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Depersonalisation in migraine.
- C. Majella Cahill (20 June 2003)
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C. Majella Cahill, Fellow in Neuropsychiatry Department of Psychiatry Beaumont Hospital
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drpsych1{at}hotmail.com C. Majella Cahill
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Sir: I read with interest Baker et al’s recent article (May 2003) on the clinical features of depersonalisation disorder, based on assessment of 204 consecutive referrals to a specialist clinic at the Maudsley Hospital, London. The authors noted that 31% of patients reported a history of migraine, “one third of whom believed that their headaches and depersonalisation were connected”. The association between migraine and depersonalisation/derealisation is worthy of further consideration. Migraine aura is a complex of focal neurological symptoms, which precedes or accompanies an attack. The International Headache Society has provided standardised criteria for diagnosis (IHS, 1988). Aura may occur in isolation without headache, but extensive investigation and prolonged follow-up is often necessary before a diagnosis of migraine is accepted. Depersonalisation/derealisation may occur as a component of migraine aura. A particularly dramatic example occurs in the Alice in Wonderland syndrome (Silberstein & Young, 1995), most common in children, where the aura is characterized by a variety of paroxysmal body schema disturbances, which may co-occur with depersonalisation, derealisation, visual illusions and disorders in the perception of time. In addition, Blau (1992) has reported that migraineurs commonly experience a feeling of being “unusually removed from reality” in the gap between termination of aura and the onset of headache, though patients do not often spontaneously volunteer this information. The authors’ observation, that their patients describing sudden onset of depersonalization/derealisation (38%) were significantly more likely to experience seeing flashes of light, may represent onset in association with visual aspects of migraine aura. The three factors identified by their patients as worsening depersonalization i.e. psychological stress, environmental lighting and physical stressors such as fatigue, are also recognised migraine triggers. Aura symptoms are usually fully reversible and individually last no longer than 60 minutes. However, the IHS also describes categories of migraine with prolonged aura (one or more aura symptom lasts greater than 60 minutes and less than or equal to 7 days, neuroimaging is normal) and migrainous infarction (aura symptoms persist for greater than 7 days and/or neuroimaging demonstrates an infarction). The term migraine aura status (not included within the IHS classification system) is used to refer to persistence of aura symptoms for greater than 7 days in the absence of cerebral infarction and symptoms may become chronic in nature. More recently, a variant of migraine with daily occurrence of aura has been described (Merims & Kuritzky, 2000). Thus, depersonalisation/derealisation occurring in the context of migrainous aura could uncommonly follow a protracted course. It has been postulated that cortical spreading depression (CSD) underlies the pathophysiology of migraine aura. CSD is a short-lasting depolarization wave that moves across the cortex at a rate of 3-5mm/min and involves an autocatalytic cycle leading to release of glutamate, which, acting on NMDA receptors, furthers the spreading depression (Lauritzen, 1994). Lamotrigine inhibits neuronal release of glutamate and case reports in the literature suggest that persistent visual aura may respond to this agent (Chen et al, 2001). Acetazolamide (Haan et al, 2000) and valproic acid (Rothrock, 1997) may also be of benefit in treatment of prolonged aura. These agents might be considered for the treatment of depersonalization/derealisation occurring as components of migraine aura. In conclusion, I would caution the authors against making a diagnosis of primary depersonalization disorder in the absence of exclusion of organic disorders, in particular migraine and epilepsy. Depersonalisation occurring in these contexts may respond to treatments appropriate to the underlying disorder. Finally, the observed association between migraine and depersonalisation may have also, in part, arisen due to the very high levels of psychiatric co-morbidity associated with migraine. References: Blau J.N. (1992) Classical migraine: symptoms between visual aura and headache onset. Lancet, 340(8815), 355-6. Chen W.T., Fuh J.L., Lu S.R., Wang S.J. (2001) Persistent migrainous visual phenomena might be responsive to lamotrigine. Headache, 41(8), 823- 5. Haan J., Sluis P., Sluis L.H., Ferrari M.D. (2000) Acetazolamide treatment for migraine aura status. Neurology, 55(10), 1588-9. Headache Classification Committee of the International Headache Society (1988) Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia, 8(supplement 7), 1-96. Lauritzen M. (1994) Pathophysiology of the migraine aura. The spreading depression theory. Brain, 117(Part 1), 199-210. Merims D., Kuritzky A. (2000) Daily migraine with aura: a new migraine variant. Headache, 40(5), 389-92. Rothrock J.F. (1997) Successful treatment of persistent migraine aura with divalproex sodium. Neurology, 48(1), 261-2. Silberstein, S.D. & Young, W.B. (1995) Migraine aura and prodrome. Seminars in Neurology, 15(2), 175-182. Author information: Dr. C.Majella Cahill, Fellow in Neuropsychiatry, Department of Psychiatry, Beaumont Hospital, Dublin 9, Telephone:00-353-1-8093354 Fax:00-353-1-8376982 e-mail:drpsych1@hotmail.com |
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