant Syndrome.Br J Psychiatry 1988;153:107-111
Andityanjee, Matthews T, Aderibigbe YA. Proposed research diagnostic criteria for neuroleptic malignant syndrome. Int J Neuropsychopharm 1999;2:129-144
Nierenberg D, Disch M, Manheimer E, Patterson J, Ross J, Silvestri G, Summerhill E. Facilitating prompt diagnosis and treatment of neuroleptic malignant syndrome. Clin Pharmacol Ther 1991;50:580-586

Smoking & Mental Health 9 March 2007

Aadil Jan Shah,
Doctor Psychiatry
Gwent Health Care NHS Trust,
Ovais Wadoo,Sheffield Care Trust
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Re: Smoking & Mental Health

aadilshah{at}gmail.com Aadil Jan Shah, et al.

Smoking remains one of the major preventable risk factors for various diseases and has been the focus of the most of the recent biochemical research. Smoking has always been implicated in aeitiology of the ischemic heart diseases,respiratory diseases & other physical problems.The prevelance of smoking is high in mental health conditions & therefore these patients are at increased risk & more susceptible to these physical problems. The prevalence of smoking in schizophrenia greatly exceeds that in the general population (75–92% v. 30–40%). Heavy cigratte smoking has been implicated in the neurobiology of the schizophrenia. Cigratte smoking induces hepatic microsomal enzymes & therefore these patients need increased doses of psychotropic medications. Nearly three quarters of people with schizophrenia, affective psychosis,and other mental health disorders who live in mental health settings are smokers, and they are more likely to be heavier and more dependent smokers than the general population. Being on psychotropic medications further increase the risk of heart,respiratory & other diseases like diabetes.Lack of activities whilst on the wards almost doubles the risk especially for long term patients. Recently there has been lots of debate on Smoking in mental health units.Under the proposed English Health Act regulations most mental health units will be smoke free,although patients will be able to smoke outside. It is going to be a great challenge for the mental heath staff as most of the patients admitted on the psychiatric units are severely distressed & some of them having no insight.They feel smoking helps them to relieve their tension & usually they spend most of their time in smoking rooms whilst inpatient. It is very difficult to predict if these new regulations will decrease the prevelance of smoking in these patients but it will definitely make it easier for staff & other non-smoker patients to avoid passive smoke exposure.
References:
Karen Jochelson, Smoke free legislation & mental health units:the challenges ahead,Karen Jochelson,The British Journal of psychiatry (2006) 189:479-480.
Kelly, C. & McCreadie, R. (2000) Cigarette smoking and schizophrenia. Advances in Psychiatric Treatment, 6, 327–332.
Moira Connolly and Ciara Kelly,Lifestyle and physical health in schizophrenia Advan. Psychiatr. Treat., Mar 2005; 11: 125 - 132.

Chess playing potentiates mental resources in schizophrenia 28 March 2007

Caroline Demily,
assistant professor
Center for Cognitive Neuroscience (CNRS and UniversitÃ© Lyon 1), Bron, France.,
Laurence Jasse, Ghislaine Bailly, and Nicolas Franck
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Re: Chess playing potentiates mental resources in schizophrenia

caroline.demily{at}isc.cnrs.fr Caroline Demily, et al.

The medicinal virtues of the game of chess have been known for some time and have been utilised as early as the tenth century by RhazÃ¨s to treat mental illness. Chess playing strategy is determined by varying configurations of pieces on the board with no significant relation between the type of chess problem and the subjectâ€™s decision rules (Scurrah et al, 1970). Chess cognition is associated with logical reasoning, with a high degree of frontal involvement, particularly in the left orbito frontal and right prefrontal cortex (Nichelli et al, 1994). Similarly, chess players do better than non-chess players on the Tower of London task (Unterrainer et al, 2006). Interestingly, Trail Making Test part B (TMT-B) failure is related to less efficient interaction between visually searching and manually connecting targets, resulting in insufficient sequencing of planning and acting. TMT-B performances seems to be sensitive to lesions of the frontal lobe. This defect is significant in patients with schizophrenia and considered to be a trait-like characteristic or even a vulnerability marker (Wolwer et al, 2002). Consequently, our small pilot study attempted to demonstrate that chess playing would have a therapeutic role in enhancing cognitive performance in schizophrenia (DSMIV criteria). The experimental group of male patients with schizophrenia (n=5, mean age: 32.8 years, mean education: 12 years, mean duration of the illness: 6.6 years, SAPS/SANS total score: 8.4/36.8) received chess training for 600 minutes (12 weekly sessions during 50 minutes). All participants were novice players and profited from individual chess training by data- processing software. We investigated TMT-B performances before (To) and after training (T1: To + 3 months). The duration of training was selected in order to limit the learning effect of repeating the TMT-B. Our results demonstrate a statistical significant influence on test and re-test performance (mean performance time: To=125.6s, T1=75.4s, p<0.05 ; mean number of errors per planning: To=1.8, T1=0, p<0.05). In conclusion, the game of chess could be a serious adjuvant in the treatment of schizophrenia and can notably potentiate capacities of patients. These promising results need replication in a larger cohort before standardized therapeutic use.
Acknowlegments : Gethin Hughes for editing the manuscript.
No declaration of interest.
References : 1 â€“ Atherton, M., Zhuang, J., Bart, W.M., et al (2003). A functional MRI study of high-level cognition. I. The game of chess. Cognitive Brain Research,16, 26-31. 2 â€“ Nichelli, P., Grafman, J., Pietrini, P., et al (1994). Brain activity in chess playing. Nature, 369,191. 3 â€“ Scurrah, M.J., Wagner, D.A., (1970). Cognitive model of problem- solving in chess. Science, 169, 209-211. 4 â€“ Wolwer, W., Gaebel, W., (2002). Impaired trail-Making test-B performance in patients with acute schizophrenia is related to inefficient sequencing of planning and acting. Journal of Psychiatric Research, 36, 407-416. 5 â€“ Unterrainer, J.M., Kaller, C.P., Halsband, U., et al (2006). Planning abilities and chess : a comparison of chess and non-chess. British Journal of Psychology, 97, 299-311.

MTAS predated by 60 years? 11 April 2007

T. C. Russ,
SHO
Tavistock Centre
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Re: MTAS predated by 60 years?

tcruss{at}fish.co.uk T. C. Russ

In the midst of all the confusion surrounding applications to specialist training via MTAS it is comforting to discover that, in the words of Gollum before the gates of Mordor and Tony Blair, “there is a third way”. From 1947 to 1957 The Menninger School of Psychiatry in Kansas studied its methods of selecting trainees and investigated what characteristics in a doctor predicted a successful training outcome, defined as:
“(1) completion of three years of psychiatric residency training; (2) entry into actual psychiatric practice; (3) certification by the American Board of Psychiatry and Neurology; (4) apparent “success” in psychiatric practice; (5) estimates, rated by fellow-residents, of level of competence during residency, in over-all performance and also in each of several major aspects of the resident’s work; and (6) the same, as rated by supervisors.” (Holt & Luborsky, 1958, p. 116).
These 60-year-old criteria seem very familiar when compared to the competency-based curriculum. However, their experimental design for trainee selection also included projective testing, a manualized interview, and a score of how much they liked the candidate.
The authors made a retrospective comparison of personality traits predicting a successful training outcome. Characteristics predictive of competence at the end of training included intelligence, empathy, capacity for good relationships with co-workers, and readiness or capacity for growth and change. Many other variables – including integrity, freedom from stereotypy of thought, psychological curiosity, and a good sense of humour – failed to correlate significantly with psychiatric competence.
It is interesting to reflect on the extent of change in selection of trainees over the last half-century. Having experienced two quite different selection processes recently in London and Yorkshire, I wonder what the outcome data for MTAS selection will be like. In conclusion and after much discussion of projective tests and unconscious motivations for career choice, Holt & Luborsky (1958) highlight that a “careful evaluation of an applicant’s past performance in psychiatric work is one of the most useful predictors of success as a resident.” Surely this cannot have changed? Despite the problems and anxiety surrounding the changeover from the current system, I remain optimistic about the future.
Holt, R. R. & Luborsky, L. (1958). Personality Patterns of Psychiatrists. Basic Books.
Declaration of Interest: TR is an SHO in psychiatry currently applying to continue his specialist training via MTAS.

Earliest evidence for malingering: There is no smoke without fire 2 May 2007

Dr. Menachem Ben-Ezra,
Researcher (Psychologist)
Department of Psychology Tel Aviv University, Israel,
Yuval Palgi
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Re: Earliest evidence for malingering: There is no smoke without fire

menbe{at}post.tau.ac.il Dr. Menachem Ben-Ezra, et al.

Menachem Ben-Ezra & Yuval Palgi
Department of Psychology, Tel Aviv University, Tel Aviv 69978, Israel. E-mail: menbe@post.tau.ac.il
Accounts of malingering prior to the modern era are scarce. Until today, the most notable evidence for malingering in medical history are those presented by the Roman physician Galen who presented two cases. The first is a patient who pretended to suffer for colic in order to avoid a public meeting, while the other faked an injured knee in order to remain home while his master was embarking on a long journey (Lurid, 1941).
We would like to present an even earlier evidence for malingering. According to the bible (Old Testament), King David lived and reigned (1005 BC – 965 BC) at the first millennium BC. In the following example, David fled from Saul after slaying Goliath heading to A’chish King of Gath domain. A’chish people capture him and David was afraid for his life.
“And David rose and fled that day from Saul, and went to A’chish the king of Gath. And the servants of A’chish said to him, “Is not this David the king of the land? Did they not sing to one another of him in dances, ‘Saul has slain his thousands, and David his ten thousands’?” And David took these words to heart, and was much afraid of A’chish the king of Gath. So he changed his behaviour before them, and feigned himself mad in their hands, and made marks on the doors of the gate, and let his spittle run down his beard. Then said A’chish to his servants, “Lo, you see the man is mad; why then have you brought him to me? Do I lack madmen, that you have brought this fellow to play the madman in my presence? Shall this fellow come into my house?” (Samuel, I, 21, 10-15). “David departed from there and escaped to the cave in Adullam” (Samuel, I, 22, 1).
This is an early historical example of malingering as a result from threat to life. The above medical condition clearly accord with the DSM-IV for malingering criteria, especially with context of presentation, and marked discrepancy between the person’s claimed stress and his actual state (American Psychiatric Association, 1994). It is interesting to see this in comparison with modern era malingering as a result of threat to life that have not changed dramatically across time and culture.
REFERENCES
American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA.
Lurid, F.B (1941). Galen on Malingering, Centaurs, Diabetes, and Other Subjects More or Less Related. Proceedings of the Charaka Club, 10, 52-55.

Learned Helplessness: Doctor's in the MTAS experiment? 8 May 2007

Asif M Bachlani,
SHO in psychiatry
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Re: Learned Helplessness: Doctor's in the MTAS experiment?

mad_docasif{at}yahoo.co.uk Asif M Bachlani

During a recent balint group attended at my local posting we were talking about the recent malaise, poor motivation and malaise that was being felt by most of the junior doctors. This was all related to the MTAS fiasco which apart from most of us facing unemployment in august has recently led to personal details being available to all online.
As the discussion progressed it became apparent that most of us felt so much despair and dejection about our chances of success in the upcoming interviews. It is a common belief that no matter what we did to improve our chances that success in this MTAS system was outside our control. That any current efforts put in made no difference and thus we should all give up.
This as I'm coming up to taking my MRCPsych part II exams made me think about Martin Selegman's Dogs and "Learned Helplessness". This is as you recall is the situtation where the dogs were placed in harnesses and given electric shocks. The dog who received shocks but his lever didn't stop the shocks learned to be helpless, and suffered chronic symptoms of clinical depression.
The follow up experiment gave the dogs a warning via a light 10 seconds before giving a shock with the task of jumping over a low barrier to escape such shocks. The group of dogs who had "learned helplessness" from the previous experiment, they just lay down and whined, and even though they could have escaped the shocks, they didn't try.
To put this in context to us junior doctors in 2007 many of us love being doctors and enjoying our profession immensely. We have lost any motivation or drive to jumping this barrier ("getting a training post in the MTAS system"). The old mandate of being a good doctor where we show good competence in managing our patients as well as been trusted and respected by our consultants just seem to lead us to electric shocks. As no matter what we seem to do on a regular basis won't improve our chances in this MTAS system. The Holy Grail of passing exams ("the light warning") giving us the chance to jump over this hurdle seems almost irrelevant as this no-longer seems to guarantee any of us a job.
Being a paranoid person one could think that this was deliberately done by those in government to cause "learned helpless" in us junior doctor so that with our daily pressures we accept anything and everything the government offers no matter how unreasonable or unacceptable the situation is!
References: Petersen, C., Maier, S.F., Seligman, M.E.P. (1995). Learned Helplessness: A Theory for the Age of Personal Control. New York: Oxford University Press.

More about smoke-free mental health units 29 May 2007

Vincenzo Villari,
Psychiatryst and Psychotherapyst
Director of the Psychiatric Emergency Service, S. Giovanni Battista Hospital, Torino, Italy,
Giulio Barzega
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Re: More about smoke-free mental health units

vvillari{at}molinette.piemonte.it Vincenzo Villari, et al.

Concerning the issue of smoke-free mental health units we noticed with great interest Jochelson (2006) editorial and comments related to it by Arnone and Simmons (2007) and Williams (2007). Our experience concern a psychiatric emergency service (pes) situated in S. Giovanni Battista Hospital of Turin. Our division is an acute and admission unit and consists of fourteen bed with 24 hour\day admission from Emergency Department. According with the Italian law that had introduced a total smoking ban in all public facilities since last few years we decided to face the problem. After a complete theoretical exam of current international literature and a deep internal debeate we adopted a complete smoking ban. We noticed also, as other authors did (Lawn et al. 2002, Velasco et al 1996), that when restrictions are graduated over time, they can have the unintended consequences of focusing on the negotiation of smoking privileges, increasing the value of cigarettes as a tool for exchange and therefore heightening the potential for conflict (Jochelson 2006).
Our observation, concording with literature (Dickens et al. 2005, Stubbs et al. 2004), is that staff generally anticipated more smoking- related problems than actually occurred. In our unit infact, following the ban, as patients still had the opportunity to smoke outside, there was no increase in: aggressions and violent episodes; chemical and physical restrain; discharges against medical advice; use of as-needed medication; staff complaints and burden as misured by number of nurses’s injuries, absences and turnover rate. Patients are allowed to smoke outside the building but for some patients this may not be possible because of the risk posed to themselves or others. For these patients it should be necessary to provide indoor designated smoking facilities with specified premises ruled by staff (Williams 2007). Despite this, we noticed also a clear evidence of the lack of consideration that practitioners give to patient quit rates and relapse rates and to staff quit rates also. Clear policies and collaborative partnership between hospitals and community services are needed to provide continuous and consistent pathways of care and support. This is essential if the gains achieved in inpatient settings where bans are imposed are to continue in the community. At the moment resumption of smoking after discharge is the most likely outcome (Arnone e Simmons 2007).
Another point concerns the importance of working on boundaries in an institutional setting. About this we hypotized that try to face the containment issue at a more high level based on mentalization and negotiation between staff and patients helps management of behavioural problems. Often, even though of course not always, can be true that to set the potential conflictuality at a symbolic level could be useful to reduce the risk of acting outs, psysical violence and the need of restrain.
Our experience seems to suggest that introduction of smoking bans in psychiatric inpatient settings is possible but would need to be a clearly and carefully planned process involving as a growing oportunity all parties affected by the bans. On the other hand smoking bans in inpatient setting is seen as only part of a much larger strategy needed to overcome the high rates of smoking and pyshical illness among psychiatric population.
Giulio Barzega and Vincenzo Villari, Psychiatric Emergency Services, S. Giovanni Battista Hospital, Corso Bramante 88, 10126 Torino, Italia
References
Arnone, D., Simmons, LJ. (2007) Smoke-free mental health units. British Journal of Psychiatry (letter), 190, 449.
Dickens, G., Stubbs, J., Popham, R., et al. (2005) Smoking in a forensic psychiatric service: a survey of impatient views. Journal of Psychiatric and Mental Heath Nursing, 12,672-678.
Jochelson, K. (2006) Smoke-free legislation and mental health units: the challenges ahead. British Journal of Psychiatry,189,479-480.
Lawn, SJ., Pols, RG., Barbe, JG. (2002) Smoking and quitting: a qualitative study of community-living psychiatric clients. Social Science and Medicine, 54,93-104.
Velasco, MD., Ells TD., Anderson, R., et al. (1996) A two-year follow up on the effects of a smoking ban in an impatient psychiatric service. Psychiatric Services,47,869-871.
Stubbs, J., Haw, C., Garner, L. (2004) Survey of staff attitudes to smoking in a large psychiatric hospital. Psychiatric Bulletin, 28,204-207.
Williams, A. (2007) Smoke-free mental health units. British Journal of Psychiatry (letter), 190, 449-450.

Varenicline significantly reduced smoking in a mentally ill person 29 May 2007

Enrique L.-M. Ochoa,
MD, PhD
Department of Psychiatry and Behavioral Sciences, University of California, Davis, and Turning Point
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Re: Varenicline significantly reduced smoking in a mentally ill person

elochoa{at}ucdavis.edu Enrique L.-M. Ochoa

Dear Editor: Varenicline, a partial agonist of ƒÑ4ƒÒ2-neuronal nicotinic acetylcholine receptors (nAChRs) is efficacious for smoking cessation (Coe et al, 2005a). It is superior to both placebo and bupropion (Jorenby et al, 2006). The varenicline registration trials have excluded mentally ill people from their study populations (Jorenby et al, 2006), despite the fact that nicotine dependence is more prevalent in mentally ill patients when compared to non-mentally ill smokers (Hughes et al, 1986). I here report the case of a 56 year old Caucasian woman with diagnoses of Bipolar Disorder Not Otherwise Specified, and both Nicotine and Opioid dependence. In August 2005, she was clinically depressed (Montgomery Asberg Depression Rating Scale (MADRS) total score of 28. She had 3 or more in the inner tension, reduced sleep, concentration, inability to feel, pessimistic thoughts, and lassitude subscales). She was neither psychotic, nor manic or hypomanic. Her smoking status was evaluated by reports from both the patient and her case worker. Her Fagerstrom score was 9, with a daily consumption of 20-25 cigarettes, smoked mainly within 5 minutes after awakening. Other diagnoses were chronic obstructive pulmonary disease (COPD) and hypercholesterolemia. The patient had a normal electrocardiogram, a body mass index of 35, and routine laboratory work within normal limits except for elevated LDL (141 mg/dL). I treated her with escitalopram (10 mg/d), clonazepam (4 mg /d), and ziprasidone (160 mg/d). An Addiction Medicine specialist prescribed and managed methadone (20 mg /d). She was seen fortnightly. One year later, escitalopram was replaced by bupropion SR (300 mg/d) in an attempt to treat both depressive symptoms and nicotine dependence. Smoking continued. At the end of November 2006, patient decided to stop smoking due to an aggravation of her COPD symptoms. I initiated 0.5 mg varenicline daily for three days, then 1 mg daily in divided doses for four days, to reach a standing daily divided dose of 2 mg. After two months of treatment she was smoking 6 cigarettes, after three months, 6 to 3, and after 4 months (and to this date), 3 cigarettes. She never developed withdrawal symptoms neither she experienced an increase in smoking behaviour. Her Fagerstrom test after 103 days of treatment showed a score of 3.5 (low to moderate dependence). She now waits half an hour or more to smoke her morning cigarette and can refrain from smoking when ill or when exposed to tobacco-free areas. Her depression improved (MADRS total score: 13 after 3 months, with no subscale scores above 2). Bipolar disorder patients exhibit marked cognitive impairment (Green, 2006). Since nicotine has mild cognitive enhancing effects by acting on nAChRs (Ochoa & Lasalde-Dominicci, 2007), and varenicline is a selective ƒÑƒ¤ƒÒƒ¢-nAChR partial agonist (Coe et al, 2005a) we explored the possibility of a cognitive enhancing effect of the drug. I used the Purdon Screen for Cognitive Impairment in Psychosis routinely used in my practice (Ochoa & Clark, 2006). The results are depicted in Table I. Surprisingly, her cognitive scores were not improved after three months of varenicline therapy. Disclaimer: ELMO is a member of the Speaker¡¦s Bureau for Janssen Pharmaceutica and Bristol Myers-Otsuka. He wants to thank Pfizer from providing samples when the drug was not available for prescribing in the USA. REFERENCES Coe, J. W., Brooks, P. R., Vetelino, M. G., et al (2005a) Varenicline: an alpha4beta2 nicotinic receptor partial agonist for smoking cessation. J Med Chem, 48, 3474-3477. Jorenby, D. E., Hays, J. T., Rigotti, N. A., et al (2006) Efficacy of varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, vs placebo or sustained-release bupropion for smoking cessation: a randomized controlled trial. Jama, 296, 56-63. Hughes, J. R., Hatsukami, D. K., Mitchell, J. E., et al (1986) Prevalence of smoking among psychiatric outpatients. Amer. J. Psych., 143, 993-997. Green, M. F. (2006) Cognitive impairment and functional outcome in schizophrenia and bipolar disorder. J Clin Psychiatry, 67, 3-8. Ochoa, E. L. M. & Lasalde-Dominicci, J. (2007) Cognitive deficits in schizophrenia: focus on neuronal nicotinic acetylcholine receptors and smoking. Cell. Mol. Neurobiol., (in the press). Ochoa, E. L. M. & Clark, E. (2006) Galantamine may improve Attention and Speech in Schizophrenia. Human Psycopharmacol., 21, 127-128.

Personality disorder managed in the general psychiatry setting 27 June 2007

Rosemary Smyth,
SpR in Psychiatry
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Re: Personality disorder managed in the general psychiatry setting

rhsmyth{at}doctors.org.uk Rosemary Smyth

With the anticipated changes in the proposed Mental Health Bill, we will be expected as psychiatrists to broaden our conceptualisation of treatment and treatability, especially where people who would come under the remit of DSPD are concerned. This is causing controversy as change does, particularly when initial motives may seem more political than therapeutic (Maden, 2007). However, while DSPD remains high profile, personality disorder (PD) in the broader sense occurs frequently in clinical practice for all psychiatrists, with estimates of 20-40% of psychiatry outpatients and 50% of inpatients fulfilling criteria for PD (Davison, 2002).
As PD is being re-examined as a more treatable condition, there have been discussions about changing current classification from categorical to dimensional in DSM V, and even questions raised again about the appropriateness of PD lying under a separate axis to axis I disorders (Widiger et al. 2005). If PD is to be regarded as treatable, perhaps classifying it as an axis I disorder makes sense. The concern that the diagnosis of PD would be forgotten when in competition with more florid disorders (Tyrer et al., 2007) occurs in clinical practice even while PD is on a separate axis. In general psychiatry, clinicians and CMHTs treat a significant proportion of patients with co-morbid axis II diagnoses. While there is evidence that the presence of PD impacts on use of inpatient and outpatient services (Kent, Fogarty & Yellowlees, 1995), severity of psychopathology in axis I disorders (Tyrer et al., 1990), and while we are reasonably good at agreeing on the presence of PD (albeit ‘Not Otherwise Specified’) (Tyrer, 2007) little direct attention is usually paid to the PD because the axis I symptoms are more prominent.
Personality disorder services are being set up nationwide, so people whose primary diagnosis is PD are more likely to be offered appropriate specialised treatment. I hope that as these specialist services evolve they will play a part in training and consultation to general psychiatry teams to optimise mindful, consistent and confident management for the large number of patients with co-morbid axis I and II diagnoses these teams manage.
REFERENCES
Davison, S. (2002) Principles of managing patients with personality disorder. Advances in Psychiatric Treatment, 8, 1-9.
Kent, S., Fogarty, M., Yellowlees, P (1995) Heavy utilization of inpatient and outpatient services in a public mental health service. Psychiatric Services, 46, 1254-1257.
Maden, A. (2007) Dangerous and severe personality disorder: antecedents and origins. British Journal of Psychiatry, 190 (suppl. 49), 8-11.
Tyrer, P. (1990) The Nottingham Study of Neurotic Disorder: relationship between personality status and symptoms. Psychological Medicine, 20, 423-31.
Tyrer, P. (2007) Critical developments in the assessment of personality disorder. British Journal of Psychiatry, 190 (suppl. 49), 51- 59.
Widiger, T., Simonsen, Z., Krueger, R., et al. (2005) Personality Disorder Research Agenda for the DSM V. Journal of Personality Disorders, 19, 315-339.

How Accessable are Website-Based Informational Resources for Disabled People? 6 July 2007

Gavin J. Newby,
Consultant Clinical Neuropsychologist
Western Cheshire PCT,
Christine Groom
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Re: How Accessable are Website-Based Informational Resources for Disabled People?

gavin.newby{at}wcheshirepct.nhs.uk Gavin J. Newby, et al.

The Editor British Journal of Psychiatry
Sir/Madam,
We have grave concerns that many NHS service-linked information websites may be failing in their primary purpose of helping vulnerable people become empowered through access to meaningful information.
We recently asked 21 current severely brain injured clients attending our community rehabilitation service to evaluate our service website and complete practical tasks to show how usable the site was. The website is hosted within our PCT’s larger site and aims to provide information on a range of relevant issues from “what is a brain injury?” to “returning to driving”.
Although the participants’ overall evaluations were favourable, the assessment process highlighted problems with legibility and comprehension and identified confusing elements in the layout. In common with many public service websites, neither our website nor its PCT host fully complied with the Disability Discrimination Act (HMSO, 1995)’s Code of Practice (Disability Rights Commission, 2002) or the Internet governing body, the World Wide Web Consortium (W3C, 1999)’s accessibility guidelines (Webcredible, 2005).
We feel our study shows a real need for actual users to be involved in the development and maintenance of NHS information websites to ensure maximum accessibility. We have been impressed that our PCT has taken on board the findings of our work and are willing to incorporate our suggested site modifications and have invited two of our users to join a web readers’ panel across the whole trust.
References
Disability Rights Commission (2002): http://www.drc- gb.org/the_law/legislation__codes__regulation/codes_of_practice.aspx
HMSO (1995): http://www.opsi.gov.uk/acts/acts1995/1995050.htm (paper version: Disability Discrimination Act 1995 (c. 50), ISBN 0 10 545095 2.)
W3C (1999): http://www.w3.org/TR/WAI-WEBCONTENT/full-checklist.html
Webcredible (2005): http://www.webcredible.co.uk/user-friendly- resources/web-accessibility/uk-website-legal-requirements.shtml
Dr Gavin Newby Dr Christine Groom Consultant Clinical Neuropsychologist Trainee Clinical South Cheshire Acquired Brain Injury Psychologist Service Lancaster Univ. Acorn Suite Doctoral Course in 1829 Building Clinical Psychology Countess of Chester Health Park Liverpool Road Chester CH2 1HJ
e-mail: Gavin.Newby@wcheshirepct.nhs.uk
Declaration of Interest
Dr. Newby is directly employed by the Western Cheshire PCT as Consultant Clinical Neuropsychologist for the South Cheshire Acquired Brain Injury Service
Dr. Groom is currently a trainee Clinical Psychologist with the Lancaster University Doctoral Course in Clinical Psychology. The study referred to in the letter was completed in part-fulfilment of her doctoral studies and funded by Lancaster University.

Deinstitutionalization of mental illness: At what cost? 12 July 2007

Sahoo Saddichha,
Resident in Psychiatry
Central Institute of Psychiatry, Ranchi, India
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Re: Deinstitutionalization of mental illness: At what cost?

saddichha{at}gmail.com Sahoo Saddichha

Mental illness is one of the biggest contributors to mortality and morbidity today (NASMHPD, 2006). It causes distress, not just to the individual, but also to the carer and the family of the ill. Recent trends in treatment of mental illness have aggressively targeted community participation while systematically promoting deinstitutionalization of such individuals (Parabiaghi et al., 2006; WHO, 2005). These augur well for the future of psychiatric illnesses and take care of the patients’ rights as an individual. However, most of these approaches do not often take into account the massive suffering that families go through while caring for mentally ill patients who are notorious for their poor compliance to treatment. As a psychiatry resident, who has been trained in empathy and understanding of psychopathology, I am however moved many a times by the plight of families that I see regularly in my practice. There have been numerous instances where the primary care-giver has literally begged me to admit the patient so that the family may become functional again. At other times, the carers have often been afflicted by psychiatric illnesses themselves, occurring as a reaction to the severe mental trauma that they have undergone. Such instances often put me in a dilemma whether to put the individual first or listen to the family. Is our duty as a doctor only to the patient or does it also involve his family? The principle of triage would suggest that I listen to the family rather than the individual, while the Hippocratic Oath enforces me to always do good for the patient. What then is the way out? These are questions to ponder about even when there is increasing recognition that deinstitutionalization has come at a cost of increased cost of care to the community and a poorer outcome (WHO, 2005).
Competing Interests: None.
References:
1.Morbidity and Mortality in People with Serious Mental Illness (2006). NASMHPD. Accessed on July 10, 2007 from http://www.nasmhpd.org/general_files/publications/med_directors_pubs/Technical%20Report%20on%20Morbidity%20and%20Mortaility%20 -%20Final%2011-06.pdf
2.Parabiaghi A, Bonetto C, Ruggeri M, Lasalvia A, Leese M (2006). Severe and persistent mental illness: a useful definition for prioritizing community-based mental health service interventions. Social Psychiatry and Psychiatric Epidemiology, 41(6), 457-63.
3.World Health Organization, WHO (2005). Resource Book on Mental Health: Human rights and legislation- ISBN 924156282 (PDF).

Reply to Peter Tyrer 12 July 2007

Jesper Bent-Hansen,
MD
Psychiatric Research Unit, Hilleroed, Denmark
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Re: Reply to Peter Tyrer

pebe{at}noh.regionh.dk Jesper Bent-Hansen

In ‘From the Editor’s desk’ (Brit J Psychiatry 2007), Tyrer refers to a new depression questionnaire for the screening of major depression and asks: “… will assessment favour the simple Depression Scale (Poutanen et al 2007) in the years to come or still echo with the name of Hamilton?”
A closer look at this non-Hamilton Depression Scale shows, that approximately 6 (or 60 %) of the 10 items in the simple Depression Scale in fact cover the first Hamilton item (depressed mood) (Hamilton1967). The contents of the remaining 4 (or 40 %) of the items are contained in the Hamilton items of insomnia and general somatic symptoms. It would have been of scientific interest if Poutanen et al (2007), with focus on the item of depressed mood, had compared their depression questionnaire with our self-rating version of the Hamilton Depression Scale (Bent-Hansen et al 1995).
The Major Depression Inventory (Olsen et al 2003), which is a widely used short depression questionnaire developed on the basis of the DSM-IV and ICD-10 concepts of major depression, has been found valid when using the Present State Examination or the Hamilton Depression Scale as indices of validity. The Major Depression Inventory is as simple as the questionnaire Tyrer (2007) is referring to, but covers much more exhaustively the symptoms of major depression.
References:
Bent-Hansen J, Lauritzen L, Clemmesen L, Lunde M, Kørner A. A definite and a semidefinite questionnaire version of the Hamilton/Melancholia (HDS/MES) scale. J Affect Disord 1995;33:143-150
Hamilton M. Development of a rating scale for primary depressive illness. Br J Soc Clin Psychol 1967;6:278-296
Olsen LR, Jensen DV, Noerholm V, Martiny K, Bech P. The internal and external validity of the Major Depression Inventory in measuring severity of depressive states. Psychol Med 2003; 33, 351-356
Poutanen O, Koivisto A-M, Joukamaa M, Mattila A, Salokangas RKR. The Depression Scale as a screening instrument for a subsequent depressive episode in primary healthcare patients. Brit J Psychiatry 2007;191:50-54
Tyrer P. From the Editor’s desk. Brit J Psychiatry 2007;191:96
J. Bent-Hansen, MD Psychiatric Research Unit Frederiksborg General Hospital DK-3400 Hillerød Denmark

Reinstating clozapine after associated Diabetic ketoacidosis 1 August 2007

John H M Crichton,
Consultant Forensic Psychiatrist
Royal Edinburgh Hospital,
Robert Brodick, Matthew Young, Fionnbar Lenihan
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Re: Reinstating clozapine after associated Diabetic ketoacidosis

john.crichton{at}lpct.scot.nhs.uk John H M Crichton, et al.

Reinstating clozapine after associated diabetic ketoacidosis
Sir: Diabetic ketoacidosis (DKA) is an increasingly recognised side- effect of clozapine therapy (Jin et al. 2004). Although potentially fatal, the condition is usually transient once clozapine therapy has been discontinued. There have been reports of hyperglycaemia on reinstituting the drug after remission from the acute episode (Colli et al. 1999). However, there is now some evidence that restarting clozapine in such cases is not absolutely contraindicated; Wilson et al. 2002 reported two patients which remained well after reinstating treatment.
We report a third such case, a 38 year old woman of African origin with a 9 year history of treatment resistant paranoid schizophrenia with a prominent affective element, in the context of a positive family history of schizophrenic illness. She also took sodium valproate 800mg twice daily but had no previous diabetes; her only medical history of note is a sickle cell trait and obesity. Resistant to other antipsychotics, she was commenced on clozapine, gradually increasing to 550 mg daily. 5 weeks later she began to complain of increasingly severe abdominal pain and became difficult to rouse. On hospital admission she was found to have DKA, with blood glucose of 38.1 mmol/l. She was managed with intravenous fluid and insulin. Clozapine was stopped for 3 days before being reintroduced gradually.
Having made a good recovery, insulin was gradually withdrawn over a period of months. She continues on clozapine 900 mg/day. Five years after the event there have been no further episodes of DKA and she is on neither insulin or oral hypoglycaemic medication. There continues to be glucose intolerance with a glycated haemoglobin HbA1c of 7.2% in the context of a poorly adhered to diabetic diet.
Why clozapine might precipitate DKA is not fully understood. Although antipsychotics are well known to cause insulin resistance, the condition is characteristic of Type I diabetes mellitus so is unlikely to be due to insulin resistance alone. It is thought therefore that insulin secretion itself is reduced, perhaps from transient pancreatic damage (Liberty et al, 2004) but the mechanism for this is yet to be elucidated.
This case adds further evidence that restarting clozapine therapy may be successful in patients who have suffered from DKA associated with its use previously. We would still advise great caution and strongly encourage close glycaemic-monitoring. It also highlights the need for glucose monitoring during initiation with clozapine and research into this area.
Colli, A., Cocciolo, M., Francobandiera, G., et al. (1999) Diabetic ketoacidosis associated with clozapine treatment. Diabetes Care, 22 (1), 176-177
Jin, H., Meyer, J.M., Jeste, D.V. (2004) Atypical antipsychotics and glucose dysregulation: a systematic review. Schizophrenia Research, 71, 195-212
Liberty, I.F., Todder, D., Umansky, R., et al. (2004) Atypical Antipsychotics and Diabetes Mellitus: An Association. Israel Medical Association Journal, 6, 276-279
Wilson, D.R., D’Souza, L., Sarkar, N., et al. (2002) New-onset diabetes and ketoacidosis with atypical antipsychotics. Schizophrenia Research, 59, 1-6
Robert Brodrick, Medical student The University of Edinburgh
John Crichton, Consultanbt Forensic Psychiatrist Orchard Clinic, Royal Edinburgh Hospital
Matthew Young, Consultant Physician Royal Infirmary of Edinburgh
Fionnbar Lenihan, Consultant Forensic Psychiatrist Orchard Clinic, Royal Edinburgh Hospital
Correspondence: J Crichton, The Orchard Clinic, Royal Edinburgh Hospital, Morningside Terrace, Edinburgh EH10 5HF, UK. Tel: +44 (0)131 5375858; fax: +44 (0)131 537 5857; email: john.crichton@lpct.scot.nhs.uk.
Declaration of interest: none

Smoking as a possible confounder in metabolic disease and cardiovascular risk with antipsychotics 15 August 2007

Bo-Jian Wu,
psychiatrsit
Department of Psychiatry, Yuli Hospital, Department of Health, Taiwan,
Tsuo-Hung Lan, Hsien-Jane Chiu, Tsung-Ming Hu, and Yung-Chang, Tuan
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Re: Smoking as a possible confounder in metabolic disease and cardiovascular risk with antipsychotics

jamsab{at}mail2000.com.tw Bo-Jian Wu, et al.

TO THE EDITOR: We would like to contribute comments on the article ¡§Metabolic disease and cardiovascular risk in people treated with antipsychotics in the community¡¨ by Paul Mackin and colleagues (Mackin, Bishop, Watkinson, et al, 2007). As to smoking problems between people with mental illness and controls, the authors stated that ¡§although significantly more people with mental illness smoked compared with controls, differences in smoking behavior did not account for the excess metabolic and cardiovascular risk¡¨. It implied that in this study, it appeared to be acceptable to neglect the fact of significant difference of smoking status between these two groups before reaching the conclusion of higher cardiovascular risk in people treated with anitpsychotics. We think it is kind of premature to make such a statement because of reasons as follows. As the authors described, cumulative evidence has reveals tobacco smoking is a well-established risk factor for cardiovascular disease. Therefore, we cannot neglect it in calculating the risk of cardiovascular disease in this study. Additionally, it is very clear that smoking status is an important variable in the University of Edinburgh of Cardiovascular Risk Calculator as the authors used. If we use the data of table 3 in this article, and put it to the calculator to estimate a man, aged 50, blood pressure: 135/81 mm Hg, total cholesterol 7.1mmol/L, HDL: 0.9 mmol/L. The probability of developing cardiovascular disease in next 10 years is jumping from 17.9% without smoking (moderate risk) to 26.6% with smoking (high risk). Hence, it is impossible to discount the smoking status in these two groups to gain metabolic parameters in table 3 and ten-year cardiovascular risk in table 4 in this article. Moreover, the authors indicated that there seemed to be no excessive risk caused by smoking by using ¡§univariate ANOVA¡¨ in comparing the metabolic and cardiovascular parameters between groups with smoking and without smoking. In fact, it is not enough to use this method to disregard the significance of smoking effect on metabolic and cardiovascular parameters. If we want to test whether the smoking status is a confounder for metabolic parameters between these two groups, we can test the difference before and after putting smoking status as an independent variable in a regression model which adjusting for other variables such as age, sex, BMI and so on. In fact, for the purpose of removing smoking effect from these two groups, we suggest two methods: using regression model for controlling for smoking status or comparing people taking antipsychotics with smoking status- matched normal control group. Nevertheless, the article by Paul Mackin and colleagues has shown that anitpsychotics may play an important role in increasing the cardiovascular risk and metabolic disease. In addition, we would like to emphasize that associated confounder such as smoking status is an important factor which should be deal with properly in designing similar studies. REFERENCES Mackin, P., Bishop, D., Watkinson, H., et al (2007) Metabolic disease and cardiovascular risk in people treated with antipsychotics in the community. Br J Psychiatry, 191, 23-29.
Declaration of Interest: Nil Authors: Tsuo-Hung Lan*,Bo-Jian Wu*, Hsien-Jane Chiu*, Tsung-Ming Hu* and Yung-Chang Tuan* Corresponding Author: Bo-Jian Wu *Department of Psychiatry, Yuli Hospital, Department of Health, 448 Chung Hua Road. Yuli Township, 981, Hualien County, Taiwan 886-3-8886141; jamsab@mail2000.com.tw

The heartland of psychiatry 6 September 2007

Deborah A Mountain,
Consultant Psychiatrist
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Re: The heartland of psychiatry

Debbmountain{at}aol.com Deborah A Mountain

Dear Editor
The heartland of psychiatry
The idea that schizophrenia has become the heartland of psychiatry and is responsible for the development of the profession is interesting (GoodwinG, Geddes J,2007). It is true that schizophrenia has dominated services and policy in mental health to the exclusion of other diagnoses including chronic depression (National Service Framework, Department of Health,1999). In many circumstances, clinicians have been marginalized and other stakeholders have more authority. Some aspects of modern psychiatry have been detrimental to service provision most notably the poor quality of inpatient services. Is the focus on schizophrenia responsible for this? There are a number of other possible explanations for how psychiatry has developed.
The NHS is in the political arena and politicians have taken charge of the health agenda leading to distortions of care. Interestingly, schizophrenia is almost absent from the GP GMS contract. There is also the legacy of the scandals of asylums and how people were treated before the hope of antipsychotic treatment. This has less to with schizophrenia as a diagnosis, but more to do with society’s response to psychosis and how people with severe mental illness were treated. Another factor is the involvement of the wider community in people’s lives after closure of asylums. This includes patients making connections, leading to service user involvement and development of social care. Psychiatry as a profession has struggled to adapt to the varying perceptions of mental illness and has not clearly defined its role in relation to the diverse range and agendas of organisations involved in mental health. We have been over pessimistic - hence the reluctance to tell people their diagnosis of schizophrenia (Coryall W and Tsuang M ,1986 ). The chronic nature of schizophrenia impacts on all aspects of peoples’ lives and we have continued to focus on acute care, designed services around episodic care and not engaged with patients and their families taking a longitudinal perspective. Some of this may be due to the difficulty of maintaining enthusiasm and innovation in face of ongoing disability and despair. This has given other models opportunity to become dominant, especially the social model.
Changing the focus to bipolar disorder will not change this. The argument used is doctors’ skills are best placed working with less dependant patients, those less likely to require social care, more likely to benefit from complex prescribing regimes including separate acute and long term medication. This emphasises the narrow role of doctors as prescribers and reinforces the episodic model of care. It is possible to work as doctors with the social model, speak of patients, illness and as researchers examine what models of care actually work for patients. Psychiatrists’ skills lie in developing a framework of care for our patients using knowledge of illness and understanding of symptoms. We need to be teaching junior doctors to manage patients with mental illness irrespective of diagnosis while working with a range of people and develop the skills required to maintain a longitudinal perspective.
Coryall W and Tsuang M (1986) Outcome after 40 year in DSM111 shizophreniform disorder. Archives of General Psychiatry 43 324-328
Department of Health (1999) National Service Framework for Mental Health
Goodwin G. Geddes J (2007) What is the heartland of psychiatry? British Journal of Psychiatry, 191, 189-191
Dr Deborah Mountain Consultant Psychiatrist Royal Edinburgh Hospital Morningside Terr Edinburgh EH105HF Debbmountain@aol.com
Declaration of interest - none

Australian Firearms Data Requires a Cautious Approach 6 September 2007

Samara McPhedran
1: University of Sydney, 2: The International Coalition for Women in Shooting and Hunting (WiSH),
Jeanine Baker
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Re: Australian Firearms Data Requires a Cautious Approach

samaram{at}psych.usyd.edu.au Samara McPhedran, et al.

We note with interest Kapusta and colleagues’ (2007) work on firearm suicide and homicide following legislative reform in Austria. However, a note of caution must be applied to Kapusta et al's statements concerning apparent consistency between Austrian and Australian experiences with firearms legislation.
Recent work demonstrates that Australia's 1996 gun laws had no significant impact on firearm homicide, but that the pre-existing decline in firearm suicide accelerated post-reforms (Baker & McPhedran, 2007; Chapman et al., 2006). There has been an accompanying decline in non- firearm suicides, beginning in the late 1990's.
Unfortunately, these findings may require re-evaluation due to data quality issues. The Australian Bureau of Statistics (ABS), a primary data source for researchers in the field, appear to be 'over-counting' unintentional deaths and 'under-counting' suicides.
De Leo (2007) showed that ABS data 'under-counted' the total number of suicides (all methods) in one Australian State (Queensland) by 127 cases, in 2004 alone. Re-analysis of the updated data ameliorated the apparent downward trend in suicides that had emerged from previous analyses. This finding has significant implications for assessment of suicide prevention initiatives in Australia, given that most assessments are based on ABS data.
Consequently, it has been suggested that the incidence of firearm suicide in Australia may be higher than thought, and, if so, then studies using ABS suicide figures merit re-evaluation (McPhedran & Baker, in press). In addition, the National Injury Surveillance Unit has questioned the accuracy of homicide data, which suggests firearm homicides, too, may be higher than ABS data show.
There are growing calls for ABS data to be crosschecked against coronial records, and for ABS records to be updated where discrepancies are found.
While this situation does not bear directly upon the findings of the Austrian study, other than reinforcing the importance of quality control, it demonstrates that drawing conclusions about the impact or otherwise of restrictive firearms legislation in Australia may be premature.
Effective public health initiatives need to be built on accurate information. As such, we caution researchers against citing Australian figures during wider discussions of the possible role of firearms legislation in public health strategies, until and unless full data accuracy can be guaranteed.
S. McPhedran, PhD, & J. Baker, PhD.
Affiliations: Samara McPhedran is affiliated with the School of Psychology, University of Sydney, NSW, Australia, 2006. Samara McPhedran and Jeanine Baker are both affiliated with the International Coalition for Women in Shooting and Hunting (WiSH).
References: Baker, J., & McPhedran, S. (2007). Gun laws and sudden death: did the Australian firearms legislation of 1996 make a difference? British Journal of Criminology, 47, 455-469. doi:10.1093/bjc/azl084. Advance access published October 18, 2006.
Chapman, S., Alpers, P., Agho, K., & Jones, M. (2006). Australia's 1996 gun law reforms: faster falls in firearm deaths, firearm suicides, and a decade without mass shootings. Injury Prevention, 12 (6), 365-372.
De Leo, D. (2007). Suicide mortality data needs revision. Medical Journal of Australia, 186, 157.
Kapusta, N.D., Etzerdorfer, E., Krall, C., & Sonneck, G. (2007). Firearm legislation reform in the European Union: impact on firearm availability, firearm suicide and homicide rates in Austria. British Journal of Psychiatry, 191, 253-257. doi:10.1192/bjp.bp.106.032862.
McPhedran, S., & Baker, J. (in press). Australian firearms legislation and unintentional firearm deaths: A theoretical explanation for the absence of decline following the 1996 gun laws. Public Health. doi:10.1016/j.puhe.2007.05.012.

Comment on the efficacy and tolerability of sertindole (Serdolect®) 7 September 2007

Joseph C.J.R. Peuskens,
psychiatrist, medical director
UC Sint-Jozef, campus Kortenberg, Belgium
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Re: Comment on the efficacy and tolerability of sertindole (Serdolect®)

joseph.peuskens{at}uc-kortenberg.be Joseph C.J.R. Peuskens

Comment on the efficacy and tolerability of sertindole (Serdolect®) for the treatment of schizophrenia following reintroduction to the market
Dear Sir
Last year, the European Commission (EC) lifted the marketing restrictions on the atypical antipsychotic sertindole (Serdolect [H. Lundbeck A/S, Denmark]). The Committee for Proprietary Medicinal Products (CPMP) withdrew the compound from the marketplace in 1998 due to concerns about QT prolongation and sudden cardiac death but, following subsequent investigations, the suspension was lifted. The agent is now generally available on the understanding that all patients undergo regular electrocardiogram (ECG) monitoring and those at risk of cardiac events are excluded.
Clinical data have suggested that sertindole causes more dose-related QT prolongation than most other antipsychotics.1,2 However, preclinical data indicate that QT prolongation alone is not predictive of the risk of life-threatening arrhythmias,3 and extensive post-marketing follow-up shows cardiovascular mortality rates with sertindole comparable to those of other antipsychotics, such as risperidone (Risperdal® [Jansen, L.P., United States]).4
A recently published clinical trial comparing the efficacy of sertindole with that of risperidone found sertindole to be at least as effective as risperidone in patients with schizophrenia.5 Sertindole improves both positive and negative symptoms of schizophrenia. Furthermore, it is generally well tolerated, shows no sedative effects and is associated with a low rate of extrapyramidal symptoms (EPS).6 A neurocognitive study of sertindole versus haloperidol suggested superior efficacy with sertindole compared with haloperidol in several cognitive domains, including working memory, speed of processing, and planning and problem-solving.7
The usefulness of an antipsychotic lies in its day-to-day performance, how patients feel and function during treatment, and how well they comply with prescriptions. As with the introduction of every new antipsychotic, considerable hope is attached to the launch of sertindole. It is anticipated that sertindole may prove helpful in reducing the negative symptoms, EPS and sedation that are typically associated with antipsychotics and that this agent may also enhance cognition, thus improving quality of life in patients with schizophrenia.
Word count: 299
Declaration of interest: Consultant for H. Lundbeck A/S, Denmark
References
1. van Kammen D, McEvoy JP, Targum SD, Kardatze D et al. A randomized, controlled, dose-ranging trial of sertindole in patients with schizophrenia. Psychopharmacol Ser (Berl) 1996;124:168–75
2. Pezawas L, Quiner S, Moertl D, Tauscher J et al. Efficacy cardiac safety and tolerability of sertindole: a drug surveillance. Int Clin Psychopharmacol 2000;15:204–14
3. Eckardt L, Breithardt G, Haverkamp W. Electrophysiological characterization of the antipsychotic drug sertindole in a rabbit heart model of torsade de pointes: low torsadogenic potential despite QT prolongation. J Pharmacol Exp Ther 2002;300:64–71
4. Moore N, Hall G, Sturkenboom M, Mann R et al. Biases affecting the proportional reporting ratio (PPR) in spontaneous reports pharmacovigilance databases: the example of sertindole. Pharmacoepidemiol Drug Saf 2003;12:271–81
5. Azorin JM, Strub N, Loft H. A double-blind, controlled study of sertindole versus risperidone in the treatment of moderate-to-severe schizophrenia. Int Clin Psychopharmacol 2006;21:49–56
6. Murdoch D, Keating GM. Sertindole: a review of its use in schizophrenia. CNS Drugs 2006;20:233–55
7. Lis S, Krieger S, Gallhofer B et al. Sertindole is superior to haloperidol in cognitive performance in patients with schizophrenia: a comparative study. Eur Neuropsychopharmacol 2003;13(Suppl. 4):S323–S324

High psychological distress among internally displaced women in West Darfur, Sudan 7 September 2007

Marwan Khawaja,
Professor
American University of Beirut,
Mohammed D.A. Omer
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Re: High psychological distress among internally displaced women in West Darfur, Sudan

mk36{at}aub.edu.lb Marwan Khawaja, et al.

To the Editor The situation in the Darfur region of Sudan was recently described by the United Nations (UN) as the most severe humanitarian crisis that the world has ever witnessed, and the living conditions there may be deteriorating1. Three years of acute conflicts have resulted in widespread population displacements with negative health consequences for people there, especially women. Mortality rates among the internally displaced persons (IDPs) are known to be high, resulting mainly from violence and malnutrition2. However, little attention has been given to common mental disorders (CMDs) which are potentially serious in the context of conflict. We examined the prevalence of CMDs among women living in West Darfur’s camps, and the association between psychological distress and satisfaction from health services in the camps.
The study was based on data from a household survey conducted in four IDPs camps in west Darfur State in January 2006. Face-to-face interviews were conducted with a randomly selected sample of 722 households, with a response rate of 94.2%. All ever married women aged 15-49 (n=791) found in the sampled households were selected for interview, and 778 of them were successfully interviewed to obtain information on mental health and a range of reproductive health issues. CMDs were measured by the widely used 12-item General Health Questionnaire (GHQ) 3. The items were summed, and a cut-off point of 4/5 was used to distinguish cases of CMDs.
The overall prevalence of CMDs was 75.8%, which is much higher than those found in other refugee settings4. Findings from a multivariate binary logistic regression model revealed that women dissatisfied with health care services were 1.51 (95% CI = 1.06 - 2.15) times more likely to report CMDs than other women, adjusting for age, education, and camp of residence. The relationship between mental health and satisfaction with health care has been documented elsewhere5.
Prolonged violence, insecurity, loss of home and relatives, and reported gender-based violence, particularly rape, were some of the underlying factors behind such dire poor mental health within IDPs in West Darfur. Although emergency responses from UN agencies and NGOs were evident, the area of mental health received little attention from the health care service providers in West Darfur. Elements of mental health and quality of health services should be taken into account when addressing intervention towards IDPs especially since they may be facing a prolonged conflict before resettlement.
References
1. UN. Sudan: UN rights chief paints grim picture of worsening Darfur crisis. http://www.un.org/apps/news/story.asp?NewsID=18367&Cr=Sudan&Cr1=Darfur (accessed on December 22, 2006). 2. Depoortere E, Checchi F, Broillet F, Gerstl S, Minetti A, Gayraud O et al. Violence and mortality in West Darfur, Sudan (2003-04): epidemiological evidence from four surveys. Lancet 2004;364(9442):1315-20. 3. Goldberg DP, Gater R, Sartorius N, Ustun TB, Piccinelli M, Gureje O et al. The validity of two versions of the GHQ in the WHO study of mental illness in general health care. Psychol Med 1997;27(1):191-7. 4. de Jong JP, Scholte WF, Koeter MW, Hart AA. The prevalence of mental health problems in Rwandan and Burundese refugee camps. Acta Psychiatr Scand 2000;102(3):171-7. 5. Lang AJ, Rodgers CS, Moyer R, Laffaye C, Satz LE, Dresselhaus TR et al. Mental health and satisfaction with primary health care in female patients. Women’s Health Issues 2005;15(2):73-9.
Acknowledgement This study was conducted with financial support from a Wellcome Trust grant to the Faculty of Health Sciences at the American University of Beirut, and the UNFPA, Sudan country office. Additional in-kind support was provided by the State Ministry of health, Sudan.

Orthorexia Nervosa: who cares? 7 September 2007

Arthur Kummer,
Psychiatrist
Department of Internal Medicine, School of Medicine, Federal University of Minas Gerais (UFMG),
Fernando M.V. Dias, Antonio L. Teixeira.
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Re: Orthorexia Nervosa: who cares?

r2kummer{at}hotmail.com Arthur Kummer, et al.

The psychiatric diagnostic categories are historically and culturally determined. Eating disorders, despite the description of similar symptoms since the first millennium in the Western world, were recognized as psychiatric disorders only in the 20th century. A series of studies identified eating disorders to be prevalent, frequently severe and even life-threatening.
Recently, some scientific articles and, mainly, the mass-media have emphasized the emergence of a new eating disorder known as orthorexia nervosa (ON). ON was first described by Dr. Steven Bratman in the non- scientific Yoga Journal [1]. According to his definition, ON is an obsession for healthy food which may lead to strict diets, sometimes with a shortage of essential nutrients, and a modification of social relationships due to this behavior [1-3].
Despite the fact Dr. Bratman has never written about orthorexia in scientific journals, he describes in his book an alarming situation regarding ON incidence in USA [2]. Although the first description of ON dates back to 1997 [1], it seems that ON has been neglect by the scientific community. We searched the term “orthorexia” in Pubmed by the end of July, 2007. We retrieved only 10 articles, most of them discussing ON concept. When we searched “orthorexia” in Google at the same period, we retrieved impressive 70,300 sites related to ON.
Motivated by the lack of scientific data regarding ON, Donini et al. investigated ON prevalence in a population-based study [3, 4]. These authors considered the presence of both “health fanatic” eating habits and obsessive-compulsive traits (according to Minnesota Multiphasic Personality Inventory) as “gold pattern” to the diagnosis of ON. A prevalence of 6.9% was found [3]. Interestingly, the prevalence of ON was higher in men and in those with a lower educational level, just the contrary of what is seen in anorexia and bulimia [5]. Bagci-Bosi et al. used the same criteria and questionnaire of the previous study to assess ON prevalence in resident medical doctors. They found a prevalence of 45.5% of ON [6]. They hypothesized that the high prevalence of ON in this population may be due to the fact that medical doctors tend to be more concerned about a “healthy nutrition”.
However, in our view, it seems that a major issue, which defines psychological phenomena as a psychiatric disorder, has been forgotten. As DSM-IV states, psychiatric disorder must have caused and continue to cause significant distress or negative consequences in different aspects of the person's life. This premise seems to have been forgotten by current researches about ON. Curiously, people with ON have been described to even have a feeling of superiority over the lifestyle of others [1-4]. For instance, how many medical doctors diagnosed as orthorexic by Bagci-Bosi et al. on their study had attended specialized help due to this eating disorder?
Although we agree that the matter of eating disorders urges for further researches, a conceptual discussion must be made in order to clarify the relevance of ON and even if it is actually a psychiatric disorder. Otherwise, orthorexia will continue to be neglected by the scientific community.
References
[1] Bratman S. Original essay on orthorexia. Available at: http://www.orthorexia.com/index.php?page=essay. Accessed: July, 2007.
[2] Bratman S, Knight D. Health food junkies. New York, Broadway Books, 2000.
[3] Donini LM, Marsili D, Graziani MP, Imbriale M, Cannella C. Orthorexia nervosa: a preliminary study with a proposal for diagnosis and an attempt to measure the dimension of the phenomenon. Eat Weight Disord 2004; 9: 151-7.
[4] Donini LM, Marsili D, Graziani MP, Imbriale M, Cannella C. Orthorexia nervosa: validation of a diagnosis questionnaire. Eat Weight Disord 2005; 10: e28-32.
[5] Characteristics of eating disorders in a university hospital- based Spanish population. Rodríguez Martín A, Novalbos Ruiz JP, Martinez Nieto JM, Escobar Jiménez L, Castro de Haro AL. Eur J Clin Nutr 2005; 59: 459-62.
[6] Bagci Bosi AT, Camur D, Guler C. Prevalence of orthorexia nervosa in resident medical doctors in the faculty of medicine (Ankara, Turkey). Appetite 2007; [Epub ahead of print]

HIGH DOSES OF LONG-ACTING RISPERIDONE IN RESISTANT SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER 7 September 2007

Sergio Ruiz-Doblado,
Chairman, Psychiatric Services
Osuna Hospital, Spain,
Sánchez-Araña T, Rueda-Villar T, Baena-Baldomero A, Ruiz-Doblado S
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Re: HIGH DOSES OF LONG-ACTING RISPERIDONE IN RESISTANT SCHIZOPHRENIA AND SCHIZOAFFECTIVE DISORDER

sergioruiz{at}ozu.es Sergio Ruiz-Doblado, et al.

Since its launch, long-acting risperidone (LAR) has become an alternative to conventional treatment with oral atypical antipsychotics for patients with poor compliance to oral treatments or with severe or poorly tolerated side effects. Recent pharmacoeconomic studies (Edwards et al, 1995) evaluating clinical response and global sanitary expenses in a 1-year longitudinal follow-up, show that LAR can be an cost-effective alternative to haloperidol decanoate, oral risperidone, and oral olanzapine. LAR is the first available atypical antipsychotic with this formulation is Spain. However, there is a limited amount of available information concerning its pharmacokinetic characteristics when uses in naturalistic settings. The scarce studies performed point to a high interindividual variability in the plasma active moiety of risperidona and 9-hydroxyrisperidone with similar parenteral doses (Riedel et al, 2005). Reasons for this variability are not very clear, although interindividual differences in liver cytochrome P450 system –especially in CYP2D6 sub- system- related to genotyped major polymorphisms have been suggested. Pharmacodynamic aspects, such as D2 receptor occupancy rate in the striatum and 5-HT2 receptor occupancy in neocortex at different doses could also be involved in this interindividual variability in the clinical response (Farde et al, 1995; Gefvert et al, 2005).
On the other hand, existing divergences between Summary of Product Characteristics of drugs, the results of randomized clinical trials –performed in “ideal” or “prototypical” patients- and the real utilization of psychoactive drugs in naturalistic settings and in daily clinical conditions, are well known by clinicians. In this sense, we present data from six patients from a Psychiatric Intensive Care Unit (Hospital de Osuna, Spain) diagnosed for schizophrenia (4 patients) and schizoaffective disorder (2 patients), who showed a partial response to recommended doses of LAR (50 mg or 75 mg every two weeks). In all these patients, LAR doses were increased up to 100 to 175 mg every two weeks, after obtaining patient’s informed consent and written authorization. Approval and monitoring from Spanish Pharmacovigilance Authorities (known as “Compassionate use”) was also obtained. The patients (5 males, 1 female; range 23-43 years; duration of illness 8-21 years) followed a schedule of 100 mg LAR every two weeks (patient 1), 125 mg LAR every two weeks (patients 2 and 3), 150 mg LAR every two weeks (patients 4 and 5), and 175 mg LAR every two weeks (patient 6). All patients were followed up for three months (6 consecutive doses of LAR), and clinical response (positive and negative symptoms), tolerability, weight gain, extrapyramidal symptoms (EPS) and benzodiazepine or antiparkinsonian drugs needed were evaluated.
Five patients showed a moderate to important improvement in Clinical Global Impression (CGI) at three months. The remaining patient showed no clinical change. The global clinical improvement was mainly attributable to the reduction in positive symptoms (delusions, hallucinatory symptoms, formal thought disorder positive type, bizarreness), while negative symptoms experienced few changes. No significant changes in weight were observed (maximum weight gain 2 kg.), although this observation is limited due to the short evaluation period (only three months). Only one patient experienced extrapyramidal side effects (EPS) that required treatment with biperiden. The most frequent side effect was akathysia, which required treatment with benzodiazepines (lorazepam 3 mg/day, clonazepam 2 mg/day) in four cases. These initial results seem promising, pointing to good clinical outcome and acceptable tolerability of LAR high doses (100-175 mg every two weeks), without significant EPS. Interindividual variability in CYP2D6 major polymorphisms or in D2 receptor occupancy rate in the striatum and 5HT2 receptor occupancy in neocortex could explain part of the variance in concentration/dose (C/D), although additional studies with a bigger sample size and longer follow-up seem necessary to confirm these preliminary findings.
Sánchez-Araña T, MD PhD *
Rueda-Villar T, MD **
Baena-Baldomero A, MD **
Ruiz-Doblado S, MD PhD *
From Psychiatric Intensive Care Unit * and Community Mental Health Services **, Osuna Hospital, Seville (Spain).
References:
Edwards NC, Rupnow MF, Pashos CL, et al (1995) Cost-effectiveness model of long-acting risperidone in schizophrenia in the US. Pharmacoeconomics, 23, 299-314.
Riedel M, Schwarz MJ, Strassing M, et al (2005) Risperidone plasma levels, clinical response and side-effects. European Archives of Psychiatry and Clinical Neuroscience, 25. 261-268.
Farde L, Nyberg S, Oxenstierna G, et al (1995) Positron emission tomography studies on D2 and 5-HT2 receptor binding in risperidone-treated schizophrenic patients. Journal of Clinical Psychopharmacology, 15, 19S- 23S.
Gefvert O, Eriksson B, Persson P, et al (2005) Pharmacokinetics and D2 receptor occupancy of long-acting injectable risperidone (Risperdal Consta) in patients with schizophrenia. International Journal of Neuropsychopharmacology, 8. 27-36.
Declaration of interest: None.

The influence of the military institution on psychiatric practice in war zones 7 September 2007

Emilio Bolla,
Psychiatrist
Università degli Studi dell'Insubria, Varese ITALY
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Re: The influence of the military institution on psychiatric practice in war zones

emiboll{at}hotmail.com Emilio Bolla

To the Editor. Working as an army medical officer engaged in a military mission overseas (Iraq 2005), I have been able to highlight the ethical quandaries inherent in military psychiatric practice. Consciously or not, the medical officer embodies a hybrid condition, due to his need to reconcile deontological principles with the demands and duties imposed by his military role. The army is a highly structured institution, partially independent of civil society. This condition is emphasized during overseas missions. Moreover, for functional reasons, the army necessarily differs from the ideal of an “open society” (as understood with reference to modern democracy), and the ethical unease and difficulties provoked by this situation are increased in the field of psychiatry. There are several reasons for this. First, in the military setting, psychiatric diseases can directly affect efficiency and safety. Second, mechanisms of stigmatization among fellow soldiers can be very common. Third, diagnostic and therapeutic decisions taken in the field can have significant repercussions in the sphere of forensic medicine. In a previous report (1), based on a few case histories and using an ethical analytical-descriptive approach, we tried to identify clearly the problems relating to the doctor-patient relationship, the principles of medical deontology and the relative ethical system. There exist several models of the doctor-patient relationship, whose application depends on the particular social and historical setting. Models based on the principle of patient autonomy or on “beneficence in trust”, as Pellegrino & Thomasma suggest (2), are not easily applied in the field of military psychiatry practised in war zones. The only approach capable of reconciling the patient’s health needs with the safety and efficiency demanded by the military purposes is the “paternalistic” model. Military priorities do not affect only the doctor-patient relationship: all the decision making processes on a military field are based primarily on the principle of distributive justice and the principle of the common good. Since the common good is mainly taken to correspond to the demands of the military machinery, another principle, that of the physician’s professional integrity, can be undermined. Therefore, medical practice within the armed forces cannot be based primarily on deontological ethics. It is not implemented according to absolute a priori moral principles. In the army, more than anywhere else, the physician complies with a system of teleological ethics. Weber (3) described this as the “ethics of responsibility”, where the moral aim has to be pursued rationally and in consideration of the consequences of the actions taken. Individual-oriented psychiatrists operating in the civil sphere may fail to appreciate this fine ethical dilemma and therefore be ill-equipped to appreciate the main issue facing military healthcare providers, which is to balance harm and benefit while respecting their dual loyalties.
References
1 Bolla E: Fra Ares e Asclepio: l’influenza dell’istituzione militare nella pratica psichiatrica in teatro operativo. Psichiatria Oggi. 2006 May;19(1):46-52
2 Pellegrino ED, Thomasma DC. For the Patient’s Good: The Restoration of Beneficence in Health Care. New York: Oxford University Press; 1988
3 Weber M. Geistige Arbeit als Beruf. Berlin: Duncker & Humblot; 1919

Nicholas Rodney Drake (1948-1974) 7 September 2007

Oz Malkesman,
post-doc fellow at nih
LMP, NIMH, NIH. Bldg. 35, Rm. 1C-1014; 35 Convent Drive, MSC 3711,
Bethesda, MD, 20892
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Re: Nicholas Rodney Drake (1948-1974)

malkesmano{at}mail.nih.gov Oz Malkesman, et al.

The first time I was exposed to Nick Drake music was at the age of 25, and I guess that was the story of Nick’s Drake life; people get acquainted with his work only later in his life, some may say a little bit too late. Nicholas Rodney Drake was an English folk singer-songwriter and musician best known for his acoustic, autumnal songs. His primary instrument was the guitar, though he was also proficient at piano, clarinet, and saxophone. Nick Drake has released only three records in his life (Island records): Five Leaves Left (1969), Bryter Layter (1970) and Pink Moon (1972). None of these records had become to be a best seller, or even close to it, in his lifetime. In the early hours of 25 November 1974, Nick Drake died from an overdose of amitriptyline, a type of antidepressant. The title of his first record 'Five Leaves Left' in some sense became prophetic, as the album was released five years before Nick's death. Drake battled with depression and insomnia throughout his life, and the topics were often reflected in his lyrics. Some say that records born exclusively of misery and catharsis can do little besides depress their listeners. I beg to differ. Nick Drake’s albums came solely from misery and catharsis one can reasonably argue. But I can assure you that they affected me in more ways than just to depress me. If you listen carefully you hear some words of hope, or at least a story of beauty: “I never held emotion in the palm of my hand” – just try to envision yourself holding emotions, any of them, in the palms of your hands; or try to find among you “A soul with no footprint” that “came with the dawn”. Drake was pathologically shy and resented touring. The few concerts he did play were usually in support of other British folk acts of the time, such as Fairport Convention or John Martyn, and were often brief and awkward. Partially because of this, his work received little attention and sold poorly. Whilst in the recording studio, he was so shy that he would always play into the wall so as to avoid people's gazes. In his university years, Drake began to smoke cannabis, and one spring he traveled with friends to Morocco, because, according to traveling companion Richard Charkin, "that was where you got the best pot.” Drake likely took his first LSD trip while in university and lyrics written during this period - in particular for the song "Clothes of Sand" - are suggestive of an interest in hallucinogenics. In the autumn of 1969 Drake moved to London to concentrate on a career in music. He spent his first few months in the capital drifting from place to place, occasionally staying at his sister's Kensington flat, but usually sleeping on friends’ sofas and floors. Eventually, in an attempt to bring some stability and a telephone into Drake's life, Boyd (the producer of Nick's two first albums) organized and paid for a ground floor bed sit in Belsize Park, Camden. Island Records was keen to have Drake promote Bryter Layter through press interviews, radio sessions and live appearances. Drake, who was by this time smoking what Kirby has described as "unbelievable amounts" of cannabis and exhibiting "the first signs of psychosis," refused. By the winter of 1970, he had isolated himself in London. Disappointed by the reaction to Bryter Layter, he turned his thoughts inwards, and withdrew from family and friends. He rarely left his flat, and then only to play an occasional concert or to buy drugs. Although Island records neither expected nor wanted a third album, Nick released his third album “Pink Moon” after only two nights of recording. Afterwards things got even worse, as Nick described it: “I can't cope, all the defenses are gone. All the nerves are exposed." In the months following Pink Moon's release, Drake became increasingly introverted and distant from those close to him. He returned to live at his parents' home in Far Leys. Nick brought to his mother Molly a copy of Albert Camus' Le Mythe de Sisyphe when he returned home, short time before he committed suicide. Though he failed to find a wide audience during his lifetime, since his death Drake's work has grown steadily in stature, to the extent that he is now widely considered one of the most influential English singer-songwriters of the last 50 years. Several modern musicians, such as Lucinda Williams, Badly Drawn Boy, Matthew Good, Sebadoh's Lou Barlow, R.E.M. guitarist Peter Buck, Blur’s Graham Coxon, and Belle and Sebastian, consider Drake an important influence.
“Take your time and you'll be fine And say a prayer for people there Who live on the floor…” (Things behind the sun/Nick Drake)
Acknowledgement
The author thanks Dr. Lisa Catapano for revising a draft of the article.
References:
MacDonald, Ian (2000). “Exiled from Heaven”. Mojo Magazine, January.
Dann, Trevor (2006). Darker than the deepest sea: the search for Nick Drake, Da Capo Press. London. ISBN 0-306-81520-6.
Humphries, Patrick (1997). Nick Drake: The Biography, Bloomsbury, USA. ISBN 1-58234-035-8.

Re: Australian Firearms Data Requires a Cautious Approach 25 September 2007

Nestor D. Kapusta,
Psychiatrist
Department of Psychoanalysis and Psychotherapy,
Elmar Etzersdorfer, Gernot Sonneck
Send letter to journal:
Re: Re: Australian Firearms Data Requires a Cautious Approach

nestor.kapusta{at}meduniwien.ac.at Nestor D. Kapusta, et al.

McPhedran and Baker point out an unsolved problem of Australian suicide research. There are concerns about the quality of mortality data sources and statistics based upon them. Therefore, they urge researchers to approach Australian firearms data with caution. The authors cite a letter to the editor of the Medical Journal of Australia written by Diego De Leo (2007).
Professor De Leo highlighted inconsistencies of Australian mortality data since the year 2001 and called for homogenized certification procedures of deaths according to ICD-10 and for other improvements of death registries. However, in Austria autopsies are performed when there is any uncertainty regarding the cause of death. The autopsy rate is high in international comparison and was in average 29% in 1991-2000 (Waldhoer et al, 2003). If the cause of death is not clear, an additional investigation by Statistics Austria takes place. Statistics Austria registers deaths as suicide if that is the most probable cause of death. The International Classification of Diseases (ICD-8, -9, -10) has been applied for many years and there are no signs of a decrease of the data quality of Statistics Austria. The work of Kapusta et al. (2007) is based on these data.
Furthermore, De Leo (2007) realistically states that some under- reporting is ubiquitous and has to be tolerated in suicide statistics. On the other hand, under-reporting of firearm-deaths seems less probable than under-reporting of e.g. deaths due to poisonings (longer survival periods) which tend to be classified as disease-related deaths.
We agree with McPhedran and Baker, that Australian firearm laws should be re-evaluated on the basis of more reliable data. But as long as sufficient evidence is not available, theoretical assumptions that Australian firearm laws had no life-saving effects remain speculative - from a scientific point of view. This applies also to Europe, where independent scientific firearm law evaluations are still rare.
Declaration of interest: None
De Leo, D. (2007). Suicide mortality data needs revision. Medical Journal of Australia, 186, 157.
Kapusta, N.D., Etzerdorfer, E., Krall, C., & Sonneck, G. (2007). Firearm legislation reform in the European Union: impact on firearm availability, firearm suicide and homicide rates in Austria. British Journal of Psychiatry, 191, 253-257.
Waldhoer, T., Berzlanovich, A., Vutuc, C., & Haidinger, G. (2003). Rates of postmortem examination in Austria: the effect of distance between location of death and site of examination. Journal of Clinical Epidemiology, 56(9), 891-5.
-----------
Nestor D. KAPUSTA, M.D.
Department of Psychoanalysis and Psychotherapy, Medical University of Vienna, Austria nestor.kapusta@meduniwien.ac.at
Elmar ETZERSDORFER, Prof. M.D. Furtbach Hospital for Psychiatry and Psychotherapy Stuttgart,Germany
Gernot SONNECK, Prof. M.D. Institute for Medical Psychology, Medical University of Vienna, Austria

Firearms suicide in Queensland, 1990-2004 25 September 2007

Professor Diego De Leo,
Centre Director
Australian Institute fo Suicide Research and Prevention, Griffith University,
Helen Klieve and Michael Barnes
Send letter to journal:
Re: Firearms suicide in Queensland, 1990-2004

diegodeleo1{at}gmail.com Professor Diego De Leo, et al.

In Australia, the 1996 National Firearms Agreement (NFA) was introduced following the Port Arthur massacre, in which 35 people were killed. The NFA introduced: access restrictions (particularly of assault weapons); storage regulations; and, a gun buy-back scheme to reduce firearms in the community. The recent Virginia Tech killings have refuelled the debate on the causal impact of the NFA, with rates of homicides virtually unchanged but substantial reductions in numbers and rates of firearms suicide (Chapman et al, 2006). However, the dramatic decrease in suicide deaths by firearms in Australia began prior to 1996.
In Queensland, on the basis of the Queensland Suicide Register (QSR), rates of firearms suicide in 1994 were more than 30% down the figures recorded in 1990 (approx. 10/100,000). In addition, in 1994 there was the crossing-over between declining rates of firearms suicide and increasing rates of hanging suicide. Both trends, between 1990 (year of constitution of QSR) and 2004 showed statistically significant variations (R²=0.88 firearms, and R²=0.70 hanging), with firearms suicide being more than 5 times less frequent than hanging suicide in 2004 (it was 2 times more frequent in 1990). Most firearms suicides involved hunting rifles, the use of which started to appear strongly reduced by early 1990’s. Minor declines were recorded in the use of other weapons.
Kapusta et al (2007) underline the successful implementation of the Austrian reform on firearm use on both homicide and suicide rates; moreover, they did not witness any increase in suicide with other methods. We believe this has not happened in Queensland, where the current legislation has not restricted firearms within the community (around 500,000 in four million inhabitants), and there has not been a reduction in male suicide rates (De Leo et al, 2006). However, a big shift in the choice of suicide methods has occurred, with younger males increasingly choosing hanging. As pointed out by Kapusta and colleagues, causality remains speculative in this type of observations. Whilst controlling access to means remains of paramount importance in suicide prevention (De Leo, 2002), it seems that a change in societal and cultural views towards firearms has played a bigger role than NFA. To verify this interpretation, we are currently checking if those who died by suicide through other methods were also in possession (and availability) of a firearm at the time of their death.
Chapman, S., Alpers, P., Agho, K., et al (2006). Australian’s 1996 gun law reforms: faster falls in firearm deaths, firearm suicides, and a decade without mass shootings. Injury Prevention, 12: 365-372.
De Leo, D. (2002). Why are we not getting any closer to preventing suicide? (Editorial) British Journal of Psychiatry, 181: 372-374.
De Leo, D., Klieve, H., Milner, A.(2006): Suicide in Queensland, 2002-2004. Mortality Rates and Related Data, Australian Institute for Suicide Research and Prevention, Brisbane.
Kapusta, N.D., Eztersdorfer, E., Krall, C., et al (2007). Firearm legislation reform in the European Union: impact on firearm availability, firearm suicide and homicide rates in Austria. British Journal of Psychiatry, 191: 253-257.
Conflict of interest: None

Side-effects of Antipsychotics and frontal release signs among people with schizophrenia 26 September 2007

Bo-Jian Wu,
Psychiatrist
Department of Psychiatry, Yuli Hospital, Department of Health, Taiwan,
Tsuo-Hung Lan, M.D., Bo-Jian Wu, M.D., Hsien-Jane Chiu, Tsung-Ming Hu, M.D., Tsung-Yun Chuang, M.D.
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Re: Side-effects of Antipsychotics and frontal release signs among people with schizophrenia

jamsab{at}mail2000.com.tw Bo-Jian Wu, et al.

This is our opinion in response to the published article "Frontal release signs and cognition in people with schizophrenia, their siblings and healthy controls in British Journal of Psychiatry, August 2007. We sincerely hope to get authors'reply to our comments. Regarding the relationships between antipsychotic effects and the frontal release signs, the authors stated that "side-effects of antipsychotics might account for our findings... the preponderance of the findings in the psychiatric literature makes it highly unlikely that the findings in our studies are solely directly attributable to the deleterious effects of antipsychotic medications."For the authors, it appeared to be acceptable to neglect the fact that antipsychotics-induced side-effects, e.g., parkinsonism, can enhance the degree of frontal release signs before reaching the conclusions in this study. In fact, in our opinion, the side-effects of antipsychotics should be considered more seriously in similar studies. Cumulative evidence from prior studies indicates that antipsychotics can induce exrtrapyramidal effects, such as glabellar reflex which is just one of the frontal release signs assessed in this study (Klawans & Goodwin, 1969; Simpson & Angus, 1970; Vreeling, Verhey, Houx, et al, 1993). Therefore, extrapyramidal effects caused by antipsychotics in schizophrenic patients are highly likely to be a confounder when comparing with their siblings and healthy controls. This confounding effect cannot be neglected just only by reviewing literature as the authors did. For the purpose of removing antipsychotic related side-effects in similar studies, we suggest methods as follows: first, considering enrolling only antipsychotics-naïve schizophrenic patients; second, using a regression model by putting frontal release signs as a dependent variable, and putting antipsychotics dosage, three cohorts (represented by dummy variables) and other factors as independent variables; thus, we can get a more clear view on the association between frontal release signs and three cohorts with controlling for the side-effects of antipsychotics. However, this possibly causes over-adjustments for the special characteristics of schizophrenia and results in non-significant difference of outcomes among these three cohorts. Third, if two methods mentioned above cannot be put into practice, we can try to conduct a study for comparing schizophrenic patients taking antipsychotics with non-schizophrenic patients also treated with antipsychotics (e.g., depressive disorders with psychotic features) on the presentation of frontal release signs. Nevertheless, this article by Thomas M. Hyde and colleagues has revealed evidence of frontal lobe dysfunction in this disorder. In addition, we would like to emphasize that associated confounder, such as the use of antipsychotics in schizophrenic patients, is an important factor which should be dealt with more properly, and more detailed discussions concerning the methodology is necessary in designing similar studies. REFERENCES Klawans, H. L., Jr. & Goodwin, J. A. (1969) Reversal of the glabellar reflex in Parkinsonism by L-dopa. Journal of Neurology, Neurosurgery & Psychiatry, 32, 423-427. Simpson, G. M. & Angus, J. W. (1970) A rating scale for extrapyramidal side effects. Acta Psychiatr Scand Suppl, 212, 11-19. Vreeling, F. W., Verhey, F. R., Houx, P. J., et al (1993) Primitive reflexes in Parkinson's disease. Journal of Neurology, Neurosurgery & Psychiatry, 56, 1323-1326.
Declaration of Interest: Nil; Authors: Tsuo-Hung Lan*,Bo-Jian Wu*, Hsien-Jane Chiu*, Tsung-Ming Hu* and Tsung-Yun Chuang,* Corresponding Author: Bo-Jian Wu *Department of Psychiatry, Yuli Hospital, Department of Health, 448 Chung Hua Road. Yuli Township, 981, Hualien County, Taiwan 886 -3-8886141; jamsab@mail2000.com.tw

Late-onset, recurrent and potentially progressive neutropenia in a patient receiving clozapine 26 September 2007

Dr Sundararajan Rajagopal,
Consultant Psychiatrist
South London & Maudsley NHS Foundation Trust,
Dr Tony Wong, Staff Grade Psychiatrist
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Re: Late-onset, recurrent and potentially progressive neutropenia in a patient receiving clozapine

Sundararajan.Rajagopal{at}slam.nhs.uk Dr Sundararajan Rajagopal, et al.

The use of the atypical antipsychotic clozapine is associated with haematological side-effects, the most significant of which are neutropenia and agranulocytosis. As a result, the use of clozapine is licensed only in treatment-resistant schizophrenia rather than as first-line, and in addition, regular full blood count (FBC) tests are mandatory. The risk of the above side-effects is highest between weeks 6 and 18 after initiation of therapy (Atkin et al, 1996), and it declines steadily thereafter. In the United Kingdom (UK), FBC is done weekly for the first 18 weeks, fortnightly for the rest of the first year, and then every four weeks. The total white cell and neutrophil counts are categorised into 'Green', 'Amber' and 'Red': a green result indicates a satisfactory count, an amber 'alert' requires more frequent FBC testing until a normal result is again reached (clozapine can continue to be taken), while a red alert, if confirmed by a second FBC test, necessitates immediate cessation of treatment. Both total white cell count and the neutrophil count need to be normal for a green result. The neutrophil ranges used for clozapine prescription seem to be very conservative in that while a neutrophil count less than 1.5 x 109/l is a red result, the haematological definition of agranulocytosis is only a neutrophil count below 0.5 x 109/l.
Althought transient neutropenia has been reported in early stages of treatment (Hummer et al, 1994) it is rare for the neutropenia to be recurrent and progressive. Benign ethnic neutropenia has been well recognised in some non-white populations (Rajagopal, 2005). There have been case reports of patients being continued on clozapine despite a red alert (Ahn et al, 2004). Acute agranulocytosis after several years of treatment with clozapine has also been reported (Sedky et al, 2005).
We report a case of late-onset neutropenia in a white male patient with a diagnosis of schizophrenia, who had been prescribed clozapine for treatment resistance. In his case the neutropenia was becoming more frequent and also appeared to be progressively severe. Clozapine had been started when the patient was 22 years old.
The patient had 2 amber alerts in the first 2 years of treatment, which were non-consecutive and occurred between 4 and 5 months after initiation. He had a total of 23 amber alerts in the second 2 years of treatment, including a series of eight consecutive amber results. The patient had an average neutrophil count of 3.08 x 109/l during the first 48 months, but it reduced significantly to 2.34 x 109/l during the following two years; the lowest neutrophil count in the first two years was 1.80 x 109/l while in the next 2 years it was 1.50 x 109/l, with a further three results between 1.50 x 109/l and 1.60 x 109/l. Thus, not only did the amber results become more frequent with time but they were progressively more severe.
The patient did not show any physical symptoms due to reduced neutrophil count, did not need any specific medical treatment at any time, and the psychosis was reasonably well controlled for the four years since being started on clozapine. However, the repeated amber results meant that the patient was needing more frequent FBC tests (every time there is an amber alert the patient needs twice weekly FBC tests until the result is back in the green range). Also, as the reduction in neutrophil count appeared to be becoming more severe (as evidenced by the declining average neutrophil count), continuing the patient on clozapine seemed to carry with it a long-term risk of agranulocytosis. Therefore, a joint decision was made with the patient to stop clozapine treatment and he was started on another atypical antipsychotic, and has been well maintained on it in the community over the last 9 months.
Our report indicates that clozapine, in addition to causing the well recognised acute agranulocytosis typically in the first few weeks of treatment, may also contribute to a more subtle, delayed, recurrent and potentially progressive neutropenia.
References
1. Ahh, Y. M., Jeong, S. H., Jang, H. S., et al (2004). Experience of maintaining clozapine medication in patients with 'red-alert zone' neutropenia: long-term follow-up results. International Clinical Psychopharmacology, 19, 97-101.
2. Atkin, K., Kendall, F., Gould, D., et al (1996). Neutropenia and agranulocytosis in patients receiving clozapine in the UK and Ireland. British Journal of Psychiatry, 169, 483-488.
3. Hummer, M., Kurz, M., Barnas, C., et al (1994). Clozapine-induced transient white blood count disorders. Journal of Clinical Psychiatry, 55, 429-432.
4. Rajagopal, S. (2005). Clozapine, agranulocytosis, and benign ethnic neutropenia. Postgraduate Medical Journal, 81, 545-546.
5. Sedky, K., Shaughnessy, R., & Hughes, T. (2005). Clozapine- induced agranulocytosis after 11 years of treatment. American Journal of Psychiatry, 162, 814.
Authors:
1. Dr Sundararajan Rajagopal
Consultant Psychiatrist
South London & Maudsley NHS Foundation Trust
Adamson Centre for Mental Health
St. Thomas’ Hospital
London SE1 7EH
E-mail: Sundararajan.Rajagopal@slam.nhs.uk
Phone: 020 7188 6027
Fax: 020 7188 6020
2. Dr Tony Wong
Staff Grade Psychiatrist
South London & Maudsley NHS Foundation Trust
Declaration of interest: None

Biological mechanisms and clinical psychiatry 4 October 2007

Jonathan W Hill,
Psychiatrist
University of Manchester
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Re: Biological mechanisms and clinical psychiatry

jonathan.hill{at}manchester.ac.uk Jonathan W Hill

I would like to add briefly three further perspectives to the debate between David Kingdon and Alan Young, on biological mechanisms and clinical psychiatry. Firstly it is unsustainable to contend, as Professor Kingdon does, that biological approaches are based on the pursuit of physical causes for mental disorders. Causal processes in biology are both physical and intentional (Bolton D & Hill J, 2004), and modern biological psychology and psychiatry are making major contributions to our understanding of the interplay between them.
Secondly as Professor Young brings out, developmental studies show how social processes affect biology, and biology modifies susceptibility to environments. Animal studies find that early adverse experiences have long-term behavioural effects, and impact on biological processes such as gene expression (Francis, Diorio, Plotsky, & Meaney, 2002). Thus links between quality of parenting in early life and subsequent adaptation may be mediated genetically (Francis et al., 2002). Animal and human studies find that environmental effects on depression vary depending on genotype (Caspi et al., 2003). Studies of adult depression find that child maltreatment history modifies the role of interpersonal processes, the presence of structural differences in the brain, and treatment outcome, all highly relevant to clinical practice (Teicher, Andersen, Polcari, Anderson, & Navalta, 2002; Nemeroff et al., 2003). In studies of children, assessments of biological consequences of social experience, such as HPA reactivity during parent-child conversations, are integral and essential. Developmental psychopathology would not have got off the ground based on the assumptions presented by Professor Kingdon.
Finally, there is, in my view, a problem, which is not to do with the conceptual and empirical issues debated by Kingdon and Young. Investigations of treatment outcomes, for example, in relation to genotype, or maltreatment history, or genotype by maltreatment history, could be conducted within clinical practice, but are very rare. As research funding, at least in the UK, becomes increasingly compartmentalised into different types of research such as ‘health services’, ‘trials’, ‘basic sciences’, who will fund the studies that cross these boundaries and bring biology into the clinic to the benefit of patients?
Reference List
Bolton D & Hill J (2004). Mind Meaning and Mental Disorder. (2nd ed.) Oxford: Oxford University Press. Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington, H. et al. (2003). Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science, 301, 386-389. Francis, D. D., Diorio, J., Plotsky, P. M., & Meaney, M. J. (2002). Environmental enrichment reverses the effects of maternal separation on stress reactivity. J.Neurosci., 22, 7840-7843. Nemeroff, C. B., Heim, C. M., Thase, M. E., Klein, D. N., Rush, A. J., Schatzberg, A. F. et al. (2003). Differential responses to psychotherapy versus pharmacotherapy in patients with chronic forms of major depression and childhood trauma. Proc.Natl.Acad.Sci.U.S.A, 100, 14293-14296. Teicher, M. H., Andersen, S. L., Polcari, A., Anderson, C. M., & Navalta, C. P. (2002). Developmental neurobiology of childhood stress and trauma. Psychiatr.Clin.North Am., 25, 397-viii.

The use of varenicline in mentally ill persons 31 October 2007

Enrique L.M. Ochoa,
MD PhD
Department of Psychiatry and Behavioral Sciences, University of California, Davis
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Re: The use of varenicline in mentally ill persons

elochoa{at}ucdavis.edu Enrique L.M. Ochoa

DEAR EDITOR: Presynaptic nicotinic receptors (nAChR) of the alpha4beta2 type regulate mesolimbic dopamine release and are implied in the physiopathology of nicotine dependence and schizophrenia (Ochoa & Lasalde-Dominicci, 2007). The alpha4beta2-nAChR partial agonist varenicline (Mihalak et al, 2006) has recently been approved as a treatment for smoking cessation (Rollema et al, 2007a). Smoking is more prevalent in the mentally ill as compared to the non- mentally ill (Ochoa & Lasalde-Dominicci, 2007), but controlled studies on the use of varenicline in this patient population are lacking.
I have recently reported a significant reduction in smoking behaviour in a 56 year old Caucasian woman with diagnoses of bipolar disorder and nicotine dependence who presented as psychiatrically stable on antipsychotic-antimanic medications and varenicline (2 mg/d) (Ochoa, 2007).
Notwithstanding, two recent reports described exacerbation of schizophrenic symptoms in one patient (Freedman, 2007) and a manic episode in another(Kohen & Kremen, 2007)both coincidental with varenicline administration.
In the first case, the patient was a 42 year old woman with schizophrenia treated for 17 years with 1015 mg of thiotixene (Freedman, 2007). She became psychotic after her general practitioner prescribed varenicline (2 mg/d). The second case (Kohen & Kremen, 2007) described a 63 year old man with bipolar disorder treated with valproic acid for 5 years. He developed a manic episode after initiation of varenicline (2 mg/d). In both reports, a varenicline-induced release of dopamine was invoked as an explanation for the episodes.
Varenicline has 20 times more affinity for the alpha4beta2-nAChR than nicotine (Rollema et al, 2007b) but as far as mesolimbic dopamine release is concerned, its in vitro (51%) and in vivo intrinsic activities are 51% and 40-60% respectively when compared to nicotine (Rollema et al, 2007b). This may not be sufficient to trigger psychosis or mania. Henceforth, I suggest the following alternative explanations for the episodes.
In one of the reports (Freedman, 2007) it is explicitly stated that the patient had recurrent and brief psychotic episodes in the absence of varenicline. After 17 years of thiothixene treatment, the patient may have become refractory to the antipsychotic medication. This contention has abundant experimental support (Samaha et al, 2007).
In the case of the manic person (Kohen & Kremen, 2007) the admission valproic acid level was 59.7 mg/L. This blood level is not compatible with full control of manic symptoms. This datum, coupled to the fact that valproic acid is not indicated for the maintenance phase of bipolar disorder, can explain the emergence of mania.
I am currently treating 5 patients with diagnosis of schizophrenia and 3 patients with diagnosis of bipolar disorder (one of them is described in reference 4) using varenicline for smoking cessation. None of them has yet developed either psychosis or mania during the 3-5 months of therapy with this medication.
Smoking in the mentally ill is a major medical issue. There is the need for randomized controlled trials that use varenicline as a smoking cessation aid in this patient population.
The author pertains to the Speaker Bureau for Janssen Pharmaceutica and Bristol- Myers Squibb.
REFERENCES
Ochoa, E. L. M. & Lasalde-Dominicci, J. (2007) Cognitive deficits in schizophrenia: focus on neuronal nicotinic acetylcholine receptors and smoking. Cell. Mol. Neurobiol. 27, 609-639. Mihalak, K. B., Carroll, F. I. & Luetje, C. W. (2006) Varenicline is a partial agonist at alpha4beta2 and a full agonist at alpha7 neuronal nicotinic receptors. Mol Pharmacol, 70, 801-805. Rollema, H., Coe, J. W., Chambers, L. K., et al (2007a) Rationale, pharmacology and clinical efficacy of partial agonists of alpha(4)beta(2) nACh receptors for smoking cessation. Trends Pharmacol Sci, 28, 316-325. Ochoa, E. L. M. (2007) Varenicline significantly reduced smoking in a mentally ill person. Br.J.Psychiatry, 29 May eletter. Freedman, R. (2007) Exacerbation of schizophrenia by varenicline. Am J Psychiatry, 164, 1269. Kohen, I. & Kremen, N. (2007) Varenicline-induced manic episode in a patient with bipolar disorder.Am J Psychiatry,164,1269-1270. Rollema, H., Chambers, L. K., Coe, J. W., et al (2007b) Pharmacological profile of the alpha4beta2 nicotinic acetylcholine receptor partial agonist varenicline, an effective smoking cessation aid. Neuropharmacology, 52, 985-994. Samaha, A. N., Seeman, P., Stewart, J., et al(2007) "Breakthrough" dopamine supersensitivity during ongoing antipsychotic treatment leads to treatment failure over time. J Neurosci, 27, 2979-2986.

Psychophysiological and behavioural characteristics in Comorbid ASPD/SSPD 28 November 2007

Murali K Sekar,
Specialist Registrar in Psychiatry
Derbyshire Mental Health Services,
Ramanathan Ganapathy
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Re: Psychophysiological and behavioural characteristics in Comorbid ASPD/SSPD

drmurali98{at}yahoo.com Murali K Sekar, et al.

Robert Schug’s article on psychophysiological and behavioural characteristics of individuals with comorbid ASPD and SSPD was very interesting since it opens the possibility of existence of a new spectrum of personality disorders. But reading the article with care, I have few questions coming to my mind.
First of all the community based study population which was recruited from temporary employment agencies appears to have prevalence of personality disorder which is in the order of what we would observe in psychiatric in patient units (de Giraloma 2000). The total prevalence in this study population was 52.4%, which is way beyond the prevalence rate of community based samples (Jack Samuels 2002). Conducting study in such a population could possibly lead to selection bias. By nature, individuals from such sample are more likely to have more severe and complex forms of the disorder (Ajetunmobi 2002). This might explain the high prevalence rate for the combined SSPD/ASPD sufferers that are observed in the study. It would have been more interesting to know about number of individuals from this sample, who have comorbidity between SSPD and other personality disorders like narcissistic, histrionic and borderline.
The other interesting observation is the results of the psychophysiological and behavioural characteristics of the four study groups. I could observe a pattern to exist with comorbid SSPD /ASPD group to appear in the severe end of the spectrum in which abnormal characteristics are more frequently observed (four out of six characteristics studied in this research, namely self reported crime, frequency, amplitude and skin conductance arousal) than the control group which lies in the other end of the spectrum. ASPD and SSPD group of individuals lie on either side of the middle of the spectrum.
A basic structural abnormality in frontal cortex could make these individuals to have higher psychiatric comorbidity (not only of ASPD and SSPD) and the abnormal characteristics identified may not be entirely explained by the co occurrence of these two disorders. Authors have rightly identified that the results could not merely due to additive effect of both disorders but a common confounder, that made this study population to have increased prevalence of personality disorder, which is not lying in the causal pathway between ASPD/SSPD and abnormality in characteristics, might operate.
Declaration of interest: None
References:
Ajetunmobi.O (2002) Making sense of critical appraisal, Arnold Publication
De Giraloma and Gitto (2000); Epidemiology of Personality Disorders, The New Oxford Textbook of Psychiatry- Chapter 4.12.5
Samuels.J et al Prevalence and correlates of personality disorder in a community sample (2002), 180; 536-542

Reclaiming the meaning of 'medical model' 28 November 2007

Tony B Benning,
specialist registrar in General adult psychiatry
Kendray hospital Barnsley, UK
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Re: Reclaiming the meaning of 'medical model'

tonybbenning{at}hotmail.com Tony B Benning

I read the editorial by Shah and Mountain (2007) with interest. In my experience, the term ‘medical model’ is commonly used in a pejorative sense, by psychiatry’s detractors, as a basis for professional attack. In this context, psychiatrists are misrepresented as drug pushing, overzealous in their use of coercive treatments and disinclined to see the person beyond the diagnosis. I used to expend a fair amount of energy defending psychiatry against this charge-arguing that it was an inaccurate representation, and protesting that I and most of my colleagues were, in fact, as holistic in orientation and as ‘touch feely’ as the next man. But this was only until I came to the realization that those who are intent on seeing psychiatry in this negative light are likely to continue to do so no matter what evidence to the contrary is presented before them and that their reasons for doing so are not so much reflective of reality as they are related to their need to create an extreme image of psychiatry as a basis for launching an attack as well as for shaping and consolidating their own personal and/or professional identities. In the service of this aim, the term ‘medical model’ is first hijacked, and then the obvious linguistic association between ‘medicine’ and ‘medical model’ is exploited. This technique of debunking something by first misrepresenting it or exaggerating its worst aspects is not an uncommon strategy in wider circles. A good recent example of this being Richard Dawkins’ trashing of religion in The god delusion. Dawkins’ attack rests on the privileging of a distorted version of religion which we might dub the ‘big R’ version. By analogy, the attack on the medical model is based on a distorted ‘big M’ version of it, which most psychiatrists would, in reality, distance themselves from and deny subscribing to. But the implication of this is that the meaning of the term ‘medical model’ is contestable and very much up for grabs and can and should be reclaimed and redefined so that it may come to represent more accurately the position taken by the overwhelming majority of psychiatrists: one that not only aspires to integrate biological and psychosocial factors and develop collaborative relationships with patients but one which increasingly looks to justify its treatments and continues to push the frontiers of neuroscience in the hope that doing so will ultimately serve our patients.
References
Shah, P. & Mountain, D. (2007) the medical model is dead – long live the medical model. British Journal of Psychiatry, 191, 375-377
Dawkins, R. (2006) The God delusion. Bantam books
Tony B Benning.
Declaration of interest . Nil

Smoke free: a plea to evaluate. 28 November 2007

Catherine Pritchard,
Specialist Trainee in Public Health
University of Nottingham,
Ann McNeill and Irene Cormac
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Re: Smoke free: a plea to evaluate.

mczcp3{at}exmail.nottingham.ac.uk Catherine Pritchard, et al.

The Health Act 2006 required the majority of workplaces in England to be smoke-free from 1 July 2007. The accompanying regulations exempted mental health units, allowing them to provide a designated room for smoking with appropriate ventilation, for patients over the age of 18, until 1st July 2008. As this date approaches, mental health units should consider how best to monitor the impact of the smoke-free policy for their organisation, staff and patients.
According to the core standards of the Healthcare Commission (2006), organisations must work towards a systematic and managed approach to tobacco smoking. NICE (2006) guidance states that the smoking status of all in-patients should be recorded on admission, and advice should be provided for smokers, together with referral to NHS ‘Stop Services’ and prescription of smoking cessation medications. NICE guidance contains an audit tool to enable organisations to identify each of these stages and provides a framework for data collection.
However, these measures will not adequately show the impact of introducing smoke-free policies within mental health units. A key organisational challenge surrounds the use of exemptions to the smoke-free policy. Across the service, a central system could collate data on smoke- free exemptions to show where they are occurring, and thus help to ensure a consistent approach across the organisation. Mechanisms to prevent double counting need to be in place.
One of the principal concerns of staff centres on the potential for an increase in aggression and violence. Whilst research from other countries does not support these concerns, monitoring should be undertaken to assess such changes. Incident report forms, with simple tick boxes, could be used to record smoking-related incidents, and whether incidents were verbal or physical abuse. It will also be important to monitor significant changes in psychiatric symptoms, psychotropic medication and physical health status, in relation to those who have quit or reduced smoking.
Sharing of the above information will promote a dialogue between patients and staff and will encourage an evidence-based appraisal of the impact of introducing smoke-free policies into mental health services.
Dr Catherine Pritchard, Specialist Trainee in Public Health, University of Nottingham, Division of Epidemiology and Public Health, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham. NG5 1PB. Telephone 01158231725. Fax 01158231946. Professor Ann McNeill, University of Nottingham, Division of Epidemiology and Public Health, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham. NG5 1PB. Dr Irene Cormac, Consultant Forensic Psychiatrist, Mental Health Service Directorate, Fleming House, Rampton Hospital, Nottinghamshire.DN22 OPD.
References
Health Care Commission 2006. The annual health check in 2006/2007. Assessing and rating the NHS. London: Commission for Healthcare Audit and Inspection.
National Institute for Health and Clinical Excellence 2006. Audit criteria. Brief interventions and referral for smoking cessation in primary care and other settings. London: NICE.

Why do we bother with evidence if we are only going to ignore them? Observations on psychosis EIS 28 November 2007

Patapia M Tzotzoli,
Psychologist
Institute of Psychiatry
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Re: Why do we bother with evidence if we are only going to ignore them? Observations on psychosis EIS

patapia.tzotzoli{at}iop.kcl.ac.uk Patapia M Tzotzoli

One of the clinical priorities of the NHS Plan blueprint (2000) is about early intervention in psychosis which aims to “reduce the period of untreated psychosis in young people”, and “improve long-term outcomes” by establishing “50 early intervention teams…over the next three years” and “by 2004...7,500 young people each year…will receive the early and intensive support they need”. The amount of money granted for this policy was £50 million. Early intervention services continue to develop and attract research funding as well as the interest of pharmaceutical companies, thus it is more that certain that the above figure has been dramatically increased during the last years and will continue to increase.
However, one cannot but notice the discrepancy between the clinical world’s preaching of “evidence-based practice” and its actual practice. Hippocrates philosophical utterance that “prevention is better than cure” became a medical truism which is currently being used as a professional argument to partly justify the presence of the early intervention services. Yet, to follow good practice’s steps there is a set of challenges such services need to overcome in order to show their effectiveness:
 Easy identification of cases in the population
 Non-invasive interventions which have minimal side-effects, if any.
 Demonstrably service evaluation
 Cost-effectiveness
Early intervention services refer mainly to individuals who experience a prodromal syndrome. Theoretically, the term refers to a period of prepsychotic disturbance, representing a deviation from a person's previous experience and behaviour (Birchwood, 1989; Malla and Norman 1994). However, evidence indicates that we are still far from defining the concept of “prodromal syndrome”. According to the Dunedin Multidisciplinary Health and Development Study (2002) early emerging motor, language and cognitive developmental deficits can only be considered as valuable clues to the processes affected in schizophrenia- related illnesses. Researchers found emotional problems and poor interpersonal functioning in childhood but at the age of 26 these associations did not exhibit any specific disorder but a host of different adult psychiatric outcomes, including schizophreniform disorder, manic episodes and anxiety/depression disorders. The only safe conclusion from these results is that this constellation of childhood behaviour indexes a generally, vulnerable personality that is at risk for all adult psychiatric disorders. In clinical medicine, prodrome is a retrospective concept, diagnosed only after the development of definitive symptoms and signs. Therefore, when considering schizophrenia, it is clear that we should have serious reservations before claiming early identification of cases, let alone the high false positives and low false negatives that occur in practice. Who are these services referring to, then?
Regarding treatment the early intervention services offer psychological therapy and drugs as the first line of treatment. Yet, medicating young adults with an unclear diagnosis and without troublesome symptoms but with unavoidable drug side effects sounds absurd. Studies reporting high transition rates to psychosis from prodromal states have been recruiting individuals who are already “at risk” due to family history or decline in function, for example. Thus, attempting to identify individuals in the prodromal state in the general population may have less predictive power. Other studies identified a remarkable low number of individuals despite the high risk of transition (e.g. Hambrecht et al, 2002), which questions further allegations of successful identification of cases. Yet, a great percentage of people are being medicated unnecessarily.
The lack of a proper service evaluation enterprise is striking. On the top of this, attempts to test the early intervention hypothesis violate two golden rules of objective research. First, is the fact that despite evidence of infallible early cases’ identification, the early intervention services fail to reflect on their premises, appointing the hypothesis as ultimate. Second, supportive evidence comes only from those who have an interest in its success and not from an independent source. Yet, these services absorb a great degree of valuable resources in the name of the “treatable person” in the detriment of the sickest despite the unknown benefits of early intervention. It seems astonishing the fact that these services persuaded the appalling governmental bureaucracy to fund them. I cannot but wonder whether clinicians’ “evidence-based practice” plight is actually an approximate evidence-based one.
References:
 Birchwood, M.; Smith, J.; MacMillan, J.F.; Hogg, B.; Prasad, R.; Harvey, C.; and Bering, S. Predicting relapse in schizophrenia: The development and implementation of an early signs monitoring system using patients and families as observers: A preliminary investigation. Psychological Medicine, 19:649-656, 1989.
 Cannon, M., Caspi, A, Moffitt, T.E., Harrington, H., Taylor, A. Murray, R.M. and Poulton, R. Evidence for early-childhood, pan- developmental impairment specific to schizophreniform disorder: results from a longitudinal birth cohort. Arch Gen Psychiatry. 2002; 59:449-456.  Department of Health, The NHS plan. Executive summary 2000. Crown Copyright.
 Hambrecht, M., Lammertink, M., Klosterkotter, J., Matuschek, E., Pukrop, R., 2002. Subjective and objective neuropsychological abnormalities in a psychosis prodrome clinic. Br. J. Psychiatr.,Suppl.; 43: 30– 37.
 Malla, A.K., and Norman, R.M. Prodromal symptoms in schizophrenia. British Journal of Psychiatry, 164:487-493, 1994.

Diagnosis and management of non-organic paraplegia with Transcranial Magnetic Stimulation 28 November 2007

SN Deftereos,
Neurologist
Department of Neurology, Athens General Hospital, 153 Mesogeion av, 11527, Athens, Greece,
G Panagopoulos, D Georgonikou and CE Karageorgiou
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Re: Diagnosis and management of non-organic paraplegia with Transcranial Magnetic Stimulation

deftereo{at}gmail.com SN Deftereos, et al.

A 44-year old woman presented with paraplegia that developed suddenly, two months prior to her admission. She had already been investigated by MRI of the brain, cervical and thoracic spinal cord and by lumbar puncture (ten days after the paraplegia developed), as well as by EMG and nerve conduction studies (four days prior to her admission). The results of these tests were unremarkable. She had received Methylprednisolone (1gr daily, for five days), but did not notice any improvement. Neurological examination disclosed paraplegia (Medical Research Council power grade 0 on both lower extremities). Plantar responses were flexor. There weren't any signs of spasticity nor sensory deficits, while bladder and bowel function were normal. There weren't any abnormal signs or symptoms in the upper extremities or the cranial nerves. Her personal history was unremarkable. Follow-up MRI scans of the brain, cervical, thoracic and lumbar spinal cord were again normal. Following these results we re-evaluated the patient, focusing on potential non-organic causes of her symptoms (hysteria or malingering). Although she did not report any strenuous events, her husband confirmed that they were having personal problems in the last few months. A positive Babinski-trunk sign supported a non- organic cause. In order to confirm this hypothesis we proceeded to a Transcranial Magnetic Stimulation (TMS) evaluation. Single-pulse TMS was delivered with a Magstim Rapid2 stimulator (the Magstim Company Ltd, Whitland, UK). The hand motor cortex was targeted with a 70mm figure-of-eight coil, while a double-cone coil was used to activate the foot motor cortex. Stimuli were delivered at 100% stimulator output. Motor Evoked Potentials (MEPs) were recorded by a Medelec Synergy EMG monitoring system (Medelec ltd, Oxford, UK) from the Abductor Digiti Minimii (ADM), Extensor Digitorum Brevis (EDB) and Vastus Medialis (VM) muscles bilaterally. The Central Motor Conduction Time (CMCT) was calculated for each muscle as CMCT = (MEP latency) – (peripheral conduction time).[1] CMCT was within normal limits in all muscles (Right ADM=6.3ms, Left ADM = 6.5ms, Right EDB=15.2ms, Left EDB=14.9ms, Right VM=13.6ms, Left VM=13.9ms). The patient was pleased by this result and, more importantly, she was surprised by the effect TMS had on her limbs; she could see her arms and legs moving briskly in response to the magnetic pulses. We capitalized on these two facts to assure her that things were much better than she thought so far and that her paraplegia would improve as long as she tried hard her self. Indeed, a considerable improvement was noted in the hours following the TMS study. By the next day the patient could walk with support and she was released from hospital. At follow-up examination, fifteen days later, she had regained full power and had return to her normal activities. TMS is a relatively new technique that is not used frequently in every day practice. Patients are unaccustomed to it and can be surprised by its effects. Thus TMS can prove useful in the management of non-organic paralyses, in addition to providing neurophysiologic evidence on the integrity of the corticospinal tracts.

BRIEF TRAINING IN PSYCHOLOGICAL THERAPIES 28 November 2007

Alasdair J Macdonald,
temporary consultant in child psychiatry
Dorset County Hospital Foundation Trust,
Mark McKergow
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Re: BRIEF TRAINING IN PSYCHOLOGICAL THERAPIES

macdonald{at}solutionsdoc.co.uk Alasdair J Macdonald, et al.

The UK government has broadly supported Professor Lord Layard's hypothesis (London School of Economics 2006) that provision of talking therapies requires an additional 10 000 therapists in the United Kingdom over the next seven years. These staff are proposed to come from expansion of clinical psychology (5000) and from existing mental health staff (5000) who will be given 'one- or two-year part-time off-the-job courses in therapy.' It seems likely that most psychiatrists would be happy to see this additional provision of skills. However, there are many practical difficulties in training so many ‘brief CBT’ enthusiasts.
One option to achieve these valuable goals may be the use of solution -focused brief therapy. Developed in the USA during the 1980s, it has world-wide applications and a very substantial evidence base, showing an effectiveness comparable with CBT and other talking therapies. A meta- analysis by Kim 2007 showed solution-focused therapy to be as effective as other therapies, requiring an average of 6.5 sessions. A Dutch meta- analysis in 2006 (Stams) gave similar results for a different group of studies. Moreover, training in solution-focused therapy can be much shorter than brief CBT: between 20 and 100 hours of training and supervision is required.
The approach can also be effective with groups not normally responsive to psychotherapy including offenders and those with learning disability. A randomised controlled trial (one of six) showed that imprisoned repeat offenders in Sweden showed a 26% reduction in reoffending, as well as other improvements (Lindforss and Magnusson 1997). It is widely used for management and organisational change around the world. Many mental health staff and many teachers already have some training in the method and its applications.
More detailed information can be found for the UK at www.brieftherapy.org.uk and www.solutionsdoc.co.uk and at www.sfwork.com for management consultancy. www.ebta.nu reports the activities of the European Brief Therapy Association and www.brieftherapysydney.com.au provides extensive links to sites in Australasia and elsewhere.
Iveson, C. (2002) ‘Solution-focused brief therapy’, Advances in Psychiatric Treatment, 8: 149-157.
Kim, J.S. (2006) Examining the Effectiveness of Solution-focused Brief Therapy: A Meta-Analysis Using Random Effects Modeling. SFBTA conference, Denver (University of Michigan dissertation database). (Research In Social Work Practice, 2008, in press)
Layard, Lord (2006) The Depression Report: A New Deal for Depression and Anxiety Disorders. The Centre for Economic Performance Mental Health Policy Group. London School of Economics: London.
Lindforss, L., Magnusson, D. (1997) Solution-focused therapy in prison. Contemporary Family Therapy, 19: 89-104.
Stams, G.J., Dekovic, M., Buist, K., de Vries, L. (2006) Effectiviteit van oplossingsgerichte korte therapie: een meta-analyse (Efficacy of solution focused brief therapy: a meta-analysis). Gedragstherapie, 39(2): 81-95. (Dutch; abstract in English).
A.J.Macdonald Child and Adolescent Mental HealthService, Dorset County Hospital, Dorchester DT1 2JY. Email: macdonald@solutionsdoc.co.uk
Mark McKergow Director sfwork, 26 Christchurch Road, Cheltenham GL50 2PL Email: mark@sfwork.com
Declaration of interest: We both provide workshops and training courses in solution-focused approaches.

Withdrawal symptoms after missing a single dose of Venlafaxine ER 3 December 2007

Zoran M Pavlovic,
Psychiatrist
Private Practice
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Re: Withdrawal symptoms after missing a single dose of Venlafaxine ER

zoki67pavlovic{at}yahoo.com Zoran M Pavlovic

Venlafaxine hydrochloride is a phenylethylamine - derivative antidepressant and anxiolytic agent that acts as a serotonin - and noradrenaline - reuptake inhibitor ( SNRI )1. Placebo - controlled clinical studies indicate that 78 % of the venlafaxine ER treated - subjects experience adverse events, although the medication was tapered during three - week period.2 Discontinuation adverse events have also been reported with other SNRIs such as duloxetine3. During withdrawal of venlafaxine, both serotonin and noradrenaline levels decrease which suggests that the withdrawal symptoms are partly the result of the rapid deprivation i.e. “bursting" activity of noradrenergic receptors in locus coeruleus in the absence of a customary neurotransmitter presence. Also, it has been found that at the doses of / and above 150 mg / day, venlafaxine inhibits the reuptake of noradrenaline more than at 75 mg / day, when acting mainly as a typical SSRI. However, little mention is found of the possibly severe effects due to postponing ingestion of the daily dose of venlafaxine, for instance by forgetting to take the single dose just as little as for 5 hours. Mr A. was a 20 – year old man who came for an appointment following a suicide attempt with benzodiazepine overdose. His main complaints were depressed mood, insomnia, feeling of guilt, desperation and suicidal thoughts. His initial Beck Depression Inventory Score was 30. He was started on venlafaxine ER 75 mg and titrated during a course of three days to 225 mg / day. Our decision to augment venlafaxine so rapidly was due to a good tolerability of its higher therapeutic dose range by our patient. After three days of continuous 225 mg daily dose of venlafaxine Mr. A noted some improvements in his depressive symptoms, and decided to take only one capsule on this morning at 7 AM. At noon he started to exhibit following symptoms: palpitations, chest pain, insomnia, hot and cold flushes, fatigue, dizziness and shortness of breath, which he rated as incapacitating. On the next morning following our advise, Mr. A . took his regular dose of venlafaxine ER, which was three capsules of Venlafaxine ER 75 mg and experienced no withdrawal symptoms afterwards. According to our case, the physician must sufficiently point out the need for a strict adherence to a fixed medication daily routine to every patient on venlafaxine ER.
References 1. Ellingrod VL, Perry PJ. Venlafaxine: a heterocyclic antidepressant. Am J Hosp Pharmacy. 1994 ; 51 : 3033 - 3046. 2. Fava M, Mulroy R, Alpert J, Nierenberg AA, Rosenbaum JF, Emergence of adverse events following discontinuation of treatment with extended - release venlafaxine. Am J Psychiatry 1997; 154: 1760 - 1762. 3. Perahia DG, Kajdazs DK, Desaiah D, Haddad PM. Symptoms following abrupt discontinuation of duloxetine treatment in patients with major depressive disorder. J Affect Disord 2005; 89: 207 - 212

Significant Weight Gain Occurring With Escitalopram 6 December 2007

Daniel C White,
Senior Registrar in Psychiatry ,
MacDara McCauley, Consultant Psychiatrist
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Re: Significant Weight Gain Occurring With Escitalopram

danwhite_ireland{at}yahoo.co.uk Daniel C White, et al.

In recent months we have reported cases of significant weight gain in two female patients occurring during treatment with escitalopram (Lexapro).
Case 1. A 33 year old unemployed single mother with recurrent depression and panic symptoms, improved on escitalopram 25 mg daily and bromazepam 1.5 mg daily. She gained 10 kg over 6 months on this medication regime. Consequently, she began to suffer distress regarding her weight gain but insisted on continuing escitalopram because of the improvement in her symptoms.
Case 2. A 55 year old married mother with a mixed anxiety/depressive illness was recently reviewed at an out patient clinic. She opted to discontinue escitalopram 20 mg despite a good clinical response, following a weight gain of 11kg over the period of one year. At the time of the weight gain she was not taking any other medication and denied recent lifestyle changes.
The psychological effects of medication induced weight gain are distressing for many patients, resulting in reduced adherence and poorer outcomes (Papakostas, 2007).
The SSRI’s are commonly associated with weight loss in the initial stage of treatment, however the potential for weight gain with ongoing treatment (Masand et al, 2002) and the risks associated with this are often overlooked. Weight gain is one of the features of the metabolic syndrome (a cluster of disorders comprising obesity, dyslipidaemias, glucose intolerance, insulin resistance/hyperinsulinaemia and hypertension) which places patients at an increased risk of developing type 2 diabetes, cardiovascular disease and stroke.
Whilst the association between schizophrenia, atypical antipsychotics and the development of the metabolic syndrome is causing increasing concern (Thakore et al, 2002, Newcomer et al, 2007), very few studies have looked for any association between depression, SSRI’s and the metabolic syndrome (Reader et al, 2006).
It is important that clinicians are alert to patients who gain weight during the course of treatment with SSRI’s because of the potential for the development of the metabolic syndrome. This is especially true of patients with recurrent depressive and anxiety illnesses who are more likely to be on long term therapy with an SSRI.
Declaration of interest: None
References:
Masand, P.S. and Gupta, S. (2002) Long-Term Side Effects of Newer- Generation Antidepressants: SSRI’s, Venlafaxine, Nefazodone, Bupropion, and Mirtazapine. Annals of Clinical Psychiatry, 14, 175-182.
Newcomer, J.W. (2007) Antipsychotic medications: metabolic and cardiovascular risk. Journal of Clinical Psychiatry, supplement 4, 8-13.
Papakostas, G.I. (2007) Limitations of contemporary antidepressants: tolerability. Journal of Clinical Psychiatry, supplement 10, 11-17.
Raeder, M.B., Bjelland, I., Emil Vollset, S., et al (2006) Obesity, dyslipidemia and diabetes with selective serotonin reuptake inhibitors: The Hordaland Health Study. Journal of Clinical Psychiatry, 67, 1974-1982. Thakore, J.H., Mann, J.N., Vlahos, I., et al (2002) Increased visceral fat distribution in drug-naïve and drug-free patients with schizophrenia. International Journal of Obesity Related Metabolic Disorders, 26, 137-141.
Authors:
D. White, Senior Registrar St Brigid’s Hospital, Ardee, County Louth, Republic of Ireland. Tel 00 353 41 6853264, Fax 00 353 41 6853503. E-mail: danwhite_ireland@yahoo.co.uk (Please send correspondence to D. White).
M. McCauley, Consultant Psychiatrist St Brigid’s Hospital, Ardee, County Louth, Republic of Ireland. Tel 00 353 41 6853264, Fax 00 353 41 6853503

Author's Response 19 December 2007

Robert A. Schug,
Graduate student
University of Southern California,
Adrian Raine, Rand R. Wilcox
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Re: Author's Response

schug{at}usc.edu Robert A. Schug, et al.

We are grateful for Murali Sekar’s thoughtful critical points. We agree that the prevalence for personality disorders in our sample is high. This sample was chosen for its elevated rates of ASPD—perhaps attributable to a downward drift in occupational functioning due to antisocial features. It is certainly vulnerable to selection bias for several reasons (among them being the fact that some individuals did not meet inclusion criteria), and the 52.4% PD prevalence rate should not be mistaken for a typical community population base-rate, or a general rate applying to other populations (claims which were not made in our article). Also, the prevalence rates of other individual personality disorders (e.g., narcissistic personality disorder—around 3%) were consistent with general population estimates (APA, 2000; Levy et al., 2007). Additionally, our focus was the characteristics of this SSPD/ASPD group, rather than making any assertions about its prevalence in the general population.
Upon reading Dr. Sekar’s comment about SSPD comorbidity with other PDs, we too became intrigued with this possibility and have since conducted further analyses. These revealed, among the other PDs, significant SSPD comorbidity only with narcissistic personality disorder (NPD). In fact, all three of our sample’s NPD individuals had comorbid SSPD and ASPD. This additional comorbidity among our SSPD/ASPDs is not surprising, given the problematically high overlap of NPD with ASPD and other Cluster B disorders (Millon & Davis, 1996; Levy et al., 2007), the conceptual link between the narcissistic and antisocial personalities (e.g., Kernberg’s “malignant narcissism;” see Millon & Davis, 1996), and the positive correlations observed between NPD and other antisocial personalities such as psychopathy (Hare, 2003). We still believe SSPD/ASPD comorbidity to be meaningful, and not an artifact of the sample, as 50% of our SSPD/ASPD comorbids were not characterized by any additional Axis II comorbidity.
We agree with Dr. Sekar that the frontal cortex (specifically the PFC) may be a common abnormality and that this needs further investigation. Clearly, additional research is needed on this comorbid group, in both clinical and nonclinical populations—including in “unique” community samples such as our own.
Declaration of interest: None
References American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (text revision). Washington, DC: Author. Hare, R. D. (2003). Hare Psychopathy Checklist—Revised (PCL-R): 2nd edition. Toronto, Ontario, Canada: MHS. Levy, K. N., Reynoso, J. S., Wasserman, R. H., Clarkin, J. F. (2007). Narcissistic personality disorder. In W. O’Donohue, K. A. Fowler, & S. O. Lilienfeld (Eds.), Personality disorders: Toward the DSM-V (pp. 233-277). Thousand Oaks, CA: Sage Publications, Inc. Millon, T., & Davis, R. D. (1996). Disorders of personality: DSM-IV and beyond. New York: John Wiley & Sons, Inc.

Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT) 30 January 2008

Markus Huber,
Psychiatrist
Departement of Psychiatry General Hospital Bruneck-Italy,
Erwin Kirchler
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Re: Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT)

markus.huber{at}sb-bruneck.it Markus Huber, et al.

Dear Editor: Involvement of zinc deficiency has been suggested in patients suffering from ADHD. The findings reinforce that zinc as a supplementary medication and/or adjunct to stimulants (mostly methylphenidate) might be beneficial in the treatment of ADHD [1]. Next to iron, zinc is the most abundant trace mineral in the body. For the brain zinc is an important cofactor for metabolism relevant to neurotransmitters, prostaglandins, and melatonin. Dietary changes and nutritional supplements have also been used to treat ADHD. Some of these results suggest a link between zinc deficiencies and low essential fatty acids. The cause of ADHD is unknown but is believed to involve multiple factors. The potential role for zinc in the treatment of ADHD is not understood. To the best of our knowledge we haven’t found any references by Pubmed-search which highlighted the neuromodulating function of zinc on the human DAT by ADHD. Neurochemistry studies show (in vitro) that binding of zinc to the three endogenous zinc-binding sites on the extracellular face of the human DAT (His 193, His 375, and Glu 396) leads to potent inhibition of dopamine uptake [2]. This is in line with the action of methylphenidate, the most commonly used and first-line stimulant of ADHD- treatment [3]. It acts as a potent striatal DAT-uptake inhibitor (like other amphetamines and cocaine). Zinc however inhibits the inward dopamine translocation process by enhancement of the carrier-mediated dopamine efflux on the DAT (facilitated reverse transport) [4] [5]. Zinc is the first example of an allosteric modulator that can regulate DAT-function by potentiating a specific uncoupled ion conductance [4]. It could be suggested that zinc-supply by ADHD-zinc-deficiency-patients inhibit the dopamine translocation process. Furthermore, it is also known that zinc enhances the binding of cocaine analogues to the DAT [5]. In this context, it is also important to note that children who are unresponsive to stimulant drugs are more likely to be zinc deficient than children who respond favourably to this medication [1]. It is conceivable that the application of zinc to ADHD-zinc-deficiency-patients facilitates the binding of cocaine analogues by conformational change of the DAT-protein. In this way zinc could surely used as a therapeutic tool in the treatment of ADHD. To verify these hypotheses however more research is needed. The data available at this time does not prove that low zinc causes ADHD nor makes zinc supplementation an established treatment. Although pharmacological treatment with stimulants is the most widely studied and effective treatment for ADHD their use in children is often polarized. Some critics object to the prospect of millions of children being prescribed controlled substances that are potentially addictive and injurious to the brain. ADHD is a complex disorder and of great public health importance. In this regard, the existing evidence tends to support the supplementary or adjunctive treatments of ADHD rather than single neuropharmacological targets.
Conflict of interest: None
References: 1) Arnold, L.E., DiSilvestro, R.A. (2005) Zinc in attention deficit hyperactivity disorder. J Child Adolesc Psychopharmacol, 15, 619-627. 2) Norregaard, L., Frederiksen, D., Nielsen E.O., et al (1998) Delineation of an endogenous zinc-binding site in the human dopamine transporter. EMBO J, 17, 4266-4273. 3) Huber, M., Kirchler, E., Niederhofer, H., et al (2007) Neuropsychiatric bases of the methylphenidate-therapy of the attention deficit/hyperactivity disorder (ADHD). Fortschr Neurol Psychiatr, 75, 275- 284. 4) Meinild, A.K., Sitte, H.H., Gether, U. (2004) Zinc potentiates an uncoupled anion conductance associated with the dopamine transporter. J Biol Chem, 279, 49671-49679. 5) Scholze, P., Norregaard, L., Singer, E.A., et al (2002) The role of zinc ions in reverse transport mediated by monoamine transporters. J Biol Chem, 277, 21505-21513.
Authors:
Markus Huber, MD & Erwin Kirchler, PhD. Department of Psychiatry General Hospital Bruneck-Italy. E-Mail: markus.huber@sb-bruneck.it

One hundred and fifty years of evolutionary theory, psychology and psychiatry 30 January 2008

Henry P O'Connell,
Senior Registrar in Psychiatry
Clare Mental Health Services, Stella Maris Day Hospital, Lisdoonvarna, Co. Clare, Ireland.
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Re: One hundred and fifty years of evolutionary theory, psychology and psychiatry

hpoconnell{at}yahoo.ie Henry P O'Connell

‘In the distant future I see open fields for more important researches. Psychology will be based on a new foundation, that of the necessary acquirement of each mental power and capacity by gradation.’ Charles Darwin.
Charles Darwin first recorded his ideas on ‘transmutation’, a word used to signify the changeable nature of species, in 1844. However, he did not publish his ideas then but instead embarked on painstaking studies of molluscs and other subjects for many years in his home-based laboratory, publishing widely and making some novel discoveries in the area of mollusc biology. We will never know if he would have got around to publishing his theory of evolution if it had not been for the work of a young Naturalist called Alfred Russel Wallace, who forwarded his own (remarkably similar) ideas on the subject to Darwin in 1858. As a result, the two men had their findings jointly presented to the Linnaean Society one and a half centuries ago this year, on July 1st 1858 (Darwin and Wallace, 1858), an event that initially passed by relatively quietly, but that was soon to rock the scientific establishment and society as a whole. Darwin’s notebooks prove that he had been developing his theories on ‘transmutation’ for the previous twenty years, based on his observations on the HMS Beagle and his own ‘home-work’ on molluscs and numerous other subjects. Potential reasons as to Darwin’s delay in publishing his findings include his own wish to produce as much supportive scientific evidence as possible, an ambivalence about publishing a Godless theory in a religious society and, at a personal level, a reluctance to offend his devoted wife Emma, who was a devout Christian (Quammen, 2006).
Charles Darwin contributed directly to modern psychology and psychiatry in the form of his book, ‘The Expression of the Emotions in Man and Animals’, which was effectively the first textbook on human evolutionary psychology and psychiatry (Darwin, 1872). His indirect contribution is far more significant, and involves the application by many others of evolutionary principles to psychology and psychiatry (Nesse, 2000; Stevens and Price, 2000; Buss, 2004). However, despite the universal acceptance of evolutionary theory in all branches of the biological sciences, evolution is effectively ignored in mainstream medicine and in psychiatry and psychology, partly due to difficulties with providing empirical evidence or ‘proof’ and partly due to the corruption and perversion of such ideas in the abuses of Social Darwinism and Eugenics. Perhaps most importantly, there is only yet an emerging evidence base on the clinical applications of evolutionary theory to psychology and psychiatry, and this area remains a challenge to researchers and clinicians with an interest in the subject.
Despite these problems and shortcomings, an undeniable fact remains that evolution is one of the central platforms of biology and, if psychology and psychiatry are to be considered as belonging to the biological (as opposed to the social) sciences, then evolutionary theory must have relevance to the study of the human mind (Abed, 2000).
In a time when ‘biological psychiatry’ has taken on hopelessly reductionistic connotations, for example relating the complexity of human emotions and psychopathology to often questionable and over-simplistic neurotransmitter theories, psychiatry and psychology were never more in need of the fresh perspectives that evolutionary theory would bring to the study of the human mind. A 21st Century presentation to the Linnaean Society is needed, this time on evolutionary psychology and psychiatry.
Declaration of interest: none
References
Abed RT. Psychiatry and Darwinism. Time to reconsider? Br J Psychiatry 2000;177:1-3.
Buss DM. (2004) Evolutionary Psychology. The New Science of the Mind. (2nd edn): Allyn and Bacon, Boston.
Darwin C and Wallace AR. ‘On the Tendency of Species to Form Varieties; and on the Perpetuation of Varieties & Species by Means of Natural Selection’. Read on July1st, 1858, and first published in the Journalof the Linnaean Society of London, vol. 3, 1858.
Darwin C. The Expression of the Emotions in Man and Animals. London: John Murray, 1872.
Nesse RM. ‘Is Depression an Adaptation?’ Arch Gen Psychiatry. 2000;57:14-20.
Quammen D. The Reluctant Mr. Darwin.An Intimate Portrait of Charles Darwin and the Making of His Theory of Evolution. 2006. Atlas Books, New York.
Stevens A and Price J. (2000) Evolutionary Psychiatry: A New Beginning (2nd edn). London: Routledge.

Hot weather and suicide: not the same risk as other causes of mortality 30 January 2008

Antonio Preti,
Professor
Department of Psychology University of Cagliari,
Matteo Cella
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Re: Hot weather and suicide: not the same risk as other causes of mortality

apreti{at}tin.it Antonio Preti, et al.

We read with interest the letter of Salib et al. (2007), about the Page et al. (2007a) paper investigating the relationship between abrupt upwards changes in temperature and suicide, and the reply by Page, Hajat and Kovats (2007b). In this correspondence we would like to take issue with Salib et al’s (2007) opinion that “the mechanism by which high temperature affects the rate of suicide should not be expected to differ from that operating for other causes of death”. Page, Hajat and Kovats (2007b), in their reply listed the most likely factors that are involved in death by thermometric discomfort. These, and other mechanisms, are likely to be common to self-inflicted violence and the other causes of death.
Individuals specifically sensitive to heat, such as children, the elderly and chronically ill patients can be protected from hot temperatures by using many procedures that can be exerted both at home and in hospitals. However, suicide is the lethal outcome of self-initiated behaviours, and it can not be foreseen where, when, and how anyone who attempts suicide will be exposed to heat. It follows that procedures aiming to protect those at risk from heat shock could not be effective in suicide.
Another issue of concern is the positive relationship between temperature and aggression (Anderson, 1989). Many studies indicate that aggressiveness is linked to suicidal behaviour, both directly and indirectly, via the common dimension of impulsivity (Mann et al., 1999). It is still debated whether the link between temperature and aggression is linear or non-linear (Bushman et al., 2005). It is likely that in extreme conditions, the effect of hot or cold temperatures decreases as a consequence of humans being unable to behave effectively due to bodily impairment caused by environmental conditions. Page et al (2007) found that the relationship between the number of suicides and temperature was not significant for the 2003 heat wave: the negative result in this case could be explained as a consequence of an overly elevated or sudden increase in temperature. If it is true that high temperatures induce inhibition in behaviour this should be true for suicidal behaviour and the lower number of suicides found by Page et al (2007) in 2003 could be dependent on that. We believe that there is ample ground to investigate the relations between weather and suicide further and unlike Salib et al. (2007), we think that the impact of the current changes in climate will be more significant on suicide than on other causes of death. (Preti et al., 2007)
References
Anderson, C. (1989). Temperature and aggression: ubiquitous effects of heat on occurrence of human violence. Psychological Bulletin, 106, 74- 96.
Bushman, B.J., Wang, M.C. & Anderson, C.A. (2005). Is the curve relating temperature to aggression linear or curvilinear? Assaults and temperature in Minneapolis reexamined. Journal of Personality & Social Psychology, 89, 62-66.
Mann, J.J., Waternaux, C., Haas, G.L. & Malone, KM. (1999). Toward a clinical model of suicidal behavior in psychiatric patients. American Journal of Psychiatry, 156, 181-189.
Page, L. A., Hajat, S. & Kovats, R. S. (2007a) Relationship between daily suicide counts and temperature in England and Wales. British Journal of Psychiatry, 191, 106-112.
Page, L. A., Hajat, S. & Kovats, R. S. (2007b) Authors’ reply. British Journal of Psychiatry, 191, 561-561.
Preti, A., Lentini, G., & Maugeri, M. (2007). Global warming possibly linked to an enhanced risk of suicide: Data from Italy, 1974- 2003. Journal of Affective Disorders, 102, 19-25
Salib, E., Cortina-Borja, M. & Anderson, D. (2007) Hot weather and suicide: a real riskor statistical illusion? British Journal of Psychiatry, 191, 560.

Authors’ reply to: Mentalising impairment as a trait marker of schizophrenia? by Pousa et al 30 January 2008

Mirjam Sprong,
research, psychologist
Rudolf Magnus Institute for Neuroscience, UMC Utrecht,
Patricia Schothorst, Ellen Vos, Joop Hox, Herman van Engeland
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Re: Authors’ reply to: Mentalising impairment as a trait marker of schizophrenia? by Pousa et al

m.sprong-2{at}umcutrecht.nl Mirjam Sprong, et al.

We would like to thank Pousa et al for their interest in our meta- analysis of Theory of Mind (ToM) impairment in schizophrenia (Sprong et al 2007). They comment that our conclusion that ToM impairment represents a possible trait marker for schizophrenia should remain tentative for two reasons. Regarding their first argument, data on remitted patients are indeed limited and have methodological shortcomings. Only five studies in remitted patients were available, and the number of remitted patients in each of these studies was small. In our paper, we also remarked that the criteria for remission used may have varied across studies, and that other factors may have influenced the results. Thus, we agree that the conclusion that ToM impairment represents a trait marker for schizophrenia should be tentative. In fact, in our paper we did describe it as a possible trait marker. It is important to note that meta-analyses are about effect sizes (ESs) rather than significance levels. By synthesizing data of multiple studies there is more statistical power to detect smaller group differences. Thus, although in 3/5 studies the ToM impairment in remitted patients was not statistically significant, when the studies were combined, the overall effect was significant (Mean d=-0.692, p<.01). So when Pousa et al do no find ToM impairment in stable remitted patients, we are not only interested in the p-levels, but also in the ES. We also agree with the second point that there is evidence of an association between psychotic symptoms and ToM impairment, but do not see why this would argue against our conclusion. Frith (1992) already proposed associations between specific schizophrenia symptoms (e.g. paranoid delusions) and mentalizing impairment, and in their upcoming paper Pousa et al apparently also find significant associations between ToM impairment and psychotic symptoms. Perhaps we should have stated that ToM impairment is a possible trait marker for psychosis rather than schizophrenia. We believe that ToM probably does not represent an all or nothing skill, and that schizophrenia should perhaps be studied using a dimensional in stead of a categorical approach.
References Frith, C.D. (1992) The cognitive neuropsychology of schizophrenia. Psychology Press, Hove, United Kingdom. Sprong, M., Schothorst, P.F., Vos, E., Hox, J., and Van Engeland, H. (2007) Theory of mind in schizophrenia: meta-analysis. British Journal of Psychiatry, 191, 5-13.

PSRHD versus PTSD 30 January 2008

Chris H Cantor,
Psychiatrist
University of Queensland
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Re: PSRHD versus PTSD

cantor98{at}powerup.com.au Chris H Cantor

Rosen, Spitzer and Mc Hugh’s editorial (1) raised problems associated with criterion creep in the diagnosis of PTSD. Conditions including grief, relationship problems, dental care, abortion, traumatic television and humiliating events have entered the arena of PTSD. I support their appeal to psychiatrists to adopt a narrower definition, but beg to go further.
The DSM series has been invaluable for taking the science of psychiatry from its infancy to its adolescence of today. However, we now need to look towards maturity when we will use conceptualizations that involve true entities instead of symptom collections. What do we currently mean by PTSD? Both the “Stress” and “Traumatic” words are so non-specific they are now virtually meaningless – not to mention the “P” and “D”. According to the authors’ concerns the broadened concept of PTSD might euphemistically be described as “Post Something Really Horrible Disorder (PSRHD).”
Panksepp (2) proposed a preliminary taxonomy of distinct emotional modular systems (i.e. core emotions), supported by neuroscientific findings complimented by an evolution-based approach. I suggest that for the high prevalence conditions comprising most of psychiatry, neuroscience without consideration of evolutionary adaptiveness is plain stupidity, as many of the relevant genes would not have persisted without adaptiveness.
Much of the PTSD bracket creep relates to the multiple forms of depression (a loss phenomenon) already catered for in the DSM. I have proposed that PTSD should be viewed as a disorder of defence involving extreme fear as the core emotion (3). As such some improvements to the DSM criteria can easily be accommodated such as differentiating the sleep disturbance associated with depressive ruminations from the listening for the bump in the night of PTSD. Criterion C7 sense of foreshortened future should be scrapped as it clearly is depressive. Space here does not permit other commonsense improvements (see Cantor pages 124-128 (3)).
The notion of “Post Terrible Scare Disorder (PTSD)” might be a more scientifically valid concept if somewhat lacking in elegance as a term.
References
1 Rosen, GM, Spitzer, RL, McHugh, PR. Problems with the pos- traumatic stress disorder diagnosis and its future in DSM-V. Brit J Psychiatry 2008; 192: 3-4. 2 Panksepp, J. Affective Neuroscience: the Foundations of Human and Animal Emotions. Oxford University Press, 1998. 3 Cantor, C. Evolution and Posttraumatic Stress: Disorders of Vigilance and Defence. Routledge, 2005.
Author Dr Chris Cantor Senior Lecturer Department of Psychiatry, University of Queensland, PO Box 1216, Noosa Heads, Queensland 4567 Australia
Ph 61 7 5449 2992 Fax 61 7 5455 4633 Email: cantor98@powerup.com.au

Esomeprazole induced taste impairment associated with olfactory hallucinations 6 February 2008

Adebusola A Akinmokun,
Registrar, Psychiatry of Later Life
St fintans Hospital, Portlaoise, Co. Laois, Ireland, 00353578692874.,
Sabina Fahy, Consultant, Psychiatry of Later Life
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Re: Esomeprazole induced taste impairment associated with olfactory hallucinations

busolakin{at}yahoo.co.uk Adebusola A Akinmokun, et al.

Dear Editor,
I wish to highlight the importance of having a high index of suspicion to drug side effects in all patients complaining of unusual symptoms.
A 76year old caucasian lady was admitted for treatment of a depressive episode associated with olfactory hallucinations and a delusion of smelling foul.
She also complained of inability to taste her food. Due to central representation of gustatory and olfactory functions in the insula(hypothalamus) as well as the link between taste and smell contributing to flavour, we assumed that all these symptoms were attributable to her mental state. However following treatment with antidepressants and antipsychotics the olfactory hallucinations and delusion of smell resolved but the taste impairment persisted. A review of her physical medication side effect profiles showed that esomeprazole can rarely cause taste impairment. Following discussion with her GP a decision was taken to discontinue the drug and her taste improved significantly within a period of 2 weeks
The adverse event report form was completed. This case highlights the need to be aware of patients physical medications in the context of unusual psychopathology or symptoms that do not appear to respond appropriately to prescribed medications.
References:British National Formulary March 2007 page 49

Treatment-resistant depression as an onset of multiple sclerosis 8 February 2008

Pierre LOULERGUE,
MD, MSc
Teaching Hospital Bicetre, Le Kremlin Bicetre, France,
Alexandre ORGIBET
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Re: Treatment-resistant depression as an onset of multiple sclerosis

pierre.loulergue{at}cch.aphp.fr Pierre LOULERGUE, et al.

Psychiatric symptoms are known in patients with multiple sclerosis (MS) for many years (1). According to retrospective studies, depressive symptoms are frequently associated (up to 80%), but scarcely present at the onset of the multiple sclerosis (1%) (2). We present a patient who was admitted to acute psychiatry unit for treatment-resistant depression. The final diagnosis was MS.
A 56-year-old woman was admitted to the psychiatric inpatient unit of our hospital for a resistant depression that started two years ago. She experienced several antidepressants treatments (fluoxetine, paroxetine, citalopram, venlafaxine and climipranine performed at maximal dose during 2 months at least) without any efficacy. She was addressed to discuss convulsivotherapy. Her psychiatric symptoms were dominated by an amotivational state with lack of initiative, a very important ideomotor decrease and a important feeling of tiredness, but no depressive mood, sadness or clinical cognitive deficits were observed. She didn’t report negative or positive psychotic symptoms or suicidal ideas. Her clinical examination revealed ideomotor decrease and a mild cerebellar syndrom. Syphilis serology was found positive (TPHA 1/2560, VDRL negative). The patient was referred to internal medicine for further tests. Lumbar puncture was performed. Cells were inferior to 2/mm3, glucose level was normal and protein level was 0.4 g/L. Neurosyphilis was ruled out (VDRL negative in the CSF). An intrathecal IgG production was found. CT scan was considered normal, whereas brain MRI showed several Gadolinium -enhancing periventricular and juxtacortical lesions. Neuropsychological tests showed cognitive impairment (decline in memory, attention and executive functions). The final diagnosis was chronic progressive multiple sclerosis. High dose steroids were started, and the patient will receive interferon b 1 b course, under strict medical surveillance. Her psychiatric symtpoms were at the end of the treatment of steroids much decreased.
MS is always of unknown etiology, although the autoimmune hypothesis is still privileged. Besides neurological manifestations, psychiatric findings are known for many years. Almost all patients with MS experienced psychiatric dysfunctions, above all thymic dysfunctions (3). But psychiatric features are rarely reported as an onset of MS. Some reported cases found a correlation between symptoms and brain localizations (4). In our case, symptoms and brain localizations were unspecific, although classical. Diagnosis was difficult because the presentation was atypical: late-onset, pure and atypical psychiatric features. Psychiatrists should be aware that MS is a differential diagnosis to atypical psychiatric illness, such as late onset, atypical features, resistance to classical treatment, cognitive disorders, and a brain imagery is much necesssary in those cases to eliminate an organic etiology of the psychiatric symptoms. Treatment is also a major issue, because of the depressive effects of interferon, which is widely indicated in MS. Interferon should be administered under tight medical surveillance, and patients should be educated about the side effects.
REFERENCES 1. Thomas PW, Thomas S, Hillier C, Galvin K, Baker R. Psychological interventions for multiple sclerosis. Cochrane Database Syst Rev.2006; 1:CD004431. 2. Rickards H. Depression in neurological disorders: an update. Curr Opin Psychiatry 2006; 3:294-298 3. Diaz-Olavarrieta C, Cummings JL, Velazquez J, Garcia de la Cadena C. Neuropsychiatric manifestations of multiple sclerosis. J Neuropsychiatry Clin Neurosci 1999; 1:51-57 4. Ashgar-Ali AA, Taber KH, Hurley RA, Hayman LA. Pure neuropsychiatric presentation of multiple sclerosis. Am J Psychiatry 2004; 2:226-231

PTSD's Future 21 February 2008

Gerald M. Rosen,
Clinical Psychologist
University of Washington,
Robert L. Spitzer, Paul R. McHugh
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Re: PTSD's Future

grosen{at}u.washington.edu Gerald M. Rosen, et al.

We welcome the responses to our editorial on problems with the PTSD diagnosis and its future in DSM-V. On the lighter side, we observe that yet more proposals for posttraumatic conditions are proposed (e.g., PSRHD), thereby demonstrating an ever increasing incidence of “acronymitis.” This disorder, characterized by a seeming compulsion to develop acronyms, was to the best of our knowledge first labeled by Isaac Marks.1
On a more serious note, we would like to use our limited space to highlight several observations that we have taken from an extensive review of the PTSD construct.2 This review proposes that PTSD’s defined clinical syndrome might best be conceptualized as encompassing a broad range of reactions to adverse events, that are in turn influenced by multiple dimensionally distributed factors (e.g., pre- and post-incident risk variables, peri-traumatic appraisals, and real-life consequences). The long history of general stress studies, and more recent research on PTSD, has demonstrated that these multiple factors and their complex interrelations yield a wide range of outcomes after adverse events. Within this framework, it remains an open question whether any attempt to define a distinct posttraumatic syndrome can lead to a true disorder in nature that is specific to a subset of stressors. Perhaps such a disorder exists, and PTSD or some other acronym should remain in the psychiatric nomenclature. For the moment, however, it appears that the very literature spurred by the creation of PTSD has demonstrated, somewhat ironically, that the construct is flawed. It is in the context of these issues, that we acknowledge concerns raised in the Journal’s letters and encourage continued discussion on the validity of the PTSD diagnosis.
References
1. Marks, I. Personal communication. Seattle, Washington: January 15, 2005. 2. Rosen GM, Lilienfeld, SO. Posttraumatic stress disorder: An empirical analysis of core assumptions. Clin Psychol Rev in press; doi.org/10.1016/j.cpr.2007.12.002

Fall in the Rate of Usage of Electroconvulsive Therapy: Clinical and Research Implications 21 February 2008

Allan I Scott,
Consultant Psychiatrist and Honorary Senior Lecturer
Royal Edinburgh Hospital,
Tracy Fraser
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Re: Fall in the Rate of Usage of Electroconvulsive Therapy: Clinical and Research Implications

Fiona.Morrison{at}lpct.scot.nhs.uk Allan I Scott, et al.

Our interest in this topic was re-awakened when, in 2003, the then National Institute for Clinical Excellence (NICE) published clinical guidelines that intended to restrict the circumstances for the use of electroconvulsive therapy (ECT) (1). The guidance was controversial, and the Royal College of Psychiatrists subsequently published its own guidance that argued that NICE was too restrictive about the place of ECT in the treatment of major depression, the commonest contemporary indication for ECT (2). It was therefore unclear if NICE would achieve its aim of reducing the use of ECT. We have already reported that there was no early effect of the NICE guidance in that the rates of usage of ECT in the City of Edinburgh were virtually identical in the individual years 2003-2005 (3).
We now report the most dramatic fall in the rate of usage of ECT that we have ever observed between consecutive years. In the years 2006 and 2007 the rates of usage of ECT were only 0.82 and 0.88 patients per 10,000 total population. This is approximately one-third less than the rate in 2005, and three quarters less than the rate in 1993 (3).
The clinical significance of the fall in the rate of usage of ECT has never been systematically assessed. Observers have suggested that there is less need for ECT as the number of effective alternative options increase, and as psychiatrists become more experienced with these options. One only hopes that those severely ill people who were formally treated with ECT are now offered equally effective alternatives, but this is open to doubt. ECT is still the most efficacious treatment for major depression, particularly when the symptoms are severe (4). The results of the recent STAR*D trial were salutary: the cumulative remission rate from major depression was only 67% after four sequential and carefully supervised acute treatment schedules (5).
The research implications are clearer. Edinburgh has a long history of ECT research, but the latest fall in usage has meant that we have not been able to complete a controlled comparison of magnetic seizure therapy and orthodox ECT. If the Edinburgh experience is replicated elsewhere, the only options for future clinical research would be to support collaborations among several ECT clinics or the establishment of a regional or national affective disorders research centre, part of the research programme to include ECT.
Declaration of interest: none

Re: Goya Painting on BJP cover 27 February 2008

Anne Weatherhead,
Psychiatrist
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Re: Re: Goya Painting on BJP cover

anneweatherhead{at}doctors.org.uk Anne Weatherhead

Dear Editor,
While I can understand that those producing the Journal of Psychiatry wish to give the cover some colour and interest, I feel constrained to express concern about the Goya painting reproduced on the cover of the current issue.
I am a lover of art, and have no quarrel at all with the inclusion of a work such as this in the body of a professional magazine, but placing it on the cover is quite another matter.
The Journal will be placed on many library shelves, and will be viewed by many ordinary people as it lies on coffee tables in the homes of members. To my mind it can only serve to undermine all the good work which is being done to try and reduce the stigma associated with mental illness.
It is more than just an evocative painting of a bygone age, but surely not an image we wish to present on a journal of contemporary psychiatry.
Yours faithfully,
Anne Weatherhead

Confidentiality 17 March 2008

Robin Jacoby,
Prof Emeritus of Old Age Psychiatry
University of Oxford
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Re: Confidentiality

robin.jacoby{at}psych.ox.ac.uk Robin Jacoby

The March issue of the Journal showed a photograph of a named, unfortunate Bethlem patient, whilst the Contents page gave a potted clinical history. Was I the only recipient of this issue gnawed by the question: at what point, if any, does our duty of confidentiality end? Is it simply a matter of time, and that the passage of 150 years or so deprives a patient of the right to confidentiality? I do not know the answer to these questions, but they trouble me. This might be because I have had one or two well-known people as my own patients. Iris Murdoch’s husband named me in a book and a national newspaper as a doctor who cared for her when she had Alzheimer’s disease. However, the journalists who telephoned me for information were told that I would say nothing because her death did not end my own duty of confidentiality to her.
I am sorry if this letter sounds self-righteous which is not my intention. Rather, I should hope to start a debate in these columns..

Evolutionary Psychiatry on the 150th anniversary of Darwin's Origin 9 April 2008

Riadh T Abed,
Psychiatrist
Rotherham District General Hospital
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Re: Evolutionary Psychiatry on the 150th anniversary of Darwin's Origin

abedrt{at}btinternet.com Riadh T Abed

It was Theodosius G. Dobzhansky, the renown geneticist and evolutionary biologist who wrote that nothing made sense in biology except in the light of evolution yet psychologists and psychiatrist, 150 years after the publication of Darwin’s Origin, and when Darwinian principles have become the organizing framework for all biological sciences, continue to think in pre-Darwinian terms. Dr O’Connell’s letter is therefore, a welcome reminder of this rather anomalous state of affairs. The most common challenge leveled at evolutionary approaches to mental disorders is that they are ‘Just So’ stories (i.e. that they are untestable and irrefutable). This challenge can be easily met. Evolutionary-based hypotheses are propositions that stand or fall by the evidence and by their predictive value and should be discarded if refuted. Hence the evolutionary theories that propose that schizophrenia is a disorder of the social brain (Brune, 2003; Burns, 2007) or related to the evolution of brain asymmetry and language (Crow, 2003) await support or refutation by empirical evidence. Similarly the theory that eating disorders (an area where non-evolutionary theorizing has been particularly sterile) represent disorders of female mating strategy (Abed, 1998; Faer et al, 2005) will be tested and discarded or amended based on empirical evidence. One major insight of evolutionary theory is that species not only have traits and characteristics but also a distinctive history during which these traits were shaped by a process of natural and sexual selection. And it is the careful piecing together of this history, utilizing evidence from a myriad of disciplines (archeology, geology, primatology, molecular biology etc.) that produces the consilience of evidence that is unique to the evolutionary approach (see Wilson, 1998). Thus, placing the human mind back within the realm of evolutionary biology where it belongs has the potential of generating insights that would otherwise be impossible to conceive. It is rather intriguing that whereas there is a determined and vocal opposition to the application of Darwinian theory to human psychology and the mind there is almost no objection to the hermeneutic approach to psychiatry which is a self-confessed antiscientific approach that excludes mental phenomena from the laws of causality altogether. Is it time to for our college to consider incorporating evolutionary psychiatry/psychology into the training curriculum for the MRCPsych? Also, is the time ripe for members/fellows of the college to form a college special interest group and to demand sessional time at the college annual meeting to present and debate research and theoretical work within these fields?
References:
Abed, R. T. (1998). The sexual competition hypothesis for eating disorders. British Journal of Medical Psychology, 71, 525–547.
Brune, M (2003) Social cognition and behaviour. In The Social Brain: Evolution and Pathology (eds M. Brune, H. Ribbert and W. Schiefenhovel) pp277-313. Wiley.
Burns, J (2007) The Descent of Madness: Evolutionary Origins of Psychosis and the Social Brain. Routledge.
Crow, T.J. (2003) ProtocadherinXY—a candidate gene for cerebral asymmetry and language. In The Social Brain: Evolution and Pathology (eds M. Brune, H. Ribbert and W. Schiefenhovel) pp61-78. Wiley.
Faer, L., Hendricks, A., Abed, R. and Figueredo, A.J. (2005) The evolutionary psychology of eating disorders. Psychology and Psychotherapy: Theory, Research and Practice,78, 397–417
Wilson, E.O. (1998) Consilience: The Unity of Knowledge. Little, Brown and Company.
Declarations of Interests: None

Buspirone induced Hypomania 16 April 2008

Nand Kumar,
Assistant Professor Psychiatry
All India Institute of Medical Sciences ,New Delhi, India,
Jain Pramit
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Re: Buspirone induced Hypomania

nandkm2001{at}yahoo.co.in Nand Kumar, et al.

Buspirone hydrochloride is an anxiolytic agent that is not chemically or pharmacologically related to the benzodiazepines, barbiturates, or other sedative/anxiolytic drugs and its anxiolytic effectiveness is comparable to that of benzodiazepines. To date there has been two published reports of buspirone induced mania in patients with Bipolar affective disorder and resistant depression with anxiety (1,2). However there is no reported direct association of buspirone with generalized anxiety disorder. In our outpatient unit we recently observed a patient with generalized anxiety disorder who developed hypomania which we feel directly associated with with Buspirone. Mr. P 23 year old unmarried male, student presented with history of 18 months of psychiatric illness characterized by predominant anxious mood, difficulty in concentration, restlessness, and light headedness which would last for most of the time with occasional, sweating and palpitation when he has to face some interview. On assessment the patient reported no predominant sustained mood changes and well adjusted pre morbid personality with non- contributory past, family or personal history. The patient received diagnosis of generalized anxiety disorder as per ICD 10 clinical and diagnostic guidelines. To rule out associated organic condition routine investigations (CBC, LFT /KFT) with urinary drug screening and thyroid function test were done which were within normal limits. The patient was started with tablet buspirone 10 mg /day in two divided doses and clonazepam 0.25mg BD. Within two months the doses of buspirone was increased to 30 mg /day in two divided doses and clonazepam was tapered and stopped. The Patient remarkably improved with Buspirone (30 mg per day) and he remained asymptomatic in subsequent follow up once in two months for 18 months. Subsequently the patient reported over cheerfulness, increased self esteem, overconfidence, over socialization, increased sexuality, little overspending and decreased sleep since last two months. He did not report perceptional disturbances and substance abuse during this period. His YMRS score was found to be 9. Buspirone was discontinued and the patient returned to his pre morbid condition within 2 weeks. After 6 months of discontinuation of Buspirone Currently the patient is asymptomatic. We observed that there is direct association between continuation of buspirone therapy and development of hypo manic symptoms. Buspirone has a high affinity for serotonin (5-HT1A) receptors and moderate affinity for brain D2-dopamine receptors and its action seems to be that of a presynaptic dopamine agonist and a 5-HT1A agonist. Buspirone enhances CNS catecholaminergic activity while inhibiting CNS serotonergic cell activity. CNS serotonergic and catecholaminergic systems are both hypothesized to be involved in the etiology of BPAD. Thus the net enhancement of noradrenergic activity relative to serotonergic activity is consistent with current hypothesis regarding the neurobiology of mania. This case suggests buspirone may leads to development of hypomania and it would be prudent to watch for similar effects in patients taking this class of anxiolytic drug. References: 1. Liegghio NE, Yeragani VK. Buspirone-induced hypomania: a case report.J Clin Psychopharmacol. 1988 Jun; 8(3):226-7. 2. McDaniel JS, Ninan PT, Magnuson JV. Possible induction of mania by buspirone. Am J Psychiatry. 1990 Jan;147(1):125-6.

Salt Ingestion To Disguise Water Loading in a Patient With Anorexia Nervosa 18 April 2008

Matthew O Cahill,
Specialist Registrar
Eating Disorders,
Sean Lubbe, and Eric Johnson-Sabine
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Re: Salt Ingestion To Disguise Water Loading in a Patient With Anorexia Nervosa

matthew231{at}btinternet.com Matthew O Cahill, et al.

Sir: We report a case of excess salt ingestion as a feature of anorexia nervosa. Morgan and Lacey reported a case of pathological salt ingestion, or ‘salinophagia,’ advising that it be added to the list of maladaptive behaviours associated with anorexia nervosa.
We continue this discussion by presenting a 32-year-old single woman with a seventeen-year history of anorexia nervosa (World Health Organisation, 1992) who has had several inpatient admissions at a BMI of 12. She has acknowledged that she usually tries to disguise her weight by water loading in order to avoid admission. Water loading is a behaviour frequently seen in severe anorexia nervosa, where it is employed to disguise the degree of weight loss from professionals and carers. Our patient has previously been aware that her water loading was exposed by hyponatraemia on measurement of serum electroytes.
In addition to water loading, she has used other methods to disguise her weight, such as sewing items into her underwear prior to weighing. Despite being closely supervised, she managed to water load by concealing water in shampoo containers during showering. We are fortunate in that our patient recognises her struggles with her eating disorder, and has begun to work with us in attempt to overcome her difficulties.
A random room search following poor weight gain revealed copious amounts of salt packets. Our patient subsequently admitted to excess salt ingestion. She believed that the salt would lead to retention of the water, which she was drinking to excess, and would therefore assist in disguising her weight. She also believed it would help to prevent coma due to possible hyponatraemia.
Another theory postulated is that our patient was attempting to conceal her water loading by preventing hyponatraemia, and was in fact self-medicating to avoid discovery. Prior to finding the salt, our patient was chronically hyponatraemic, the lowest value being 129 mmol/l. Had she not regularly ingested the salt, her plasma sodium could have fallen lower than this, possibly to fatal levels.
The phenomenology of her behaviour appeared to be neither self- punitive nor ego-syntonic, as in Morgan and Lacey’s case study. Her salt ingestion also lacked the features of obsessive-compulsive disorder or pica. By placing the patient on constant close supervision, combined with health education, (and simply instructing her to stop), she managed to control the behaviour. She remarked that it was a relief to know that her behaviours had been discovered.
Clinicians working with similar cases should be vigilant regarding possible salinophagia to disguise water loading. We also agree with previous authors in that salinophagia should be added to the list of maladaptive behaviours associated with anorexia nervosa and bulimia nervosa.
Morgan, J.F, Lacey, J.H. (1998) Salinophagia in Anorexia Nervosa. British Journal of Psychiatry 173, 352-353.
World Health Organisation (1992) Tenth Revision of the International Classification of the International Classification of Diseases (ICD10). Geneva: WHO

Clozapine-Induced Stammer and EEG abnormalities in a bipolar patient 18 April 2008

Lena N Abreu,
Psychiatrist, research fellow
University of Sao Paulo Medical School,
Cilly K. Issler, Beny Lafer
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Re: Clozapine-Induced Stammer and EEG abnormalities in a bipolar patient

lenabuco{at}hotmail.com Lena N Abreu, et al.

TO THE EDITOR: Stammer and seizures has been previously described in 4 cases of schizophrenic and schizoaffective patients during clozapine treatment (1,2,3,4), but to our knowledge this side effect has not been described in bipolar patients. In this letter, we describe a case of clozapine induced stammer associated with abnormalities in EEG on a bipolar I patient and discuss the clinical implications in the light of previous reports in schizophrenia .
Ms. F, a 32 year-old woman who had been diagnosed with bipolar disorder type I, with onset at age 15, was treated with clozapine for treatment of refractory manic episodes. When she was discharged from the hospital she was using clozapine at the dose of 150mg/day. When the dose was increased to 175mg, she developed stammer in a fluctuating pattern. As she still presented manic symptoms and even with eletroconvulsive therapy she was not showing improvement, clozapine was increased to 225mg/day. At this point, the stammer became more severe and incapacitating. An EEG showed the appearance of sporadic theta waves with projections in left temporal area. Valproate was introduced in order to minimize this side effect and the dose was increased to 1.500 mg/day with a blood level of 82µg/dl. Even after the introduction of valproate, the stammer did not improve. Due to the severity of stammer, clozapine was discontinued. After 3 weeks,the stammer disappeared and a new EEG was performed with normal pattern.
This case complements the four other cases that we know about clozapine induced stuttering (1,2,3,4) and abnormal electric brain activity (2,4). This report is the first described in a bipolar patient (the others were in three schizophrenic patients (1,3,4) and one in a schizoaffective patient (2). Furthermore, it presents different aspects when compared with the other cases reported previously: the stuttering started at lower doses of clozapine , it did not respond to anticonvulsant therapy (valproate) and the patient even in the presence of EEG abnormalities did not present any type of seizure. After the discontinuation of clozapine all the symptoms remitted and the EEG normalized. The pathogenesis of development stuttering is unclear, but recent observations related this condition to epileptic-like brain activity (3) and clozapine shows more often alterations in EEG and induced seizures compared to other antipsychotics (5). Although clozapine is not frequently prescribed in bipolar disorder, it has been described to be beneficial in refractory cases (6) Therefore clinicians should be aware of this uncommon side effect, witch can lead to treatment failure.
References: 1.Ebeling T, Compton A, Albright DW: Clozapine-induced stuttering. Am J Psychiatry 1997; 154:1473. 2.Thomas P, Lalaux N,Vaiva G, Goudemand M: Dose-Dependent stuttering and Dystonia in a patient taking clozapine. Am J Psychiatry 1994; 151:1096. 3.Supprian T, Retz W,Deckert J:Clozapine-induced Stuttering: epileptic Brain activity. Am J Psychiatry 1999; 156:1663. 4.Duggal HS, Jagadheesan K, Haque Nizamie S: Clozapine-induced stuttering and seizures. Am J Psychiatry 2002;159:315. 5.Haller E, Binder R: Clozapine and seizures. Am J Psychiatry 1990; 147:1069-1071.

Mental Health related paintings of Vincent van Gogh 25 April 2008

Arabinda Narayan Chowdhury,
Consultant Psychiatrist
Northamptonshire Healthcare NHS Trust
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Re: Mental Health related paintings of Vincent van Gogh

arabinda.chowdhury{at}btinternet.com Arabinda Narayan Chowdhury

I wish to thank the Editorial Board of British Journal of Psychiatry for printing the portrait of Dr. Felix Rey, painted by Vincent Van Gogh on the cover of April 08 issue.1 This is definitely a way of honorouing this genius artist who inspite of his episodic mental illness creatively contributed to the repertoire of impressionistic art of his time. But I wonder why this painting was chosen? May be this portrait is currently on exhibition at the Royal Academy in London. Otherwise, I think a different choice could have been more meaningful. Following are a few thoughts on this matter. Records show the names of three medical doctors who were involved with the treatment of van Gough. Dr. Felix Rey (1867-1932), who diagnosed Vincent’s epilepsy and was credited for prescribing potassium bromide for his recovery.2 Dr. Théophile Zacharie Auguste Peyron (1827- 95), of Saint-Remy asylum who also diagnosed “a type of epilepsy” and gave him hydrotherapy. He was a very understanding physician who arranged facilities within the asylum so that van Gogh would be able to continue his paintings and artwork. Dr. Paul Gachet (1828-1909), a homeopathic therapist living in Auvers-sur-Oise, near Paris, where Vincent spent last ten weeks of his life.
We have no picture of Dr. Peyron but Van Gough, as a token of friendship painted two portraits and an etching of Dr. Gachet, one of which (Portrait of Doctor Gachet, June 1890) was auctioned in 1990 for an astounding sum of US$ 82.5 million, the highest price ever paid for a painting till now! Young intern Dr. Rey probably maintained distance because he saw van Gogh in the context of his psychotic state, after the ear mutilation, and episode with a young prostitute. He failed to value the creativity in the artist and thus was not possessive of the gift presented to him. This was well exemplified in his own account as: “Vincent was above all a miserable, wretched man, ... He often complained that he was the only painter in town and therefore could not talk to anyone about his art. For lack of such a colleague, he would talk to me about complementary colors. But I really could not understand why red should not be red, and green not green! . . . When I saw that he outlined my head entirely in green (he had only two main colors, red and green), that he painted my hair and my mustache--I really did not have red hair-- in a blazing red on a biting green background, I was simply horrified. What shouldn’t I do with this present? Nor did I know what to do with other paintings, The Hospital Garden and Dormitory in the Hospital, that were also presented to me. I offered them to the Administrator of Hospitals, who happened to be visiting, but he would have no part of them and passed them on to the secretary of the clinic. You see, this gentleman is himself a painter . .Unfortunately, Van Gogh’s paintings did not find favour with him either. This gentleman called them "dirty obscenities" and presented them, now for the fourth time, to the druggist. More careful than the previous owners, this man kept them and sold them much later, when the value of the works by the dead Van Gogh had reached a very high level, for fabulous prices.” 3
Dr Gachet, on the other hand, was himself an artist and was very supportive of van Gough and valued his creative instinct. Vincent had found a “true friend” in him. It is a matter of pride for the medical fraternity that Dr. Gachet was highly admired by Vincent and that he tried his best to keep Vincent’s torment soul in peace and allow his creativity to flourish in the village atmosphere of Auvers. Vincent, under the care of Dr. Gachet, begins to paint with incredible energy, producing more than 80 paintings in the last two months of his life. “The importance of Dr.Gachet’s positive influence can hardly be exaggerated. It was Gachet who brought home to van Gogh the significance and value of his art, Gachet who used his natural authority to persuade van Gogh to do a new series of portraits, and a number of townspeople to sit for him”. 4 The sketch of van Gogh on his deathbed was done by Dr. Gachet. Moreover, van Gogh created a series of paintings illustrating the Saint-Remy asylum, few of the masterpieces are: Ward in the Hospital in Arles (Apr 1889); The Courtyard of the Hospital at Arles (Apr 1889); at least four paintings on Trees in the Garden of Saint-Paul Hospital (Oct 1889); four on The Garden of St Paul Hospital (Oct 1889); Fountain in the Garden of Saint-Paul hospital (May 1889); Stone Bench in the Garden of Saint Paul Hospital (Nov 1889); Portrait of a patient in Saint-Paul hospital (Oct 1889), Corridor in Saint Paul Hospital (Oct 1889), and A road at Saint-Remy with female figure (Dec 1889). Any of them may be appropriate for the BJP to focus on his creativity in using colour and space to astonishing effect. Those paintings are carrying the historical value of the mental health perspective so far as the asylum culture of his time is concerned.
Conflict of Interest: None
Arabinda Narayan Chowdhury, Stuart Road Clinic, Northamptonshire NHS Trust, Corby, Northants NN17 1RJ.
1. Editorial Board. Cover picture. Br J Psychiatry 2008,192,4: first cover.
2. Blumer D. The illness of Vincent van Gogh. Am J Psychiatry 2002, 159: 519-526.
3. Brauman M. With friends of Van Gogh's in Arles. Kunst and Kunstler 1926. Coated by Auden WH in Van Gogh: A self-portrait: Letters revealing his life as a painter. Greenwitch, Connecticut: New York, 1961, pp. 353-54
4. Walther IF, Metzger R. Van Gogh: The complete paintings.2006, Taschen
GmbH: Koln, pp 648.

Cannabidiol and psychotic symptoms 30 April 2008

Satish K Karunakaran,
Consultant Psychiatrist
Queensland Health
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Re: Cannabidiol and psychotic symptoms

Satish_Karunakaran{at}health.qld.gov.au Satish K Karunakaran

An interesting paper. The notion that cannabis smokers may differ in their metabolism of cannabis and this may affect the pharmacological properties experienced and in turn the propensity for developing psychotic symptoms need further exploration.
However, some issues need discussion. The sample is from a population of substance abusers. It is highly likely that some of them also abuse other psychotomimetic substances including cocaine, amphetamines and LSD. Although the authors state that the groups were similar in their “recreational drug use”, it is unclear whether they specifically controlled for these substances. Differential use of these drugs could easily account for the observed differences between the groups with regard to ‘psychosis proneness’ and ‘delusional thinking’. Moreover, stimulants can also significantly affect ‘introvertive anhedonia’ factor scores.
It should also be pointed out that the numbers mentioned do not add up. ‘Methods’ section report that the sample consisted of 140 individuals, of whom 54 tested positive for a cannabis related compound (20 with THC only; 26 with THC+CBD and 8 CBD only) with presumably 86 with no cannabinoids. Yet, when they divided the sample, it became 20 (THC only); 27 (THC+CBD) and 85 (no cannabinoids).

Mental Health related paintings of Vincent van Gogh 22 May 2008

Arabinda Narayan Chowdhury,
Consultant Psychiatrist
Northamptonshire Healthcare NHS Trust
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Re: Mental Health related paintings of Vincent van Gogh

arabinda.chowdhury{at}btinternet.com Arabinda Narayan Chowdhury

Many thanks to BJP for printing the Vincent Van Gogh’s work on Dr. Felix Rey1 for honorouing this genius artist who inspite of his episodic mental illness creatively contributed to the repertoire of impressionistic art of his time. But I wonder why this painting was chosen? I think a different choice could have been more meaningful. Three medical doctors were involved with the treatment of van Gough. Dr. Felix Rey (1867-1932), who diagnosed Vincent’s epilepsy. Dr. Théophile Zacharie Auguste Peyron (1827-95), of Saint-Remy asylum who also diagnosed “a type of epilepsy”. He was a very understanding physician who arranged facilities within the asylum for his paintings and artwork. Dr. Paul Gachet (1828-1909) treated him during his last ten weeks of life.
Vincent painted two portraits and an etching of Dr. Gachet, one of which (Portrait of Doctor Gachet, June 1890) was auctioned in 1990 for an astounding sum of US$ 82.5 million. Young intern Dr. Rey probably maintained distance because he saw van Gogh in the context of his psychotic state, after the ear mutilation episode with a prostitute. He failed to value the creativity in the artist and thus was not possessive of the gift presented to him, which he disclosed afterwards: “Vincent was above all a miserable, wretched man, ... he would talk to me about complementary colors. But I really could not understand why red should not be red, and green not green! . . . When I saw that he outlined my head entirely in green (he had only two main colors, red and green), that he painted my hair and my mustache--I really did not have red hair--in a blazing red on a biting green background, I was simply horrified. What shouldn’t I do with this present?...” 2 Dr Gachet was very supportive of Gough and valued his creative instinct. Vincent had found a “true friend” in him. It is a matter of pride for the medical fraternity that Dr. Gachet was highly admired by Vincent and that he tried his best to keep Vincent’s torment soul in peace and allow his creativity to flourish in the village atmosphere of Auvers. van Gogh created a series of paintings, at least 14, illustrating the Saint-Remy asylum. Any of them may be appropriate for the BJP to focus on his creativity in using colour and space to astonishing effect. Those paintings are carrying the historical value of the mental health perspective so far as the asylum culture of his time is concerned.
Conflict of Interest: None
Arabinda Narayan Chowdhury, Stuart Road Clinic, Northamptonshire NHS Trust, Corby, Northants NN17 1RJ.
1. Editorial Board. Cover picture. Br J Psychiatry 2008,192,4: first cover.
2. Brauman M. With friends of Van Gogh's in Arles. Kunst and Kunstler 1926. Coated by
Auden WH in Van Gogh: A self-portrait: Letters revealing his life as a painter.
Greenwitch, Connecticut: New York, 1961, pp. 353-54

“TRUMAN” SIGNS AND VULNERABILITY TO PSYCHOSIS 30 May 2008

Paolo Fusar-Poli,
Lecturer
Institute of Psychiatry, London,
Oliver Howes, Lucia Valmaggia, Philip McGuire
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Re: “TRUMAN” SIGNS AND VULNERABILITY TO PSYCHOSIS

p.fusar{at}libero.it Paolo Fusar-Poli, et al.

Dear Editor,
Prospective studies indicate that individuals meeting a range of clinical criteria such as attenuated psychotic symptoms, brief psychotic episodes or functional decline and family history of schizophrenia, have a high risk of being in the prodromal phase of a psychotic disorder (1). However, these studies do not differentiate between different symptom characteristics. Understanding the phenomenology of attenuated psychotic symptoms may aid the discrimination of truly prodromal from low risk individuals.
Mr. MA, a 26 year old postman, presented with the feeling there was something subtle going on around him that others knew about but he didn’t. He had a vague sense that people around him were “acting”, he was the focus of their interest and they knew a secret that was kept from him. Furthermore he felt “detached from the environment” and had a sense the world was slightly unreal, as if he was the eponymous hero in the film “The Truman Show”. He was preoccupied with the belief that he was the focus of something that he couldn’t quite understand. At no point did his conviction reach delusional intensity. There was no evidence of hallucinations, thought disorder, odd behaviour or other features of psychosis. The symptoms met the criteria for an “At Risk Mental State, ARMS”, which is associated with a 25-45% risk of developing psychosis in the next 12 months. Over the ensuing nine months these preoccupations became more pronounced he developed grandiose and persecutory delusions, and marked thought disorder. He was diagnosed with DSM-IV schizophrenia. Following treatment with quetiapine 150mg bd these delusions and the thought disorder have resolved, although he continues to experience occupational impairment, and has not been able to return to work.
In this case MA had a pre-occupying belief that the world had changed in some way that other people were aware of, which he interpreted as indicating he was the subject of a film and living in a film set (a ‘fabricated world’). This cluster of symptoms, which we have termed the ‘Truman syndrome’ is a common presenting complaint in individuals attending the OASIS clinic for people who may be in the prodromal phase of schizophrenia. Underlying the phenomenology of these symptoms are several features that are consistent with theories of delusion formation resulting from a process of aberrant salience (2). Firstly there is the sense that the ordinary is changed or different, and that there is particular significance in this. This is coupled with a searching for meaning, which, in this case, results in the ‘Truman explanation’. The third features is a profound alteration of subjective experience and of self-awareness, resulting in unstable first-person perspective with varieties of depersonalization and derealisation, disturbed sense of ownership, fluidity of the basic sense of identity, distortions of the stream of consciousness and experiences of disembodiment (3). We suggest that these experiences characterize the earliest clinical manifestation of aberrant salience leading to delusion formation. The qualitative phenomenology of the prodrome has not been widely studied, but may, as in this case, be a useful indicator of impending psychosis.
References:
1) Rossler W, Riecher-Rossler A, Angst J, Murray R, Gamma A, Eich D, van Os J,Gross VA. Psychotic experiences in the general population: a twenty-year prospective community study. Schizophr Res 2007;92(1-3):1-14.
2) Kapur, S., Mizrahi, R. & Li, M. From dopamine to salience to psychosis--linking biology, pharmacology and phenomenology of psychosis. Schizophr Res 2005;79:59-68.
3) Sass, L. & Parnas, J. Self, consciousness, and schizophrenia. Schizophrenia Bulletin, 203;29:427-444.

Re: Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT) 5 June 2008

H Niederhofer,
NPI
General Hospital of Bolzano, Serv. NPI
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Re: Re: Zinc, Attention-Deficit/Hyperactivity Disorder (ADHD) and the Dopamine Transporter (DAT)

helmutniederhofer{at}yahoo.de H Niederhofer

Involvement of zinc deficiency has been suggested in patients suffering from ADHD [1]. The findings reinforce that zinc as a supplementary medication and/or adjunct to stimulants (mostly methylphenidate) might be beneficial in the treatment of ADHD. However the biochemical mechanism of zinc by the ADHD remains unknown. Neuroimaging studies show a higher striatal DAT-density by ADHD-patients (methylphenidate responder) as compared to healthy controls. Methylphenidate the most commonly used and first-line stimulant of ADHD- treatment acts as a potent DAT-uptake inhibitor (like other amphetamines and cocaine). The decrease in available striatal DAT-binding sites via DAT -blockage under treatment with methylphenidate, corresponding with an increase of dopamine in the synaptic cleft, correlates well with the clinical improvements of the ADHD-symptoms (hyperactivity, impulsiveness, inattention, impaired socialization) [2] [3]. Zinc, however, seems to have a stimulant-like action on the DAT. Binding zinc to the three endogenous zinc-binding sites on the extracellular face of the human DAT (His 193, His 375, and Glu 396) leads to potent inhibition of dopamine uptake (blockage of the inward DAT-translocation process) [4] [5]. Moreover, zinc was found to enhance binding of cocaine analogues to the DAT and that zinc differentially enhances the carrier-mediated dopamine efflux on the DAT (facilitated reverse transport) [4] [5]. So it is obvious that zinc deficiency may be correlated with ADHD. Zinc deficiency could intensify the DAT-inward translocation process and inhibit the DAT-reverse transport. In contrast zinc as a supplementary medication and/or adjunct to stimulants could equalize (increase) the chronical dopamine deficit by ADHD-patients – through: (i) inhibition of the DAT-inward translocation process, (ii) facilitating of the DAT-reverse transport, (iii) and/or through an enhanced DAT-binding of prescribed stimulants. Zinc so may be surely a therapeutical tool in the treatment of ADHD. We verified this hypothesis in a 8year old patient, suffering from ADHD combined type according to DSM-IV criteria. Before initiating zinc treatment, he received 20mg Methylphenidate daily for approx. 2 years. On the 18 item Conner Scale (maximum score 54, cut off 27) there was an improvement from 39 to 28, which rose again up to 36 after having sospended Methylphenidate treatment. Being medication-free for 2 months, his serum zinc level was 527 ug/ml (range 700-1200ug/ml) and rose up to 982 ug/ml after 3 weeks of zinc treatment (every day one tablet containing 15 mg Zinc, as well as 70 mg Histidin and 19 mg Cysteine to facilitate assumption). The Conner-Score improved up to 25. Although there was an obvious improvement, we added Methylphenidate 20mg daily once again (intended by the mother because of the start of a school.year) and obtained an additional improvement of the Conner-Score of 22. Another two patients, also diagnosed with ADHD combined type according to the DSM-IV criteria, who also received Methylphenidate 20mg daily, had an zinc serum level of 779ug/ml and 836 ug/ml respectively. While continuing Methylphenidate therapy, additional zinc therapy (also 1 tablet daily of the same preparation as described above) (final serum zinc level 1256ug/ml and 1045ug/ml respectively) also aumented the improvement of the Conner Score (without Methylphenidate 41(38), under Methylphenidate but without zinc 28(27), under Methylphenidate and zinc 32(21). To verify these observations, however, more research is needed

Exposure Therapy for Paranoid Anxiety: a Case Report 5 June 2008

Dr Nir Essar,
Psychiatrist
Psagot Institue,
Menachem Ben-Ezra, Yuval Palgi, Merav Barkavi-Shani
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Re: Exposure Therapy for Paranoid Anxiety: a Case Report

nir{at}psagot.com Dr Nir Essar, et al.

Nir Essar, MD1, Menachem Ben-Ezra, PhD2, Yuval Palgi, MA3, & Merav Barkavi-Shani MSW1
1Psagot Institute, Tel Aviv, Israel. 2 School of Social Work, Ariel University Center of Samaria, Ariel, Israel 3 Department of Psychology, Tel Aviv University, Tel Aviv, Israel
Correspondence: Dr. Nir Essar, Psagot Institute, Tel Aviv, Israel. E- mail: nir@psagot.com
To the Editor: There are mixed results regarding the impact of cognitive therapy on paranoid delusions (Key et al., 2003). Schizophrenia that erupts at an early age is known to have bad prognosis (Remschmidt & Theisen, 2005). In addition, low response to antipsychotic medication leads to disorganized thought process, difficulties in conversation. In that case, psychotherapy targeted at the cognitive biases such as selective attention is impractical.
We would like to present the case of “Ms. A,” a 23 years old female remitted schizophrenic patient. Ms. A suffered from disorganized psychosis (between ages 11-14.5) and later from disorganized/paranoid psychosis (between ages 14.5-16) with extreme intensity and tenaciousness. Today, she works to sustain herself, and has ended a four years relationship as "she thinks that she deserves a better mate". A written informed consent was obtained from the patient for the publication.
At the age of thirteen, her treating psychiatrist recommended to hospitalize her in a children's closed ward because her condition was too severe and untreatable. Her parents did not comply with his recommendation and changed the psychiatrist. During the following year, “Ms. A” engaged in uncontrolled sexual behavior and sometimes conducted intercourse with more than ten men a day without any apparent enjoyment.
This behavior was replaced by being bounded at home, due to the appearance of delusions that: "people would penetrate her mind and harm her by looking at her eyes". She tried to avoid eye contact by confining herself to her home. As medication continued to have no positive outcome, poor quality of life and dysfunction occurred. She skipped school, lacked social skills and other developmental skills. The therapeutic team was desperate about her situation and thought of an unorthodox method in order to help her, using exposure therapy.
The rationale was that the persecutory delusions, (fears that lead to avoiding eye contact), were perceived by her as extremely threatening. The therapists saw little difference between this situation and other anxiety states. The only difference was the diagnosis of schizophrenia. Other clinicians and researchers arrived to the same conclusion but avoided recommending exposure therapy (Bentall et al., 2001; Fear, Sharp, & Healy, 1996; Freeman, Garety & Kuipers, 2001; Martin & Penn, 2002). We chose a more direct approach, explaining the patient that according to our experience, the more anxiety is felt without trying to avoid it, the better she would master the situation. We anticipated that making eye contact would initially increase her anxiety, but then her anxiety will decrease with every exposure.
We decided to expose gradually her in vivo – from a nearly deserted location to crowded places. She was asked to become calm for a fifth of the duration during the exposure time. During each exposure session, she was escorted by a therapist or an assistant. Each exposure lasted for several hours. The frequency was 3-5 times a week for four months, then the number of weekly exposures remained stable while the accompanying person gradually spent less and less time with her in each session (which remained 2-3 hours long) and gradually skipped more exposure sessions.
Seven months after the beginning of the exposure therapy, the patient reported less than 20% anxiety while being alone in a mall and staring at people’s eyes. In an interview approximately 5 years later (and after making incredible advances in all domains of life) she stated that her delusions faded away during these years. During this period, a suitable medication was found and prescribed for her: Seroquel (Quetiapine) 100 mg/d, that made an impressive improvement with her negative symptoms, Oralep (Pimozidum) 4 mg/d which is supposed to act as antipsychotic and Tegretol (Carbamazepine) CR 400 mg, for augmentation.
DSM-IV considers paranoid delusions as unshakable beliefs considered untreatable by psychotherapy. Cognitive therapy (CT) argues that there is no substantial difference between delusions and basic assumptions as seen in the cognitive schemata (Brockington, 1991), thus using cognitive restructuring with proven favorable results (Cather, 2004; Kingdon & Turkington, 2005), which is used by CBT clinicians would lead to good outcome (Cannon, McKenzie & Sims, 2003).
CT is limited by the need to have a coherent patient, which is not the case with some disorganized schizophrenic patients, especially if they are suspicious and do not admit that they have a mental disease. Such a patient can easily accept being tense or anxious. These negative emotions are noxious and can easily become a common ground for therapy. Ignoring the psychiatric diagnosis, as well as the causes for anxiety, allows to suggest a bold speculation that avoidance has a major role in maintaining the current negative feelings, while exposure to the feared situations ends up in mastery, at the end of a well-designed process. Aiming to treat anxiety facilitates adherence to the treatment plan. Once anxiety levels are diminished, a domino effect occurs and reduces the levels of paranoid delusions.
Clinicians tend to be cautious with exposure, as schizophrenia constitutes a criterion of exclusion in the literature (e.g. Foa, Molnar & Cashman, 1995).Our outcome calls for a controlled trial to establish the validity of exposure technique for treating paranoid anxiety, as we conducted.
Footnotes The authors report no competing interests. References Bentall RP, Corcoran R, Howard R, Blackwood N, Kinderman P. Persecutory delusions: A review and theoretical integration. Clin Psychol Rev. 2001;21:1143-1192.
Brockington I. Factors involved in delusion formation. Br J Psychiatry Suppl. 1991;14:42-45.
Cannon M, McKenzie K, Sims A. Is cognitive-behavioural therapy a worthwhile treatment for psychosis? Br J Psychiatry. 2003;182:477-479.
Cather C, Penn DL, Otto M, Goff DC. Cognitive therapy for delusions in schizophrenia: models, benefits, and new approaches. J Cog Psychother: An Int Q 2004;18:207–221.
Fear C. Sharp H, Healy D. Cognitive processes in delusional disorders. Br J Psychiatry. 1996;168:61-67.
Foa EB, Molnar C, Cashman L. Change in rape narratives during exposure therapy for posttraumatic stress disorder. J Trauma Stress. 1995;8:675-690.
Freeman D, Garety PA, Kuipers E. Persecutory delusions: developing the understanding of belief maintenance and emotional distress. Psychol Med. 2001;31:1293-1306.
Key FA, Craske MG, Reno RM. Anxiety-Based Cognitive-Behavioral Therapy for Paranoid Beliefs. Behavior Therapy. 2003;34:97-115.
Kingdon D, Turkington D. Cognitive Therapy of Schizophrenia. New York: Guilford Press; 2005.
Martin JA, Penn DL. Attributional style in schizophrenia: an investigation in outpatients with and without persecutory delusions. Schizophr Bull. 2002;28:131-141.
Remschmidt H, Theisen FM. Schizophrenia and related disorders in children and adolescents. J Neural Transm Suppl. 2005;69:121-141. Key words: CBT, CT, Exposure Therapy, Psychotherapy, Paranoia, Paranoid anxiety, Schizophrenia.

Protecting Mental Health from Climate Change 11 June 2008

Anne M. Doherty,
Registrar, General Adult Psychiatry
Mater Misericordiae University Hospital, Eccles St., Dublin 7, Ireland.,
Brendan D. Kelly, Consultant Psychiatrist Mater Misericordiae University Hospital; Senior Lecturer University College Dublin.
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Re: Protecting Mental Health from Climate Change

anne_m_doherty{at}hotmail.com Anne M. Doherty, et al.

The World Health Organisation (WHO) devoted World Health Day 2008 to the theme of “protecting health from climate change” with particular focus on malnutrition, natural disasters, diarrhoeal disease, rising temperatures and infectious diseases (1). Other threats to physical health will stem from the effects of climate change on livestock, wildlife, forests, crops and marine organisms (2). We are deeply disappointed with the low priority accorded to the effects of climate change on mental health: the only reference to mental health in the WHO issues paper was a brief allusion to increased rates of post-traumatic stress disorder in women affected by natural disasters (1).
There is a bi-directional relationship between physical and mental illness (3): any substantive deterioration in population physical health will have a substantial negative effect on population mental health too. In addition, climate change is likely to have its most devastating effects amongst the poor (1) who are already at increased risk of mental illness. Natural disasters are also expected to increase in number and severity as a consequence of climate change and this, too, will have a strongly negative effect on mental health, as demonstrated by the 2004 tsunami in South East Asia (4).
It is also expected that climate change will cause a further increase in trans-national migration, as people in the areas worst affected are forced to flee their homes as a result of natural disasters, faltering infrastructure, disturbed eco-systems, infectious diseases, malnutrition and resultant socio- political unrest. Migration is associated with increased rates of both physical and mental illness, including serious mental disorders such as schizophrenia (4); as result, the effects of climate change will further increase the global illness burden stemming from migration.
Finally, there is the possibility that the environmental effects of climate change may contribute directly to the causation of mental illness through biological mechanisms that are not yet understood; in the absence of detailed biological understandings of most mental illnesses, precise prediction is not feasible but the possibility of direct biological effects remains.
The best way to protect mental health from the effects of climate change is to strengthen general mental health services, especially in low- and middle-income nations (5). Broader and deeper recognition of the importance of the mental health consequences of climate change by organisations such as the WHO would also represent an important step in safeguarding global mental health against the effects of climate change.
1. World Health Organisation. Protecting Health from Climate Change. Geneva: World Health Organisation (2008). 2. Epstein P.R. Climate Change and Human Health. N Eng J Med. 2005; 353: 1433-1436. 3. Prince M et al. No health without mental health. Lancet 2007; 370: 859- 877. 4. Hollifield M., Hewage C., Gunawardena C.N., Kodituwakku P., Bopagoda K., Weerarathnege K. Symptoms and coping in Sri Lanka 20-21 months after the 2004 tsunami. Br J Psychiatry 2008; 192: 39-44. 5. Lancet Global Mental Health Group. Scale up services for mental disorders: a call for action. Lancet 2007; 370:1241-1252.

aripiprazole is not first choice in delusional parasitosis 18 June 2008

Peter Lepping,
Consultant Psychiatrist, Associate Medical Director, Honorary Senior Lecturer
North East Wales NHS Trust, University of Wales, Bangor,
Roland W Freudenmann
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Re: aripiprazole is not first choice in delusional parasitosis

peter.lepping{at}new-tr.wales.nhs.uk Peter Lepping, et al.

Dear Sir, We thank our colleagues Narayan et al for their contribution (eLetter to British Journal of Psychiatry, 9 April 2008) to the discussion around the antipsychotic treatment of primary delusional parasitosis (DP) referring to our recent systematic review in this journal (1). Narayan et al suggest that the pharmacokinetics (half-life of 60-80 hours) and side effect profile of aripiprazole may make it particularly interesting for the treatment of DP where adherence to and engagement with treatment are the most significant challenges. They mention a case report of an 85 year-old woman with primary DP, which fully responded to aripiprazole (2). It is interesting that our own systematic review in this journal showed that the best response rates were achieved with first generation depot antipsychotics. However, other first generation antipsychotics with relatively long half-lives did not differ from those first generation antipsychotics with shorter half-lives. Experience with other second generation antipsychotics with long half-lives are limited to one case with partial remission to sertindole (3) and one recent case treated with paliperidone (4). The level of efficacy of second generation antipsychotics in DP is less than certain. Our own review showed that only 25% of patient treated with a second generation antipsychotic achieved full remission in primary DP. The side effect profile of aripiprazole may be advantageous with regard to the development of metabolic syndrome, but this is often less important in DP because of the often short period of time that patients agree to take medication. Furthermore, the common side effect of insomnia is a real problem with aripiprazole in a patient group that already suffers from agitation and insomnia because of persistent itching. We do therefore not agree that the current evidence available for aripiprazole makes it the substance of choice among the group of second generation antipsychotics in DP despite its favourable pharmacokinetic profile and low risk of metabolic and cardiac complications. There are substantially more successful reports on risperidone (more than n = 30) and olanzapine (more than n = 15) as well as our own positive experience with amisulpride than case reports on aripiprazole in both primary and secondary DP. However, clinical studies, not case reports, will be needed to further establish second generation antipsychotics in DP, and show their individual effects in this syndrome. Yours sincerely Corresponding author: Dr. Peter Lepping, Honorary Senior Lecturer (University of Wales Bangor), Consultant Psychiatrist and Associate Medical Director (North East Wales NHS Trust) Roland W. Freudenmann (University of Ulm)
Declaration of Interest: PL has received honoraria for lecturing from Lilley and Bristol-Myers Squibb, producers of aripiprazole. He has been partially funded by Lilley to attend a conference in 2007. This activity was fully within the rules of CR148. RWF has nothing to declare.
References:
1. Lepping, P., Russell, I. & Freudenmann, R. W. (2007) Antipsychotic treatment of delusional parasitosis: systematic review. Br J Psych, 191, 198-205. 2. Rocha, F. L. & Hara, C. (2007) Aripiprazole in delusional parasitosis: Case report. Prog Neuropsychopharmacol Biol Psychiatry, 31, 784-786. 3. Yorston, G. (1997) Treatment of delusional parasitosis with sertindole [letter]. Int J Geriatr Psychiatry, 12, 1127-1128. 4. Freudenmann, R. W., Kühnlein, P., Lepping, P., et al Secondary delusional parasitosis treated with paliperidone. Clin Exp Derm (in press).

“Truman” signs: integrating qualitative psychopathology of Self and UHR criteria. 2 July 2008

Andrea Raballo,
Psychiatrist, Marie Curie RTN Fellow
Center for Subjectivity Research and Hvidovre Hospital Department of Psychiatry, Copenhagen, DK
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Re: “Truman” signs: integrating qualitative psychopathology of Self and UHR criteria.

anr{at}hum.ku.dk Andrea Raballo

Dear Editor,
The condensed depiction of the “Truman syndrome” as a cluster of symptoms associated with the early prodromal phase of impending psychosis (1), brilliantly illustrates the topicality of qualitative analysis in contemporary research and clinical practice (2). Qualitative analysis allows an appropriate psychopathological appreciation of those subtle pre- psychotic anomalies of subjective experience, which constitute a rather characteristic feature of schizophrenia spectrum conditions. Such subjective domain, however, has long been neglected by mainstream research and psychiatric conceptual modeling, although it belongs to the fundamentals of psychopathology, clinical practice and psychotherapeutic support.
The “Truman syndrome” exemplifies the experiential matrix which leads from relatively uncharacteristic, yet intrusive and disturbing elementary phenomena (such as basic symptoms and not-yet psychotic anomalous subjective experiences), to more sophisticated and characteristic psychotic symptoms (3). From a descriptive viewpoint indeed the “Truman syndrome” exhibits crucial features of a pre-delusional state (4), combining pervasive depersonalization-derealization feelings, primary self -reference, anomalous subjective experiences which subsequently get infused with a content-specific theme (i.e. in the presented clinical vignette: grandiosity and persecution (1)). Such altered modes of experience can be reliably explored with appropriate assessment tools (e.g. the "Bonn Scale for the Assessment of Basic Symptoms", or the recently developed "Schizophrenia Prediction Instrument - Adult Version" and "Examination of Anomalous Self-Experiences") and constitute a clinically meaningful core phenotype of psychotic liability (5).
Since the onset of schizophrenia is often associated with profound alterations of subjective experience which antedate the emergence of both subthreshold (e.g. UHR criteria) and overt diagnostic symptoms (e.g. delusions, hallucinations, psychomotor disorganization,…) a supplementation of the UHR strategy with specific instruments addressing anomalous subjective experiences might enrich current intervention-based research and early identification programs.
References:
1)Fusar-Poli P, Howes O, Valmaggia L, McGuire P. “Truman” signs and vulnerability to Psychosis. BJP Online, 30 May 2008.
2)Stanghellini G, Ballerini M. Qualitative analysis. Its use in psychopathological research Acta Psychiatrica Scandinavica 2008; 117 (3), 161–163.
3)Klosterkoetter J. The Meaning of Basic Symptoms for the Genesis of the Schizophrenic Nuclear Syndrome 1992; 46 (3), 609-630.
4)Bovet P, Parnas, J. Schizophrenic delusions: a phenomenological approach. Schizophr Bull 1993; 19 (3), 579–597.
5)Parnas J, Handest P, Jansson L, Saebye D. Anomalous subjective experience among first-admitted schizophrenia spectrum patients: empirical investigation. Psychopathology 2005; 38 (5), 259-67.

A primary care view 13 July 2008

Alan C Cohen,
General Practitioner
Sainsbury Centre for Mental Health,
Andre Tylee, Chris Manning
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Re: A primary care view

alan.cohen{at}scmh.org.uk Alan C Cohen, et al.

Sir
Craddock et al (Wake up call for British Psychiatry (2008) 193, 6-9) make some interesting points about the role of the psychiatrist. It is unashamedly made from a psychiatrist’s perspective.
We would like to comment from a primary care perspective, since many of the issues raised have a significant bearing on the way primary care works currently, and how it may work in the future.
The authors make the point that “psychiatry is a medical speciality” and that general practitioners should have the opportunity to refer patients for an opinion when they are unclear about the diagnosis or treatment. Sadly, in our experience, this rarely happens, as patients who have a mood disorder such as depression or anxiety are often told that they do not fulfil the criteria for referral (understood by the patient to mean that they are not “ill enough”) to see a psychiatrist. It is a rare occurrence where a psychiatrist will intervene in the administrative chore of “bouncing the patient” back to the GP, so that the patient does benefit from their opinion. Such referrals are often pejoratively labelled as “inappropriate” implying a lack of competence by the referrer.
This behaviour, of screening out people with certain conditions, is justified on the grounds that psychiatrists should concentrate on the most ill, that is the psychoses, and they quote the National Service Framework for Mental Health (NSF) as supporting this stance. No other medical speciality diverts patients away from a medical opinion in the same way. It is a sad testament to both primary and secondary care clinicians that the person who was able to negotiate an improved level of care for people with a significant mental illness such as depression or anxiety, was an economist, making an economic argument at the highest level of government.
The authors also make the case that they should be responsible for managing the physical health care needs of the people for whom they care. They are, according to the authors, first and foremost highly trained doctors. What has stopped psychiatrists providing this care in the past? Are the authors really making the case that they should manage not only the psychiatric needs of a person suffering from schizophrenia, but also manage that person’s diabetes, hypertension, obesity and osteoarthritis? Surely not? Readers were offered a thought experiment; we offer another thought experiment to the authors: “if you had diabetes, hypertension, obesity and osteoarthritis, would you want these conditions managed by a psychiatrist, or a GP?”
If there is a real concern that psychiatrists no longer have the opportunity to practice the speciality in which they trained, then they should do something about it. The NSF is coming to an end – so should the restrictions on who psychiatrists will see should also come to an end. If psychiatrists wish to behave as other medical consultants, then they should see the referrals made to their teams – as team leaders it is in their gift to do so. It may well be that some form of screening may be necessary, but do so based on patient need, not on the basis of a diagnosis.

Abortion Does Not Cause Mental Illness 17 July 2008

Nada L Stotland,
psychiatrist
Rush Medical College/American Psychiatric Association,
Gail Robinson, Donna Stewart, Carol Nadelson, Marta Rondon, Susan Kornfeld
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Re: Abortion Does Not Cause Mental Illness

nadast{at}aol.com Nada L Stotland, et al.

April 28, 2008
To the Editor:
We are psychiatrists who specialize in women's mental health. We have reviewed the literature on the psychiatric sequelae of abortion and have published books and papers on this subject. One of us (NLS) has testified about abortion in several state courts and the Congress of the United States, representing the American Psychiatric Association. We write now out of concern for the accuracy and impact of the Royal College of Psychiatrists’ most recent statement about abortion, which was recently reported in the London Times. Analysis of the majority of the studies published over the last ten years reveals gross errors in methodology with major misleading manipulations of the statistical data as well as a failure to consider key variables such as pre-abortion mental status, the wantedness of the pregnancy, and the motivations for and circumstances of an abortion. However, the conclusions of these studies have supported the invention of the terms 'abortion trauma syndrome' and 'post-abortion depression and psychosis,' which have no basis in medical science. The assertion that abortion causes psychiatric damage is avowedly the central strategy of anti-abortion groups, and has been successfully introduced into policy decisions and public discourse. Solid science, on the other hand, indicates that abortion, in and of itself, does not cause psychopathology. Past or current psychiatric disorder is both a reason to seek abortion and also the strongest predictor of psychiatric disorders after abortion. Women with these risk factors are among the few most likely to have psychiatric disorders after giving birth. The significant risks posed by childbirth, on the other hand, are well documented. Pregnant women in stressful circumstances have difficult decisions to make. Warning women considering abortion that the procedure may cause psychiatric harm is scientifically inaccurate; adds needlessly to their anxiety; and is likely to cause, in some women, the very psychopathology such a warning is meant to address.
Russo, N.F. & Schmiege, S. J. (2005). Debates about our design are beside the point: The Reardon and Cougle findings are invalid and cannot be reproduced with properly coded data. British Medical Journal, December 18, 2005. http://bmj.bmjjournals.com/cgi/eletters/331/7528/1303
Russo, N.F. & Schmiege, S. J. (2006). Depression and unwanted first pregnancy: Methodological issues, additional findings, British Medical Journal, February 10, 2006. http://bmj.bmjjournals.com/cgi/eletters/331/7528/1303 Posavac, E. & Miller, T. Some problems caused by not having a conceptual foundation for health research: An illustration from studies of the psychological effects of abortion. Psychol & Health 1990; 5: 13- 23. . The Royal Australian and New Zealand College of Obstetricians and Gynaecologists, Termination of Pregnancy: A Resource for Health Professionals. RANZCO, East Melbourne, Australia, 2005.
Nada L. Stotland, MD, MPH President [as of May 8, 2008], American Psychiatric Association Professor of Psychiatry and Obstetrics/Gynecology, Rush Medical College 5511 South Kenwood Avenue Chicago, Illinois 60637-1713 no disclosures
Gail Erlick Robinson MD, D.Psych, FRCPC Director, Women's Mental Health Clinic University Health Network Professor of Psychiatry and Obstetrics/Gynecology University of TorontoToronto General Hospital, 8_231 EN, 200 Elizabeth St., Toronto M4W 3M4, 416-340-3048, No disclosures Carol Nadelson, MD Clinical Professor, Harvard Medical School Director, Office for Womens Careers, Brigham and Womens Hospital Boston Massachusetts Past President, American Psychiatric Association
Donna Stewart, MD, FRCPC University Professor and Chair of Women’s Health, Professor of Psychiatry and Obstetrics and Gynecology, University Health Network and University of Toronto Past President, International Association for Women’s Mental Health, and World Psychiatric Association Section on Women’s Mental Health 200 Elizabeth St, EN-7-229, Toronto, M5G2C4, Canada Phone 416-340-3846 Fax 416-340-4185 Declaration of Interests: Research grants from Canadian Institutes for Health Research Advisory Boards: Wyeth and Eli Lilly
Marta Rondon, MD Chair, World Psychiatric Association Section on Women’s Mental Health Deputy Dean, Peruvian College of Physicians Member, Peruvian National Council on Health Past President, Peruvian Psychiatric Association Founder, Peruvian Association for Women's Mental Health Avenida Pardo 541 (1101) Miraflores, Lima 18, Peru Phone 511 445 8633 Fax 511 705 1404 No conflicts.
Susan G. Kornstein, M.D. Professor of Psychiatry and Obstetrics/Gynecology Executive Director, Institute for Women's Health Executive Director, Mood Disorders Institute Virginia Commonwealth University
Grants/Research Department of Health and Human Services National Institute of Mental Health Pfizer, Inc. Bristol-Myers Squibb Company Lilly, Inc. Forest Laboratories, Inc. GlaxoSmithKline, Inc. Mitsubishi-Tokyo Merck, Inc. Biovail Laboratories, Inc. Wyeth, Inc. Berlex Laboratories Novartis Pharmaceuticals, Inc. Sepracor, Inc. Boehringer-Ingelheim Sanofi-Synthelabo Astra-Zeneca
Advisory Boards/ Honoraria Pfizer, Inc. Wyeth, Inc. Lilly, Inc. Bristol-Myers Squibb Company Warner-Chilcott, Inc. Biovail Laboratories Berlex Laboratories Forest Laboratories Neurocrine Sepracor, Inc.

Emergence of obsessive-compulsive symptoms during clozapine treatment in a pair of monozygotic twins 17 July 2008

Kyung Sue Hong,
Associate Professor
Department of Psychiatry, Sungkyunkwan University School of Medicine, Samsung Medical Center,
Hee Jung Nam and Meerae Lim
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Re: Emergence of obsessive-compulsive symptoms during clozapine treatment in a pair of monozygotic twins

hongks{at}skku.edu Kyung Sue Hong, et al.

Previous case reports have described the de novo onset or exacerbation of obsessive-compulsive (OC) symptoms during treatment with second generation antipsychotics (SGA).1 The authors recently reported the detection of OC symptoms associated with SGA in 12.4% of schizophrenia outpatients.2 The assumption that genetic factors might be involved in the individual¡¯s response to various antipsychotic drugs is the theoretical basis of pharmacogenetic studies. However, data on the heritability of drug responses are extremely limited because it is difficult to recruit appropriate cohorts. Therefore, it is important to study drug responses in monozygotic twins in order to gain insight into the role of genetic factors in determining drug response variability.3 To our knowledge, this is the first case report of OC symptoms occurring simultaneously in a pair of monozygotic twins during clozapine treatment.
Mr. A and Mr. B, 24-year-old male monozygotic twins (zygosity confirmed by genotyping microsatellite markers) diagnosed with schizophrenia (DSM-IV), were admitted to our inpatient unit. Both patients had primary symptoms of auditory hallucinations and delusions. They were previously unresponsive to conventional antipsychotics and risperidone and were therefore switched to clozapine. At the time of discharge, Mr. A was no longer delusional, and his hallucinations were less distracting. Mr. B showed similar improvement in positive symptoms, but prominent negative symptoms persisted. Mr. A and Mr. B first reported OC symptoms 10 and 22 months after clozapine initiation, respectively. At that time, Mr. A was being treated with clozapine monotherapy (350mg/day), and Mr. B was being treated with clozapine (400mg/day), propranolol and benztropine. Mr. A initially reported intrusive thoughts pertaining to aggressive acts. He later developed repetitive checking and asking behaviors accompanied by pathologic doubts about daily events. Mr. B initially displayed compulsive behaviors, such as checking and hoarding, and later showed symptoms of repetitive washing and obsession with contamination. Neither twin had a history of OC symptoms. And their obsessive ideation could be clearly differentiated from their preexisting psychotic symptoms. They were able to attest to the ego-dystonic nature of their OC symptoms. Both patients refused the addition of anti-OC drugs, such as serotonin reuptake inhibitors. Gradual reduction of clozapine dose (A: 250mg/day, B: 325mg/day) seemed to help alleviate the OC symptoms. They have remained on clozapine treatment for the following two or three years, and they have been able to hold part-time jobs, with only mild OC symptoms.
The presented cases suggest that genetic factors might play a role in the development of clozapine-associated OC symptoms. However, further observations on twins or relative-pair cases are needed.
References 1 Lykouras L, Alevizos B, Michalopoulou P, Rabavilas A. Obsessive- compulsive symptoms induced by atypical antipsychotics. A review of the reported cases. Prog Neuropsychopharmacol Biol Psychiatry 2003; 27: 333- 46. 2 Lim M, Park DY, Kwon JS, Joo YH, Hong KS. Prevalence and clinical characteristics of obsessive-compulsive symptoms associated with atypical antipsychotics. J Clin Psychopharmacol 2007; 27: 712-3. 3 Theisen FM, Cichon S, Linden A, Martin M, Remschmidt H, Hebebrand J. Clozapine and weight gain. Am J Psychiatry 2001; 158: 816.
Declaration of interest We declare that we have no conflicts of interest. Supported by grants of the Korea Health 21 R&D Project, Ministry for Health, Welfare and Family Affairs, R.O.K. (A030001) and IN-SUNG Foundation for Medical Research.

Possible polyneuritis cranialis in a psychotic patient: diagnostic and therapeutic dilemmas 31 July 2008

Konstantinos N. Fountoulakis,
Associate Professor of Psychiatry
3rd Department of of Psychiatry, Aristotle University of Thessaloniki, Greece,
Eirini Tsirka, Maria Saiti, Melina Siamouli, Stamatia Magiria, Marina Paschalidou, Apostolos Iacovides, Nickolaos Iacovides, George S. Kaprinis
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Re: Possible polyneuritis cranialis in a psychotic patient: diagnostic and therapeutic dilemmas

kfount{at}med.auth.gr Konstantinos N. Fountoulakis, et al.

Case report
Dear Sir,
We report here the case of a 42 years old single bipolar I female with psychotic features and hypothyroidism. The index hospitalization occurred when she presented to the emergency unit with disorganized and agitated behavior, plus non congruent psychotic features.
Her treatment during her hospitalization (57 days) is shown in Figure 1 with the exception of benzodiazepines, long acting risperidone i.m., valproate and thyrohormone. The fluctuation of the clinical picture is also shown in the same figure. Her treatment included high dosages of olanzapine and latter haloperidol but the symptoms persisted. At day 18 she had 38.5o C fever, treated with paracetamol and antibiotics. Clinical and laboratory examinations were normal. At day 21 she manifested severe hypersalivation, hoarseness of voice, but no peripheral muscular rigidity. At day 25 her treatment changed and the new one was based on haloperidol 30 mg daily and valproate 1500 mg daily.
At day 35 she manifested severe dysphagia, dysarthria and hypersalivation at the absence of peripheral muscular disorder. The phenomena were considered to be extrapyramidal in nature and all antipsychotic treatment was stopped. Brain MRI was normal. At day 39 she suffered a second fever episode (37.8o C) and during days 39-41 she was lethargic. At day 45 a new neurological examination revealed the presence of skew deviation (1) and confirmed the presence of dysphagia and dysarthria. During the next 12 days the patient improved, but neither the psychiatric symptoms, dysarthia, dysphagia, nor skew deviation remitted completely. She was released and put on outpatient follow-up.
Three months latter, the patient was re-hospitalized due to a relapse of and remitted within 48 hours after aggressive treatment with 1800 mg quetiapine daily and 400 mg amisulpride daily.
She was followed up 1-2 times per month on an outpatient basis. No peripheral EPS were ever evident. Dysphagia, dysarthria and skew deviation continued to improve slowly and disappeared after another 2.5 months, that is 6 months after they first appeared.
The fact that none of the motor symptoms responded to anticholinergic treatment, they persisted for more than 1 month after stopping high dosages of haloperidol and their independent fluctuation argue against an extrapyramidal causation. The most probable cause could be multiple cranial neuritis (polyneuritis cranialis) (PC), which is a rare disorder of multiple cranial nerve palsies without spinal cord involvement. It is thought to be an acute post-infective polyneuropathy or a variant of Guillain-Barre syndrome. An additional feature which was not assessed at that time but only retrospectively is a significant reduction in the mimic of face muscles, which can easily be considered as an extrapyramidal feature but it is also a common element of PC. Sialorhea could be considered in the same frame.
References
1. Liu GT, Volpe NJ, Galetta SL. Eye movement disorders. Current Opinion in Ophthalmology 1995; 6: 27-33.
Conflict of Interest
There was no funding on which the present case report was based on. All of the authors have received support concerning travel and accommodation expenses from various pharmaceutical companies in order to participate in medical congresses. Dr Fountoulakis has received honoraria for lectures from Astra-Zeneca, Janssen-Cilag, Eli-Lilly and a research grant from Pfizer Foundation.

wake up call for british psychiatry 31 July 2008

Kamini Vasudev,
Specialist Registrar, Adult Psychiatry
Hadrian Clinic, Newcastle General Hospital, Newcastle upon Tyne, NE4 6BE
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Re: wake up call for british psychiatry

kaminivasudev{at}hotmail.com Kamini Vasudev

Dear Editor
I read with keen interest the article ‘Wake-up call for British psychiatry’ by Craddock et al, 2008;193: 6-9. I completely agree with the concerns raised by the authors. As a trainee psychiatrist working in United Kingdom for the last few years, I have had an opportunity of working with several community mental health teams (CMHTs). I have observed implementation of ‘new ways of working’ in different teams and its impact on patient care. Unfortunately, at some places the psychiatrists themselves have misinterpreted the meaning of their ‘consultative role’ in the ‘new ways of working’ model. They do not wish to assess the new referrals to the team in the assessment clinics. They rather rely on the assessments by other members of the team, who present the new cases in the weekly team meeting, to decide if the patient needs to be reviewed by them. One of the reasons for the reluctance to see new referrals may be the time-consuming paper work including the care co- ordination document and risk assessment document for the new referrals. However, this deprives the patient of the benefit of being assessed by ‘the most experienced and skilled professional of the team’, as rightly pointed by the authors.
In the best interest of the patients, most if not all the new referrals to the CMHTs should be assessed by the consultant psychiatrist or his trainee doctor under his supervision along with/without another member of the team. The management plan thus formulated could be implemented with involvement of other members of the team and sometimes in the primary care. The psychiatrist thus would have minimal number of patients in their follow-up clinic. After providing their ‘consultation’ the consultant psychiatrists should be able to discharge the care of the patients back to the primary care. Alternatively, the more complicated patients could be followed up by other members of the CMHT with once or twice yearly review by the psychiatrist. This would free-up their time to make themselves available for urgent or new referrals. It is understandable that GPs might have their reservations to take the burden of care of all the stable psychiatric patients unless they get reassurance that the consultant psychiatrist would be able to review the patients as soon as possible should the need arise.
There is a need for the psychiatrists to be forthcoming and take the initiative to implement the ‘new ways of working’ in the best interest of their patients. They would, however, need co-operation of other members of the team to make this happen, which can be challenging.

Ethnicity and mental health: precision required 8 August 2008

Jonathan S Koffman,
Lecturer in Palliative Care
King's College London, Department of Palliative Care, Policy & Rehabilitation
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Re: Ethnicity and mental health: precision required

jonathan.koffman{at}kcl.ac.uk Jonathan S Koffman

Connolly and Taylor1 have attempted to examine an on-going concern that some ethnic groups are subject to a mismeasure of care and treatment for mental health problems2. This important issue deserves consideration if health care services are to better manage the considerable burden of mental illness that impacts on society. However, there are serious concerns with the absence of specificity in a methodology that lumps ethnic groups together. There was a time in the NHS’s history when there were inherent difficulties in assigning ethnicity to an individual and ethnic aggregation represented a pragmatic solution to routinely recording a patient’s identity. However, this situation has now thankfully improved. It is therefore possible that heterogeneity in the prevalence of mental illness and its management is evident but lost in this current analysis. Crude comparisons between patients assigned to being ‘white’ and ‘black’ only reinforces the racial specificity of colonial populations3.
1. Connolly A. Taylor D. Ethnicity and quality of antipsychotic prescribing among in-patients in south London, British Journal of Psychiatry, 2008;193:161-162. 2. Koffman, J. Fulop, N., Pashley D. Colman K. Ethnicity and the use of acute psychiatric beds: findings from a recent census of acute psychiatric patients in North and South Thames regions. British Journal of Psychiatry, 1997;171:238-241. 3. Barkan E. The retreat of scientific racism. Cambridge: Cambridge University Press, 1992.

NWW: New Ways of What? 8 August 2008

Mamdouh EL-Adl,
Consultant Psychiatrist
Northamptonshire Healthcare NHS Trust
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Re: NWW: New Ways of What?

mamdouh.eladl{at}nht.northants.nhs.uk Mamdouh EL-Adl

Dear editor The special article by a group of eminent professors and consultants’ psychiatrists entitled: Wake-up call for British Psychiatry is a very important call. Craddock et al highlighted the likely multiple damages of the so called New Ways of Working “NWW”(1). Many colleagues welcomed the wake-up call but some feel concerned that this wake-up call was too late. An important question to be raised: where is the Royal College of Psychiatrists from this? As we know the College was one of the main driving parties for the introduction of NWW. The main reasons outlined by the College were: Consultants’ heavy workload across the UK and the need for change.
The problem of the overworked consultants could have been addressed by different approach including: improving recruitments, encouraging healthy retired consultants to continue to work either full or part time and encouraging new generations of medical students and trainees to join psychiatry. Change is a healthy process that none could object to although it is usually associated with challenges. However radical and uncalculated change could be damaging. The disaster of modernising medical career (MMC) has not been forgotten yet and the medical profession continues to suffer its flashbacks. In his response to being invited by Patricia Hewitt, Health Secretary, to conduct an independent inquiry on MMC, Professor Sir John Tooke stated: Seldom in my professional career has an issue provoked such an outcry from the profession and expressions of concern for the future of trainee doctors and the delivery of medical care and health service developments to which we hope they will contribute (2).
The long term planning for medical workforce has never been an easy task (3). However passing many of the important responsibilities that require the skills and expertise of the medically trained psychiatrists to non-medical disciplines is not the solution! There is a growing believe that the NWW has made a negative effect on the profession, the psychiatric training and service quality. While patients’ best interest should be at the heart of the clinical operation and healthcare strategy, many mental health clinicians (psychiatrists & non-psychiatrists) do not feel that NWW considered this carefully. I feel it was probably more appropriate instead of introducing a new system (NWW) to examine an already existing system, promote its positives and address its negatives.
Professor Tooke stated: The profession should develop a mechanism(s) for providing a coherent advice on matters that are of major significance to medicine and hence the health of the population in general (4). Therefore, I am urging the College and the Department of Health (DOH) to objectively review the situation. I suggest forming an independent group of experienced clinicians, academics and service developers to review the implementation of NWW in the trusts that adopted this model and study its impact on patients’ care, service quality and delivery and quality of training before it is too late. We need to do it for our patients, profession and for the mental healthcare of future generations. If the College does not do this, who else will do? Declaration of interest: none.
Mamdouh EL-Adl Consultant Psychiatrist, Campbell House, Northamptonshire Healthcare NHS Trust Mamdouh.eladl@nht.northants.nhs.uk
References: 1.Craddock N, Antebi D, Attenburrow M et al. Wake-up call for British Psychiatry. Br J Psychiatry 2008;193: 6–9 2.Tooke J.: MMC Inquiry. Why an Inquiry? www.mmcinquiry.org.uk. Accessed on 07.08.08 3.Pidd S. The Royal College of Psychiatrists: response to the health committee’s inquiry into workforce needs and planning for the health service (2006). www.rcpsych.ac.uk/pdf/accessed on 07.08.08 4.Tooke J.: Final report of the Independent Inquiry into Modernising Medical Careers. www.mmcinquiry.org.uk/MMC_FINAL_REVD_4Jan.pdf. Accessed on 07.08.08

Specificity of teachers and health professionals in referred pervasive developmental disorder childr 27 August 2008

Sabrina Ribeiro,
Clinical Psychologist
Mackenzie Presbyterian University, São Paulo-SP, Brazil,
Cristiane S Paula, Associated Professor at the Mackenzie Presbyterian University, São Paulo-SP, Brazil and Marcos T Mercadante, Associate Professor of Psychiatry, Dept of Child & Adolescent Psychiatry at the Federal University of São Paulo-SP, Brazil
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Re: Specificity of teachers and health professionals in referred pervasive developmental disorder childr

sabandini2{at}yahoo.com.br Sabrina Ribeiro, et al.

Specificity of teachers and health professionals in referred pervasive developmental disorder children
Dear Editor: Pervasive developmental disorders (PDD) present social, communicative and behavior impairments, which compromise the adaptive performance (1). The prevalence of this severe neurodevelopmental disorder was estimated in 4/10,000 during the 60’(2). Since then, several studies have applied modern methodologies to describe the appropriate prevalence (3). The current estimative range from 0.3 to 1% (3), however the studies have been done only in Europe, North America and Japan (3). We conducted the first PDD epidemiological study in Atibaia, a countryside city in São Paulo, Brazil.
This city has a full covered Family Health Assistance Program (Programa de Saúde da Família – PSF), a Brazilian government initiative based on assistance by under-graduated professionals. The data collection was done in two phases; first, all health and educational services for children (aged 7 to 12) were contacted. A basic training program about PDD was realized. A short 10 items symptoms-list, based in DSM-IV and CDC (4), was offered in order to indentify suspected cases. Teachers, and health professionals were asked to referee all the suspected subjects in a neighbored of 20,000 in-habitants. Second, all the parents (95% of agreement) were assessed by trained psychologists, applying Autism Screening Questionnaire (ASQ) and Strength and Difficulties Questionnaire (SDQ).
In this district it was identify two public schools, four PSF teams, two Basic Health Unit, plus four specialized services in the city (CAADE, APAE, FENIX, Travessia). Seventy-six children were referee as suspected PDD subjects. After a systematic evaluation, only 13 match DSM-IV criteria for PDD (17.1%). Interesting teachers and health professionals from the PSF program showed the same capacity in referee subjects (20% teachers; 17% PSF professionals, p=0.95). Important to mention that only one case were indicated by both teams. In addition, it is relevant to say that all referee subjects presented some mental health problem (n=55; 72,4%) (table 1). The only difference between teams are the referred of hyperactive disorder from the PSF professionals (p= 0,036).
Our study showed that PSF and educators are equally able in discriminating mental health problem, but do not have high specificity in refereeing PDD subjects. Interestingly, PSF professionals were able to referee more subjects matching attention deficit hyperactivity disorder, suggesting that the training that have been done, in our country (5), are relevant to improve the sensibility of these professionals. In this sense, we believe that more information and training would be helpful in order to improve our capacity in recognizing PDD subjects, refereeing them to the intervention programs.
Reference
1- Klin A, Mercadante MT. Autism and Pervasive Developmental Disorder (editorial). Rev Bras Psiquiatr 2006; 28 (suppl 1): s1-2.
2- Lotter, V. Epidemiology of Autistic Conditions in Young Children. Social Psychiatry 1966; 1; 124-137.
3- Fombonne E. Epidemiological Surveys of Autism and Others Pervasive developmental Disorders: An Update. J Autism Dev Disord 2003; 33: 365-382.
4- Center for Disease Control And Prevention. Prevalence of Autism Spectrum Disorders- Autism and Developmental Disabilities Monitoring Network, Six Sites, United States, 2000. MMWR Surveill Summ 2007; 56 (suppl 1): 1-11.
5- Rohde LA, Halpern R. Transtorno de déficit de atenção/hiperatividade:atualização. Jornal de Pediatria; 2004: 80 (suppl 2): s61-70.

Neuropsychiatric systemic lupus erythematosus associated with neuroleptic malignant syndrome. 27 August 2008

Philippe Verdoot,
MD
Université Catholique de Louvain, Cliniques Universitaires Saint Luc, Adult Psychiatric Unit,
Eric L Constant, Arlette Seghers
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Re: Neuropsychiatric systemic lupus erythematosus associated with neuroleptic malignant syndrome.

philippe.verdoot{at}uclouvain.be Philippe Verdoot, et al.

Neuropsychiatric manifestations such as anxiety, mood disorders, and psychosis are frequent features of systemic lupus erythematosus (SLE). A psychosis prevalence of 5% in SLE has been reported (1,2). Neuroleptic Malignant Syndrome (NMS) is a life-threatening complication of the treatment with antipsychotics (2). High-potency antipsychotics increase the risk.
We report the clinical case of a 23-year-old woman presenting early- onset neuropsychiatric SLE (NPSLE) with interstitial pneumopathy, glomerulonephritis and malar rash. When she was 20 years old, she had been hospitalized for her first episode of NPSLE with acute psychotic symptoms (mystic delusions) and agitation. The introduction of droperidol led to an NMS with high creatinine phosphokinase (CPK) levels, muscular rigidity, hyperthermia, and blood pressure dysregulation. The droperidol was stopped and benzodiazepines were used.
The patient was rehospitalized when she was 23 years old in a similar state because she had not observed the immunosuppressant treatment. No new gliotic cerebral lesions appeared on the cerebral MRI. The psychiatrist decided to introduce valproic acid and benzodiazepines in order to avoid antipsychotics. However, the mental state of the patient quickly led to delirium with repetitive, delusional and incoherent speech and behaviour. Despite the risk of NMS, a one-shot intramuscular injection of clotiapine was administered. Once again, we observed muscular rigidity, dehydration (148 mEq/L natrium), and systolic hypertension. Her clinical state became serious with lethargy, aspontaneity, disinhibition, and executive dysfunction. Biological features were abnormal with elevated CPK (3415 UI/L), increased CRP (3.7 mg/dl), and hepatic cytolysis. Her treatment consisted of cyclophosphamide and methylprednisolone, and the introduction of a titrating-dose (up to 600 mg) of quetiapine for the psychiatric symptoms was decided upon. Her CPK levels returned progressively to a normal state, and no sign of NMS were observed. Six weeks after continuing this treatment, biological and clinical features were normalized.
This case illustrates the importance of differentiating delirium caused by a NPSLE, a steroid-induced delirium (1) (which was not the case here as the patient had not been receiving any steroids when she developed the second psychotic episode) and an alteration in the consciousness level due to an NMS, which was the case here.
While there are no guidelines for the treatment of the psychiatric manifestations of SLE, it usually includes immunosuppressants associated with second-generation antipsychotics (3). The diagnosis of NMS is based on muscle rigidity, hyperthermia, delirium, and autonomic disturbances (4). The dopaminergic hypothesis of the NMS is well documented (5). NMS is not an absolute contraindication for further antipsychotic treatment, and some factors can reduce that risk : avoiding the long-term use of antipsychotics, using low-potency agents, adjunctive treatments, and slow titration (2).
In this case, we suggest that the introduction of quetiapine - a lower D2- affinity antipsychotic - was an interesting alternative.
References:
1. Brey RL et al. Neuropsychiatric syndromes in lupus : prevalence using standardized definitions. Neurology. 2002;58:1214-20.
2. Haddad PM et al. Neurological complications of psychiatric drugs : clinical features and management. Hum. Psychopharmacology Clin Exp. 2008;23:15-26.
3. Stojanovich L et al. Psychiatric manifestations in systemic lupus erythematosus. Autoimmunity Rev. 2007;6:421-6.
4. Ananth J et al. Neuroleptic Malignant Syndrome and Atypical Antipsychotic Drugs. J Clin Psychiatry 2004;65(4):464-470.
5. Strawn JR et al. Neuroleptic Malignant Syndrome. Am J Psychiatry 2007;164(6):870-6.

Moving people to combat stigma and discrimination: the challenges ahead 8 September 2008

Vanessa A Pinfold,
Director of Research
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Re: Moving people to combat stigma and discrimination: the challenges ahead

vanessa.pinfold{at}rethink.org Vanessa A Pinfold

October 2007 marked the launch of another programme in England to tackle stigma and discrimination. Moving People models national initiatives from New Zealand and Scotland drawing on an expanding stigma evidence base (Link and Phelan 2001) as well as lessons from the past projects, including Royal College of Psychiatry ‘defeat depression’ and ‘changing minds’ campaigns.
How might this programme succeed where others have stalled? It is resource rich with £18 million from the Big Lottery Fund and Comic Relief to channel into 35 linked programmes. It has four years to prove change among targeted audiences within a 30 million adult reach. It is a four- party coalition with a desire to learn from organisations across health and disability fields. It is adopting an evidence-based approach (Thornicroft 2007) - national social marketing, service user leadership and engagement, local direct action, multiple targets using stick and carrot approaches– but this does not guarantee success.
Key challenges are identifiable.
Preparatory consultation during February 2008 using a pragmatic, non- systematic survey method through the membership networks of 18 organisations generated responses from 3038 service users and 661 family or friend carers. It emphasised that:
a) Stigma and discrimination is widespread and the impacts far reaching.
• 71% reported to have stopped doing things –accessing employment, making friends, joining groups, engaging with health professionals. 73% reported anticipated discrimination including 1 in 2 who fear disclosing their health problems because of the negative reactions they might receive. • Carers reported less personal affects but 85% felt the person they supported was affected. • Moving People will need to targets its efforts to impact meaningfully in any one area.
b) Combating stigma and discrimination is not straight forward.
• Service users and carers warned that the entangled nature of mental illness and their own and other people’s reactions make generic solutions difficult to find. Pin-pointing exact goals for the 35 Moving People programmes in terms of what needs to change will be central to proving any success.
c) Moving People must set realistic goals
• Variation in experiences particularly relating to physical health disabilities, sexuality, severe mental illness diagnosis and ethnicity of carers were found. Stakeholders will not equally benefit from Moving People and the programme must be open and honest about its limitations from the outset. There is a danger that if it “fails” to impact on lived experience of stigma and discrimination – people will give up hope that any change is possible.
Health professionals have a key role to play. GPs and psychiatrists were listed as stigma generating agents whilst NHS mental health trusts were prioritised by 1 in 10 as the key target location for the social marketing campaign. However, the role goes far beyond being a target for interventions. Alongside Moving People, momentum behind recovery driven services is gathering pace (Sheppard et al, 2008). Joining up initiatives across psychiatry that impact on stigma and discrimination will assist this programme. For more information please visit: www.movingpeople.org.uk
Word count 484
References
Link B, Phelan J (2001) Conceptualising Stigma. Annual Review of Sociology, 27: 363-385.
Thornicroft G (2007) Shunned: discrimination against people with mental illness. Oxford University Press, Oxford.
Sheppard G, Boardman J, Slade M (2008) Making recovery a reality. Sainsbury Centre for Mental Health, London.
Author
Dr Vanessa Pinfold Director of Research at Rethink Royal London House 22-25 Finsbury Square London EC2A 1DX
Tel: 0207 3309116 Fax: 0207 3309102
vanessa.pinfold@rethink.org
Declaration of Interest: Employed by one of the Moving People partners – Rethink.

DSM-V: Comorbidity studies suggest that PTSD belongs in its own class of traumatic-stress disorders 24 September 2008

Mark W. Miller,
Clinical Psychologist
VA Boston Healthcare System, National Center for PTSD,
Patricia A. Resick and Terence M. Keane
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Re: DSM-V: Comorbidity studies suggest that PTSD belongs in its own class of traumatic-stress disorders

mark.miller5{at}va.gov Mark W. Miller, et al.

Principles of diagnostic taxonomy suggest that disorders of a specific class, or spectrum, should aggregate together more so than with disorders from another class. Results of recent comorbidity studies raise questions about whether this is true for PTSD—which has been classified as an anxiety disorder since DSM-III—and have implications for where the diagnosis should be located in DSM-V. Several factor analyses of diagnostic data from epidemiological and clinical samples suggest that PTSD covaries more strongly with disorders defined by anhedonia, worry, and rumination (i.e., the unipolar mood disorders and generalized anxiety disorder) than with ones characterized by pathological fear and avoidance (e.g., the phobias, panic/agoraphobia and obsessive-compulsive disorder) [1]. However, classifying PTSD among these “anxious-misery” disorders provides a poor fit to the data because PTSD is conditional on trauma exposure and, in new onset cases, typically develops before its comorbid conditions. For example, when PTSD and major depression co-occur following trauma exposure, PTSD usually precedes or develops concurrently with the depression. New onset major depression that develops in the wake of trauma rarely precedes or develops in the absence of PTSD [2]. This implies a causal influence of PTSD on comorbid psychopathology and suggests a distinct phenomenology which should be reflected in its diagnostic class membership within DSM.
Developmental studies have shown that adult psychopathology is often foreshadowed by childhood and/or adolescent problems in the same domain. Along these lines, many adults with anxiety disorders report histories of juvenile anxiety disorders but they do not typically report juvenile externalizing disorders. The exception to this is found among samples of individuals with PTSD where adult patients frequently have histories of childhood externalizing disorders [3]. Twin studies align with this finding and have shown that PTSD shares genetic influences with both internalizing and externalizing spectrum diagnoses [4]. Other work suggests that many adults with PTSD exhibit a predominantly externalizing pattern of comorbidity characterized by problems in the domain of impulse- control, antisociality, and substance abuse [5]. These findings raise concern about conceptualizing PTSD simply as the manifestation of a vulnerability to anxiety-related psychopathology.
Since its 3rd edition, the DSM has taken a largely descriptive, as opposed to etiologic, approach to defining and classifying disorders. The most notable exception to this is the PTSD diagnosis which specifies a causal relation between trauma exposure and symptom development. We believe that the most appropriate location for PTSD in DSM-V would be among a class of disorders precipitated by serious adverse life events, i.e., a spectrum of traumatic-stress disorders. Candidates for inclusion would include PTSD, acute stress disorder, adjustment disorder, a traumatic-grief or bereavement-related diagnosis, and possibly complex PTSD. These disorders are the product of an environmental pathogen (i.e., a traumatic stressor) operating on individual diatheses that span the spectrum of human variation in vulnerability to psychopathology. This diathesis-stress interaction can result in extensive heterogeneity in the phenotypic expression of psychopathology-- pathological anxiety being just one manifestation of the process.
References
1. Miller MW, Fogler JM, Wolf EJ, Kaloupek DG, Keane TM: The internalizing and externalizing structure of psychiatric comorbidity in combat veterans. J Trauma Stress 2008; 21:58-65.
2. Breslau N, Davis GC, Peterson EL, Schultz LR: A second look at comorbidity in victims of trauma: The posttraumatic stress disorder-major depression connection. Biol Psychiatry 2000; 48:902-909.
3. Gregory AM, Caspi A, Moffitt TE, Koenen K, Eley TC, Poulton R: Juvenile mental health histories of adults with anxiety disorders. Am J Psychiatry 2007; 164:301-308.
4. Koenen KC, Fu QJ, Lyons MJ, Toomey R, Goldberg J, Eisen SA, True W, Tsuang M: Juvenile conduct disorder as a risk factor for trauma exposure and posttraumatic stress disorder. J Trauma Stress 2005; 18:23- 32.
5. Miller MW, Kaloupek DG, Dillon AL, Keane TM: Externalizing and internalizing subtypes of combat-related PTSD: A replication and extension using the PSY-5 scales. J Abnorm Psychol 2004; 113:636-645.

Mirtazapine induced akathisia 1 October 2008

Ashish Aggarwal,
Senior Resident
Department of Psychiatry, G.B. Pant Hospital, New Delhi,
Manish Jain, Ram C. Jiloha
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Re: Mirtazapine induced akathisia

drashish1980{at}gmail.com Ashish Aggarwal, et al.

Dear editor, we wish to report a rare untoward side effect of akathisia following mirtazapine administration in a depressed patient. Mirtazapine is a noradrenaline and specific serotonergic antidepressant commonly used for the management of depression. In low doses (15 mg per day), mirtazapine has been found to be useful for the management of akathisia. (1) Akathisia is commonly defined as a subjective sense of inner motor restlessness. It is commonly associated with the use of antipsychotic medications, but has been reported with antidepressants, calcium channel blockers and buspirone. (2) We could find only two previous cases of akathisia induced by mirtazapine reported in the literature. (3, 4) A 42 years old male presented to us with history of sadness of mood, decreased interest in pleasurable activities, easy fatigability, marked insomnia, loss of appetite and suicidal ideation for the last 2 weeks. He had history of undergoing coronary angiography and percutaneous coronary intervention around 3 months prior top onset of symptoms. Besides this past, personal and family history was not significant. His Mental status examination revealed depressed affect, ideas of helplessness, hopelessness and worthlessness along with suicidal ideation. His psychomotor activity was decreased. A diagnosis of severe depressive episode without psychotic symptoms was made according to ICD 10 and the patient was started on mirtazapine 7.5 mg increased to 15 mg on the second day. However, after the third dose of mirtazapine, patient reported severe intense motor restlessness and inability to sit still. The patient was brought to us. He reported inner restlessness and was constantly moving his legs pacing about here and there. He was given mouth dissolving clonazepam 1 mg and his symptoms settled down in about 45 minutes. The next day the patient remained calm for the whole day but again reported similar complaints after about 2 hours of taking mirtazapine 15 mg. He was again brought to us. At this time his total Barnes akathisia score was 10. Detailed neurological examination at this time was within normal limits. His routine blood investigations including MRI brain was within normal limits. Keeping the possibility of a drug-induced phenomenon, mirtazapine was stopped, and the patient was started on nortriptyline 25 mg increased to 75 mg per day along with zolpidem on as and when required basis. The patient showed improvement in his symptoms with no recurrence of akathisia. He is currently maintaining well after about 4 months of start of nortriptyline. One unique point in our case is that the patient developed akathisia on 15 mg dose of mirtazapine whereas previously reported cases were on 30 mg dose. The neurobiological mechanism for drug induced akathisia is still not clear. Based on treatment response, role of noradrenergic and serotonergic neurotransmitters have been postulated. Blockade of α2- adrenoreceptors by mirtazapine may have role in causation of akathisia. Our report suggest that one must be vigilant for this side effect as it can lead to impulsive suicidal attempt, (5) especially in a patient with depression harboring suicidal ideations.
References:
1) Poyurovsky M, Pashinian A, Weizman R, Fuchs C, Weizman A. Low-dose mirtazapine: a new option in the treatment of antipsychotic-induced akathisia. A randomized, double-blind, placebo- and propranolol-controlled trial. Biol Psychiatry 2006; 59(11):1071-7.
2) Nelson DE. Akathisia-a brief review. Scott Med J 2001; 46(5): 133- 4
3) Gulsun M, Doruk A. Mirtazapine-induced akathisia. J Clin Psychopharmacol 2008 Aug;28(4):467
4) Girishchandra BG, Johnson L, Cresp RM, Orr KG. Mirtazapine-induced akathisia. Med J Aust 2002;176(5):242.
5) Drake RE, Erlich J. Suicide attempts associated with akathisia. Am J Psychiatry 1985; 142: 499-501

AMISULPRIDE INDUCED GYNAECOMASTIA 25 October 2008

Ashish Khandelwal,
Resident
Department of Psychiatry, GB Pant Hospital, New Delhi,
Ashish Aggarwal, Ram C Jiloha
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Re: AMISULPRIDE INDUCED GYNAECOMASTIA

drashish1980{at}gmail.com Ashish Khandelwal, et al.

Sir, We wish to report a case of gynaecomastia associated with amisulpride, a second generation antipsychotic. Mr N, a 21 years old unmarried male was suffering from schizophrenia for the last 1 year. His past and family history were non contributory. Personal history revealed history of cannabis use for the last one and a half years off and on not amounting to cannabis dependence. He was started on risperidone 2 mg per day gradually increased to 6 mg over the next 2 weeks along with lorazepam 4 mg per day. The patient showed minimal response over the next 2 months. So, it was stopped and amisulpride started at the dose of 50 mg per day. It was gradually increased to 200 mg over the next 2 week and lorazepam was continued in doses of 4 mg per day. The patient started showing improvement in his psychotic symptoms. However, after about 3 weeks of 200 mg amisulpride, he complained of swelling beneath the nipples. Local examination revealed firm, nontender round growth of approximately 2 cm in height and 2 cm in diameter under both the nipples, without any sign of galactorrhoea. There was no associated decrease in libido or any sexual dysfunction reported though the patient was unmarried. Detailed neurological examination including fundus was within normal limits. His prolactin levels were 90 ng/ml and testosterone level was 4.25 ng/ml. Other investigations including thyroid function test and MRI scan of the brain were within normal limits. Amisulpride was stopped in one week’s time and patient was started on quetiapine 100 mg per day. Gradually there was decrease in swelling around the breast which finally disappeared after 4-6 weeks. Serum prolactin and testosterone levels were 20ng/ml and 6 ng/ml respectively after 6 weeks of stopping amisulpride. Quetiapine was gradually increased to 500 mg per day over a period of 3 weeks and patient showed improvement in symptoms. He however continued to use cannabis off and on. There were no further complaints regarding the breast enlargement. In this case, appearance of gynaecomastia was associated with hyperprolactinaemia, and gynecomastia disappeared with return of circulatory prolactin to normal levels, following withdrawal of amisulpride. The adverse drug reaction probability score based on Naranjo’s algorithm, was nine for this case, denoting a definite adverse reaction due to amisulpride therapy. Gynaecomastia is not a common side effect of neuroleptics in male patients. (1) Amisulpiride is a substituted benzamide derivative a second generation antipsychotic. It has preferential action at D2/D3 receptors. At low doses, (<10 mg/kg) it blocks presynaptic receptors resulting in increased dopamine transmission. (2) It has preferential activity in limbic rather at striatal structures. Drug-induced gynaecomastia is thought to be caused mainly by enhanced oestrogen action and/or inhibited testosterone action.(3) The role of neuroleptic agents in gynecomastia is poorly defined. Recent study has shown the rate of endocrinological side effect with amisulpride to be low (0.7%). (4) Our patient also used cannabis which could have increased the chances of developing gynaecomastia. (5) We could find only one report of gynaecomastia with sulpiride. The patient however, was a case of generalized anxiety disorder. (6) Gynaecomastia in our case was an acute and early side effect of the drug. One should be vigilant for the adverse effect, even at low doses. Management options include change to other antipsychotic with lower incidence of raising prolactin level, or use of dopamine agonist such as amantadine, cabergolin and bromocriptine. (7)
References:
1. Kaneda Y, Fujii A, Yamaoka T, Morimoto T, Nagamine I. Neither gynecomastia nor galactorrhea is a common side effect of neuroleptics in male patients. Neuro Endocrinol Lett 2000;21(6):447-51. 2. McKeage K, Plosker GL. Amisulpride: a review of its use in the management of schizophrenia.CNS Drugs 2004;18(13):933-56. 3. Carlson HE. Gynecomastia. New England Journal of Medicine 1980; 303:795 -9 4. Sechter D, Peuskens J, Fleurot O, Rein W, Lecrubier Y; Amisulpride Study Group. Amisulpride vs. risperidone in chronic schizophrenia: results of a 6-month double-blind study. Neuropsychopharmacology 2002 Dec;27(6):1071-81. 5. Olusi SO. Hyperprolactinaemia in patients with suspected cannabis- induced gynaecomastia. Lancet 1980 Feb;1(8162):255 6. Kaneda Y, Fujii A. Gynecomastia with sulpiride. Journal of Clinical Pharmacy and Therapeutics 2002;27:75-7 7. Haddard PM, Wieck A. Antipsychotic-induced hyperprolactinaemia: mechanisms, clinical features and management. Drugs 2004;64:2291-314.

Mentally Disorders Prisoners in Europe 25 October 2008

Harald Dressing
Central Institute of Mental Health, Mannheim, University of Heidelberg,
Christine Kief and Hans-Joachim Salize
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Re: Mentally Disorders Prisoners in Europe

dressing{at}zi-mannheim.de Harald Dressing, et al.

The prevalence of psychiatric disorders in prisoners is substantially higher than in the general population (1). Additionally, there is scientific evidence that the number of mentally disordered prison inmates is rising. As a consequence, the World Psychiatric Association (WPA) has repeatedly voiced concern about the increasing number of mentally ill individuals being placed in correctional facilities (2). In European Union member states forensic legal provision governing the diversion of mentally disordered offenders is found spread across penal codes or in general or mental health legislation such that is uncertain whether member states place emphasis more on medical or punitive parameters in judicial deliberations (3). From a human rights perspective, depriving mentally disordered prisoners of any state-of-the-art treatment cannot be accepted (4). However, there is a serious shortage of information and data in the field. Therefore the European Commission funded the research project: EUPRIS that aimed at collecting structured information on concepts, models, and routine practices in prison mental health care in 24 European Union Member States and other European countries (5). The results of the study are alarming and should give rise to public policy and research activities. Even the most rudimentary health reporting standards for mental health care in prison are lacking almost everywhere in Europe. Almost none of the included countries provides regular national statistics on the frequency of mental disorders of prisoners or on the availability or frequency of psychiatric treatments. A major reason for the lack of data on the prevalence of mental disorders in prisons is the deficient implementation of standardized psychiatric screening and assessment procedures at prison entry and during imprisonment. In many countries, the appointment of inadequately trained staff to perform such screenings increases considerably the risk that mental disorders or psychiatric needs of the inmates will remain undetected. Furthermore the pathways to care in case of an acute psychotic episode differ significantly since referral to prison hospitals, medical prison wards, forensic hospitals or general psychiatric hospital are used in various combinations depending on different national legal regulations and on the availability of services or other regional circumstances. Therefore the equivalence of care for mentally disordered prisoners has been questioned by the cooperating national experts. As a basic prerequisite for any action taken, more awareness of the deficiencies and problems must be raised by responsible authorities and decision makers. The implementation of some basic indicators used in general psychiatry research seems to be overdue.
1.Fazel D, Danesh J. Serious mental disorders in 23000 prisoners: a systematic review of 62 surveys. Lancet 2002; 359:545-550
2.Okasha A. Mental Patients in prisons: punishment versus treatment. World Psychiatry 2004; 3: 1-2
3.Dressing H, Salize HJ, Gordon H. Legal frameworks and key concepts regulating diversion and treatment of mentally disordered offenders in European Union member states. European Psychiatry, 2007; 27: 427-432
4.Harding TW. Prevention of torture and inhuman or degrading treatment: medical implications of a new European Convention. Lancet 1989; 1: 1191-93
5.Salize HJ, Dressing H, Kief C. Mentally Disordered Persons in European Prison Systems- Needs, Programmes and Outcome (EUPRIS) http://ec.europa.eu/health/ph_projects/2004/action1/action1_2004_17_en.htm
Declaration of interest: The study was funded by a grant of the European commission.

Challenges to binge drinking prevention 25 October 2008

Napoleon Waszkiewicz,
Psychiatrist
Department of Psychiatry of Medical University of Bia³ystok, 16-070 Choroszcz, Poland,
Agata Szulc
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Re: Challenges to binge drinking prevention

napoleonwas{at}yahoo.com Napoleon Waszkiewicz, et al.

SIR—An alarming rise in binge drinking has received considerable media attention in recent years (Anonymous, 2008). Binge drinking occurs in a third of the drinking occasions. Nothing unusual in that since an increasing number of working young adults use alcohol as a recreational drug, tending to concentrate their drinking at weekends. Alcohol “bingeing” increases the risk for numerous acute adverse health and social events including poisoning, myocardial infarction, injuries, accidents, suicide, violence, etc. but other (e.g. biochemical) side effects may not be appreciated. Binge drinking is characterized by the consumption of alcohol leading to intoxication (drinking to get drunk), often measured as having more than 5/4 drinks on one occasion, etc. (Waszkiewicz et al, 2008a). Despite the current prevention strategies (increasing alcohol excise taxes, enforcing the minimum legal age for drinking, restrictions on hours of sale, reducing alcohol outlet density, banning advertising), binge drinking is still growing problem in the world (Anonymous, 2008). Therefore, it is an urgent need to improve strategies to binge drinking prevention. A feedback given to patients on the basis of biomarkers is an important challenge that has not been adequately exploited. Routine laboratory tests are not sensitive enough to detect harmful effects of single occasion drinking (except of serum aspartate aminotransferase), since changes are only measurable after very high and prolonged ethanol consumption (Sharpe, 2001). But the binge drinking session can increase some of the new harmful drinking markers (salivary, serum and urinary β-hexosaminidase, salivary immunoglobulin A) (Waszkiewicz et al, 2008a,b). However, no binge drinking marker has been established so far. The minor or lack of “answer” of alcohol abuse markers in young people has been reported. The rapid normalization of elevated serum markers and relatively light drinking may be the reasons of false-negative results (Waszkiewicz et al, 2008a). Binge drinking is characterized by occasional high alcohol intake. Hence, the statement of binge drinking markers with its biofeedback properties, might be particularly/only applicable to such a “bingeing” population. Saliva-based testing shows much promise in this way, since material can be simply and non-invasively obtained. As the majority of alcohol-rel