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Depersonalisation disorder: clinical features of 204 cases

  • Dawn Baker (a1), Elaine Hunter (a1), Emma Lawrence (a1), Nicholas Medford (a1), Maxine Patel (a1), Carl Senior (a1), Mauricio Sierra (a1), Michelle V. Lambert (a1), Mary L. Phillips (a2) and Anthony S. David (a2)...

Depersonalisation disorder is a poorly understood and underresearched syndrome.


To carry out a large and comprehensive clinical and psychopathological survey of a series of patients who made contact with a research clinic.


A total of 204 consecutive eligible referrals were included: 124 had a full psychiatric examination using items of the Present State Examination to define depersonalisation/derealisation and 80 had either a telephone interview (n=22) or filled out a number of self-report questionnaires. Cases assessed were diagnosed according to DSM–IV criteria.


The mean age of onset was 22.8 years; early onset was associated with greater severity There was a slight male preponderance. The disorder tended to be chronic and persistent. Seventy-one per cent met DSM–IV criteria for primary depersonalisation disorder. Depersonalisation symptom scores correlated with both anxiety and depression and a past history of these disorders was commonly reported. ‘Dissociative amnesia’ was not prominent.


Depersonalisation disorder is a recognisable clinical entity but appears to have significant comorbidity with anxiety and depression. Research into its aetiology and treatment is warranted.

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Corresponding author
Anthony David, Section of Cognitive Neuropsychiatry, Box 68, Institute of Psychiatry, DeCrespigny Park, London SE5 8AF, UK. Tel: +44 (0)20 7848 0138; fax: +44 (0)20 7848 0572; e-mail:
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Depersonalisation disorder: clinical features of 204 cases

  • Dawn Baker (a1), Elaine Hunter (a1), Emma Lawrence (a1), Nicholas Medford (a1), Maxine Patel (a1), Carl Senior (a1), Mauricio Sierra (a1), Michelle V. Lambert (a1), Mary L. Phillips (a2) and Anthony S. David (a2)...
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Depersonalisation in migraine.

C. Majella Cahill, Fellow in Neuropsychiatry
20 June 2003

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 illusionsand 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 diagnosisof 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.


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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 aurawith divalproex sodium. Neurology, 48(1), 261-2.

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Author information:Dr. C.Majella Cahill, Fellow in Neuropsychiatry, Department of Psychiatry,Beaumont Hospital,Dublin 9,
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Conflict of interest: None Declared

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