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Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki
Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, and Department of Psychiatry, University of Helsinki
Department of Mental Health and Alcohol Research, National Public Health Institute, Helsinki, Finland
Correspondence: Dr Laura Niemi, Department of Mental Health and Alcohol Research, KTL, National Public Institute, Mannerheimintie 166, FIN-00300 Helsinki, Finland. Tel: +358 9 4744 8894; e-mail: laura.niemi{at}ktl.fi
Declaration of interest None. Funding detailed in Acknowledgements.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Aims To compare the development of high-risk and control group children, and investigate which factors predicted future psychiatric disorders.
Method We examined information from childhood and school health record cards of 159 high-risk and 99 control group offspring. Logistic regression was used to assess whether developmental abnormalities predicted later mental disorders.
Results Compared with controls, children in the high-risk group had more emotional symptoms before school age, attentional problems and social inhibition at school age, and neurological soft signs throughout. In this group pre-school social adjustment problems (OR=9.7, 95% CI 1.8-51.8) or severe neurological symptoms (Fisher's test, P=0.006) predicted future schizophrenia-spectrum disorder. Social adjustment problems and emotional symptoms during school age predicted future non-psychotic psychiatric disorders.
Conclusions Our study supports the validity of neurological, emotional, social and behavioural markers as vulnerability indicators of psychotic and other mental disorders, particularly among children genetically at high risk of psychosis.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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METHOD |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Finnish child health guidance in child welfare clinics and schools
Child health guidance in Finland is provided by public health nurses and
primary care physicians, and it extends to all children under school age (7
years). Thereafter the children visit school health nurses and physicians in
their school area. After the initial home visit from a public health nurse
when they are 8-14 days old, infants attend the child health centre at 1 month
and thereafter at 2, 3, 5, 6, 10, 12 and 15 months of age; toddlers attend
when they are 2, 3, 4 and 5 years old. They see a doctor at age 1.5, 4, 8 and
18 months, and at 3 and 6 years. Nurses and physicians complete a standard
form with measurements (e.g. weight, height) and other standard observations
(e.g. reaching motor milestones) at every visit. School children visit the
school nurse once a year and are seen by the school doctor at age 7, 12, 15
and 17 years.
Childhood health cards
Health cards for all individuals in the sample were obtained from their
home districts. The card data cover childhood health checks for each visit
from infancy to the end of school age. The following items were extracted from
each card: whether the child was walking at 12 months and speaking words at 2
years; whether the child had a speech problem during childhood (age 5-6 years)
or at school (age 7-17 years); whether there were emotional symptoms during
childhood (before age 7 years) or at school (age 7-17 years); problems in
social adjustment (only at 5-6 years); problems in neurological development
(coded as ‘severe neurological symptoms’ in severe cases, e.g.
with hemiplegia or spasticity, and as ‘neurological soft signs’ in
less severe cases, e.g. with tics or subthreshold hypotony) during childhood
or adolescence; rating of failure to reach the age-appropriate level of mental
development (coded as delayed mental development, assessed yearly between 1
year and 6 years of age) and of need for extra follow-up in the school health
system for any reason (assessed at school age); rating during school years of
being socially inhibited, of having conduct problems, attention problems or
academic impairment (indicated by repeating the same class, having been
examined by a psychologist or doctor because of severe problems in academic
performance or having been transferred to a special school owing to severe
problems in academic performance).
Dependent variables
For this analysis, offspring who later developed a psychiatric disorder
were classified into six diagnostic groups: all schizophrenia-spectrum
disorders (n=12; 8 males), including schizophrenia, schizoaffective
disorder, delusional disorder and psychotic disorder not otherwise specified;
any psychotic disorder (n=17; 11 males); any mood disorder
(n=15; 9 males); substance-related disorder (n=15; 11
males); personality disorders (n=10; 6 males); and any mental
disorder (n=30; 21 males). Because comorbidity was common, some
offspring appeared in more than one diagnostic group.
Explanatory variables
All explanatory variables were dichotomised and coded as 0 (child had
reached expected level or had no problem with the assessed variable) or 1 (had
not reached the expected level or had the assessed problem). In a separate
analysis we also used missing data as an explanatory variable, because missing
health assessments could reflect family problems possibly associated with
increased risk of psychiatric morbidity.
Gender and social class were incorporated in the models as covariates. Socio-economic group classification was based on the City of Helsinki Social Group classification (Central Statistical Office of Finland, 1989). In the analysis, the groups were collapsed into two groups: professional/clerical became ‘upper social class’ (for the high-risk sample n=61, for controls n=53), and skilled/unskilled workers ‘lower social class’ (for the high-risk sample n=91, for controls n=44). Social class data were lacking for seven children in the high-risk group and two in the control group. We used paternal occupation to classify socio-economic status; if this was missing, we used maternal occupation.
Statistical assessment
The occurrence of developmental problems was compared between the high-risk
and control group offspring using the chi-squared test, or Fisher's exact test
when the expected number in any cell was below five. Developmental problems
were compared between offspring in each maternal diagnostic group using the
likelihood ratio test. Examination of the relationship between childhood
developmental problems and psychiatric morbidity in adulthood was confined to
the high-risk group, because the cumulative incidence of mental disorders in
the control group was low (Niemi et
al, 2004). To investigate the relationship within the
high-risk group we used logistic regression models in which the six
dichotomised diagnostic outcomes were used as dependent variables. Univariate
models were calculated for all combinations of dependent and explanatory
variables; gender and social class were incorporated as covariates. Odds
ratios with 95% confidence intervals and Wald test statistics with
significance levels were calculated. All statistical analyses were performed
using the Statistical Package for the Social Sciences for Windows, version
11.5.1.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Factors differentiating the development of high-risk and control group offspring
Offspring in the high-risk group more often had emotional symptoms during
childhood (
, d.f. = 1, P =
0.006) and neurological soft signs (
,
d.f. = 1, P = 0.024), and were more prone to social inhibition during
their school years (Fisher's exact test, P=0.044)
(Table 1).
Table 2 displays the proportion
of individuals with developmental problems in each maternal diagnostic
group.
Factors predicting later development of mental disorders in high-risk offspring
Neither of the dependent variables (social class or gender) significantly
influenced the odds of developing mental disorders. Among the high-risk
offspring, after adjusting for gender and social class, problems in social
adjustment at age 5-6 years predicted later development of
schizophrenia-spectrum disorder (OR=9.73, 95% CI 83-51.8; P=0.008).
Two offspring in this group had severe neurological symptoms in childhood and
both developed schizophrenia (Fisher's exact test, P=0.006); odds
ratios could not be calculated because of the zero denominator
(Table 3).
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Problems in social adjustment at age 5-6 years (OR=4.51, 95% CI 0.99-20.6; P=0.052) and emotional symptoms at school age (OR=2.88, 95% CI 0.99-8.34; P=0.051) tended to predict later development of any psychotic disorder.
Emotional symptoms (OR=15.7, 95% CI 3.32-74.1; P=0.001), conduct problems (OR=18.0, 95% CI 4.41-73.5; P<0.001) and social inhibition (OR=34.9, 95% CI 5.71-4100; P<0.001) at school age predicted later development of any mood disorder; attentional problems were an almost significant predictor (OR=6.71, 95% CI 0.99-45.5; P=0.051).
Emotional symptoms (OR=7.23, 95% CI 1.82-28.6; P=0.005), conduct problems (OR=13.2, 95% CI 3.14-55.8; P<0.001) and attentional problems (OR=7.62, 95% CI 1.09-53.4; P=0.041) at school age all predicted later development of substance-related disorder.
Delayed mental development (OR=10.5, 95% CI 1.95-56.4; P=0.005), problems in social adjustment at age 5-6 years (OR=6.22, 95% CI 1.0-38.7; P=0.050), and emotional symptoms (OR=9.55, 95% CI 1.91-47.8; P=0.006), conduct problems (OR=5.88, 95% CI 1.23-28.2; P=0.027) and social inhibition (OR=12.3, 95% CI 2.19-68.6; P=0.004) at school age, predicted later development of personality disorder.
Delayed mental development (OR=3.98, 95% CI 1.07-14.9; P=0.040), emotional symptoms (OR=4.70, 95% CI 1.92-11.5; P=0.001), conduct problems (OR=9.44, 95% CI 2.44-36.3; P=0.001) and social inhibition (OR=13.6, 95% CI 2.30-80.6; P=0.004) at school age, predicted later development of any mental disorder. Problems in social adjustment at age 5-6 years (OR=4.10, 95% CI 0.99-17.0; P=0.052) tended to predict later development of any mental disorder.
Factors predicting later development of mental disorders among offspring of women with schizophrenia
Separate analysis of the data for the offspring of mothers with
schizophrenia-spectrum disorder changed the results only slightly
(Table 4). Neurological soft
signs tended to predict later development of schizophrenia-spectrum disorder
(OR=4.48, 95% CI 0.98-20.5; P=0.053), whereas problems in pre-school
social adjustment no longer predicted later development of any psychotic
disorder, personality disorder or any mental disorder. Social inhibition no
longer predicted later development of any mood disorder.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Factors differentiating the development of high-risk and control offspring
The high-risk offspring more often had emotional symptoms before school age
than controls. This accords with previous findings that children at high-risk
are more depressive, hyperactive and immature
(Niemi et al, 2003).
Consistent with previous studies (Niemi
et al, 2003), high-risk children more often had
neurological signs than controls. A recent family study found that
neurological soft signs were more common among parents of patients with
schizophrenia, who were the presumed carriers of the genetic loading based on
their family history, than among parents who were presumed non-carriers,
supporting the hypothesis that neurological signs are associated with genetic
risk of schizophrenia (Gourion et
al, 2004). The high-risk offspring, particularly those whose
mothers had schizophrenia, also differed from controls in being socially
inhibited at school age. Also in previous studies the behaviour of high-risk
offspring was more often disturbed at school age compared with controls (for
review see Niemi et al,
2003).
Developmental factors predicting future development of schizophrenia-spectrum disorders
Problems in social adjustment during childhood were equally likely in the
high-risk and control offspring; however, they predicted later development of
schizophrenia-spectrum disorder, and tended to predict any psychotic disorder,
only in the high-risk group. Problems in pre-school social adjustment in our
cohort were assessed at age 5-6 years, when a health assessment priority is to
identify children who may be unable to start education at the normal age of 7
years. Two of the five high-risk boys and one of the six high-risk girls with
problems in pre-school social adjustment developed schizophrenia-spectrum
disorder. High-risk individuals who developed schizophrenia-spectrum disorders
in our cohort did not differ significantly as adolescents in their social
adjustment from high-risk offspring who did not develop a mental disorder.
Conduct and attentional problems and social inhibition at school age were more
common among high-risk offspring who developed schizophrenia-spectrum
disorders, but not to a statistically significant extent. It may be that these
children's problems did not draw as much attention at school age as they did
at the pre-school assessments.
Severe neurobiological symptoms predicted future development of schizophrenia-spectrum disorders, and neurological soft signs tended to predict the same among high-risk offspring whose mothers were diagnosed with these disorders. Severe neurological symptoms were rare, but both of the high-risk children who had these symptoms had mothers with schizophrenia, and both went on to develop schizophrenia-spectrum disorders. The girl had febrile seizures at age 2 years, and from age 5 years was found to have spasticity, to be slow and to have coordination problems; she later developed schizophrenia with depressive symptoms and alcohol misuse. The boy had hemiplegia; he went on to develop schizoaffective disorder with alcohol misuse. Previous high-risk studies have also found that neurological symptoms predicted schizophrenia (Niemi et al, 2003). It seems that problems in neurological development are more specific to schizophrenia-spectrum disorders, whereas emotional problems are more unspecific predictors of mental disorder (Gottesman, 1991; Jones & Murray, 1991; Cannon et al, 2002).
Developmental factors predicting development of other mental disorders
Emotional symptoms in school-age children tended to predict later
development of any psychotic disorder. Previous studies have found that at
school age internalising and externalising symptoms both predict future
psychotic disorder (Cannon et al,
2001). Emotional symptoms, conduct problems, social inhibition and
attentional problems at school age were strong predictors of future mood
disorders among high-risk offspring. The Dunedin Multidisciplinary Health and
Development Study found that individuals with juvenile-onset depression have
an excess of behavioural and emotional problems, as well as motor development
problems (Jaffee et al,
2002). Our results suggest that emotional and conduct problems and
social inhibition increase the risk of future mood disorders among individuals
with a high genetic risk of psychotic disorder. The odds ratios increased when
only the data for high-risk offspring whose mothers had a
schizophrenia-spectrum disorder were analysed, suggesting that the observed
associations were not caused by an elevated genetic risk of affective
disorder. Conduct and attentional problems were also highly predictive of
future mood disorders. The Dunedin study found that juvenile-onset depression
in particular is highly comorbid with conduct disorder and attention-deficit
disorder (Jaffee et al,
2002), which complements our findings. Although neurological soft
signs did not predict later development of mood disorders in our study, it is
interesting that the British 1946 National Birth Cohort found excess twitching
and grimacing among children with childhood affective disturbance
(van Os et al, 1997),
and in our cohort, neurological soft signs were most common among offspring of
mothers with affective disorder, suggesting a possible connection also between
familial risk of affective disorder and soft neurological signs.
Interestingly, besides psychotic disorders, only personality disorder was predicted by behavioural problems before school age, and was the only diagnosis for which developmental predictors were observed from early childhood through adolescence. Two children in the high-risk group developed antisocial personality disorder, five developed borderline personality disorder and two personality disorder not otherwise specified. That no cluster A personality disorder was found reflects our method of case selection. As the Copenhagen High-Risk Study showed, individuals with cluster A personality disorders rarely receive hospital treatment (Parnas et al, 1993), whereas individuals with cluster B disorders are often admitted to hospital because of their impulsive, aggressive or selfdestructive behaviour. Cluster B personality disorders being so common in our sample, our findings concerning delayed mental development in early childhood could be explained by previous research suggesting that persistent antisocial behaviour is associated with both pre-school and school-age neurocognitive deficits (Moffitt, 1993; Raine et al, 2002). Consistent with our findings, earlier studies have found that childhood aggression, withdrawal, lack of social skills, and mental health problems are risk factors for antisocial personality disorder (Holmes et al, 2001; Moffitt et al, 2002). Individuals who develop borderline personality disorder also have more emotional symptoms and conduct disorder throughout childhood and adolescence (Joyce et al, 2003). Conduct problems self-evidently predict future antisocial personality disorder, since they are part of its diagnostic criteria.
Emotional symptoms, conduct problems and attentional problems at school age predicted future substance-related disorders. Similarly, the Danish Longitudinal Study of Alcoholism found that childhood unhappiness and antisocial personality disorder predicted alcohol misuse and dependence (Knop et al, 2003).
Overall, developmental problems predicting personality, mood and substance use disorders among individuals at high genetic risk of schizophrenia do not differ from those identified in population-based cohort studies, but the observed odds ratios are much higher. Thus, the effect of these problems is more severe in the presence of genetic vulnerability to psychotic disorders.
Some developmental problems, such as speech problems, academic impairment, lateness in learning to walk and childhood emotional symptoms, did not predict any psychiatric disorder in adulthood. In cohort studies, children who later developed schizophrenia have been found to reach motor milestones later, and to learn to speak later, than those who remained unaffected (Niemi et al, 2003). Our different finding might be explained by our smaller sample size or by the less-detailed information we had (only whether the child had reached the milestones by a certain age). Because of the nature of our data, we are cautious about drawing any further conclusions at this point, although it might also be that the degree of developmental adversity necessary for the development of schizophrenia is somewhat different in offspring who have an especially high genetic risk compared with those who have no family history of schizophrenia.
Limitations
Although this was one of the largest high-risk studies, sample sizes were
still small and the statistical power was insufficient to detect
moderate-sized associations. All differences reaching significance in the
numerous statistical tests performed were in the expected direction, which
supports the reliability of our results. Multiple regression analysis was not
possible because for most developmental problems the number of affected
individuals was small, and collinearity became a problem. Thus our results
were mostly descriptive. Larger samples would be needed to assess the
significance of developmental abnormalities in relation to each other, and
possible interactive mechanisms.
Missing data could have influenced our results. This problem was more common among controls in the pre-school variables, and among the high-risk group at school age. Non-participation in child health guidance could reflect an unstable family lifestyle, possibly with frequent change of residence or social problems. However, when ‘missing data’ was entered as a separate variable in the models, it did not predict future development of any of the examined mental disorders.
The psychotic disorders developed by offspring in the high-risk group might represent a special form of psychosis, since all the individuals in this group were at high genetic risk. Thus, the findings may not be generalisable to less familial forms of the disorder. Also, all the high-risk children lived in a family environment where the mother had a psychotic disorder, or else were adopted away: this might have increased psychological and social stress in the offspring and influenced the overall outcome.
When assigning diagnoses, the researchers could not always remain masked to the offspring's risk status, since it was often mentioned in the case notes. However, they were always masked to the actual identity of the mother-child pairs.
Compared with other high-risk studies, our information was less detailed, consisting of ratings in regular childhood assessments coded in standard forms used throughout the country. The benefit of this is that ratings were made without awareness of the ongoing study, and that all these problems were severe enough to be observable in primary care. However, only severe problems were recorded in the health cards; more subtle developmental problems might have remained unrecognised or unrecorded. Despite the lack of detailed data we were able to identify predictive factors that distinguished the high-risk children who later developed mental disorders. When supportive measures for high-risk children are planned, special attention should go to children who already have neuromotor, emotional, social or behavioural problems.
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Clinical Implications and Limitations |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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LIMITATIONS
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMETHODRESULTSDISCUSSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Received for publication April 13, 2004. Revision received September 9, 2004. Accepted for publication September 10, 2004.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Psychiatric Bulletin | Advances in Psychiatric Treatment | All RCPsych Journals |
