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Does a family history of psychosis protect against psychosis in people with epilepsy ?
- Vaughan Bell, Cardiff University (23 June 2005)
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Schizophrenia & Epilepsy
- Ephraim Bental (27 June 2005)
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Epilepsy excludes diagnosis of schizophrenia
- Andrew Al-Adwani (1 July 2005)
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Epilepsy and Psychosis: Pitfalls in treatment
- Dr Adil Y. Kadri (1 July 2005)
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Possible impact of medication
- Dinah KC murray (3 July 2005)
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Schizophrenia and Epilepsy: Untenable Link from Flawed Research Design
- Stefan P Kruszewski (5 July 2005)
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Re: Epilepsy excludes diagnosis of schizophrenia
- Brian P Hallahan (5 October 2005)
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Vaughan Bell, Research Associate School of Psychology, Cardiff University
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The authors conclude from the study that epilepsy and psychosis may share common environmental and / or genetic causes. The authors also report however, that the increased risk associated with both personal and familial history of epilepsy is stronger among people with no family history of psychosis. This suggests a curious interaction, in that a family history of psychosis seems to infer some sort of protection against psychosis in people with epilepsy. Such a result is in exactly the opposite direction that one might expect from the received wisdom, and the other evidence presented in the study, and suggests that seizures and genetic and environmental influences do not produce a simple cumulative risk for psychosis. It is possible that a family history allows for an environment where reality-distortion symptoms are recognised and referred to a clinician before they become full-blown psychosis, or perhaps that a genetic susceptibility to psychosis and the presence of seizures are somehow antagonistic. Either way, the cause of this interaction would seem to be a particularly valuable point of enquiry that could lead to some important clinical interventions. Competing interests: None declared |
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Ephraim Bental, Neurologist & Psychiatrist Private 34349
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In describing the realationship between these two diseases, the historical concept of antagonism of diseases first introduced by Wagner- Jauregg in 1917 - the concept of treating a mental disease by introducing another disorder- (treating Dementia Paralytica with Malaria), should be mentioned. In 1930 Ladislaw Meduna applied this theory, based on his observation that patients who developed epileptic seizures, showed a relief of the symptoms of Dementia Praecox, thus introducing the injection of Camphor to produce an epileptic seizure. This was tried on the 23 January 1934 in a psychiatric hospital in Budapest on a schizophrenic patient who had been psychotic, mute and negativistic. He repeated the camphor injections at three days intervals and after the fifth injection the patient got up from his bed and began to talk for the first time in four years. This led to the later introduction of the Electroconvulsive therapy by U. Cerletti and L. Bini in 1938 in Rome. Competing interests: None declared |
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Andrew Al-Adwani, Psychiatrist Great Oaks, Ashby High Street, Scunthorpe, N. Lincs., DN16 2JX
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Sir: The authors of this study having used initially ICD-8 and then ICD-10 to make diagnoses of schizophrenia seem to have ingnored the ICD-8 diganostic category of 'psychosis associated with other cerebral condition' (e.g. epilepsy) and the ICD-10 exclusion criterion for a diagnosis of schizophrenia in the presence of epilepsy. The authors are not alone in this oversight as the BNF cautions against the use of atypical drugs licensed for schizophrenia in the presence of epilepsy when no such diagnosis can be made if a higher order diagnosis (organic brain disorder)is present. Competing interests: None declared |
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Dr Adil Y. Kadri, SHO Psychiatry Rotation Cefn Coed Hospital Swansea NHS Trust Swansea SA2 0GH
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Thank you for a most interesting study showing an increased risk of developing a psychotic illness in those with epilepsy. The results of this study do go against the conventional psychiatric wisdom and well-established fact that inducing a seizure provides relief in psychotic symptoms. Therefore one would have expected those with epilepsy to have had a lower incidence a psychotic illness. Having said that from my own experience (having worked in psychiatry for 6 years now) one does meet a number of patients with a psychotic illness who also suffer from epilepsy. Certainly from now on whenever I see patients with psychosis and epilepsy I will be bearing the results of this study in mind. To compound matters further, treating psychosis in those with epilepsy can be quite tricky on occasion. The reason for this is that as most anti-psychotics lower the seizure threshold they can potentially cause problems in the symptom-control of epilepsy. In this group of patients it is therefore important to carefully select an anti-psychotic with a lower epileptogenic side-effect profile. It is also of importance to optimise the dose of anti-epileptic medications if needed and have input from a Neurology Consultant whose advice can be invaluable in the care of such patients. Competing interests: None declared |
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Dinah KC murray, author; Independent researcher Autism & Computing 42 Cheverton road London N19 3AZ
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The authors appear not to have considered the possible impact of medication on the association between epilepsy and schizophrenia they find in their study. It seems to me premature to speculate about cause without taking into account potential interactions between psychotropic medications and prior dispositions. Yours truly, Dinah Murray Competing interests: None declared |
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Stefan P Kruszewski, Psychiatrist Harrisburg, Pennsylvania USA
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The recently published BMJ article by Qin et al, “Risk for schizophrenia and schizophrenia-like psychosis among patients with epilepsy: Population based cohort study” offers an untenable conclusion.(1) The first sentence of the authors’ discussion asserts, “…this large population study shows that people with a history of epilepsy have nearly 2.5 times the risk of developing schizophrenia and nearly three times the risk of developing a schizophrenia-like psychosis compared with the general population.” While it is possible that the authors’ declaration of risk might have future validity, it is unsupportable based upon their current research. An analysis of their work, partially funded by the USA-based Stanley Medical Research Institute, ignores the effects of antiepileptic medication-induced neuropsychiatric sequelae in an epileptic cohort. The oversight is significant. It is a problem addressed briefly by Dinah KC Murray, London, in her previous response to the Qin article.(2) The authors failed to account for the putative role of anticonvulsant medications in the production of psychotic symptoms, including psychoses that resemble schizophrenic-like disorders. This omission erroneously assumes that anticonvulsant-treated epilepsy in Denmark, and elsewhere, has the same natural course as unmedicated epilepsy. The evidence regarding anticonvulsant-mediated adverse side-effects suggests otherwise. In 1994, Srinivasan and Richens described a ‘schizophrenia-like syndrome' in vigabartin.(3) That paper outlined at least three subtypes of psychosis associated with vigabartin, an irreversible inhibitor of GABA transaminase whose net effect is to enhance regional GABAergic activity.(4) In similar fashion, but not to the same degree, all of the major anticonvulsants list psychosis or psychotic-like symptoms in their presentation of adverse effects. The number one and number two best-selling anti-seizure drugs in the United States (according to the 21 April 2005 story in the Wall Street Journal, “FDA Request Reviews of Epilepsy Drugs-Paper”) dramatize the problem.(5) Best-seller gabapentin (Neurontin-Pfizer), a GABAergic anticonvulsant similar to vigabartin but whose different mechanism of action also enhances GABA activity, induces comparable problems. The adverse event data for gabapentin, as observed and recorded during all clinical trials in adults and adolescents with epilepsy, according to 2004 Physicians’ Desk Reference(PDR), pages 2562-3, reveals the following neuropsychiatric side-effects: Apathy, hallucinations, agitation, depression, paranoia, depersonalization, euphoria, emotional lability, nervousness, abnormal thinking, encephalopathy, suicidal gestures and psychosis.(6) The second most widely prescribed anticonvulsant in the United States, topiramate (Topamax-Ortho-McNeil; division of Johnson and Johnson), has a mechanism of action similar to vigabatrin and gabapentin, suggesting that it also potentiates the activity of the inhibitory neurotransmitter, GABA. The 2004 PDR(pages 2486-88) lists its adverse neuropsychiatric events as follows: Psychomotor slowing, impaired concentration, encephalopathy, personality disorder, speech or language problems, confusion, exacerbation of mood disturbances(including irritability and depression), hallucinations, aggressive reaction, paranoid reaction, delusions, paranoia, manic reactions, suicidal gestures, suicide attempts and psychosis.(6) A similar picture of adverse neuropsychiatric side-effects has been reported with all of the other major anticonvulsants, including carbamazepine, valproic acid, the oxazolidinediones, the succinimides, and the hydantoins. In many cases, the co-administration of these anticonvulsants increases the risk of neurotoxicity and the production of psychotic symptoms.(4) In order to substantiate their putative link between epilepsy and schizophrenia-like psychosis, Qin et al. would have to affirm three assumptions: (a) that medicated and unmedicated epileptic cohorts are separable and have natural history courses that are comparable, (b) that antiepileptic drugs, otherwise known to produce psychotic sequelae, do not produce long-term clinical conditions similar to schizophrenia-like psychosis, and, (c) that antiepileptic drugs, despite producing serious mood and thought disturbances as side-effects, do not induce those conditions in sufficient numbers in a given cohort to be addressed in linkage studies. Since these assumptions have not been addressed, the author’s conclusions are not valid. Stefan P. Kruszewski, M.D. Harrisburg, Pennsylvania 17112 USA joeysdogma@comcast.net 1. Qin P, Huilan X, Laursen TM, et al. 2005(17 June) Risk for schizophrenia and schizophrenia-like psychosis among patients with epilepsy: population based cohort study. BMJ Publishing Group Ltd. BMJ, doi:10.1136/bmj.38488.462037.8F. 2. Murray, D, July 3, 2005 response to: Qin P, Huilan X, Laursen TM, et al. 2005(17 June). Risk for schizophrenia and schizophrenia-like psychosis among patients with epilepsy: population based cohort study. BMJ Publishing Group Ltd. BMJ, doi:10.1136/bmj.38488.462037.8F. 3. Srinivasan, J & Richens A. (1994) A Risk-Benefit Assessment of Vigabartin in the treatment of neurological disorders. Drug Saf. 10: 395-405. 4. Brown TM, Stoudemire A. (1998) Psychiatric Side Effects of Prescription and Over-the-Counter Medications: Recognition and Management. Washington, DC. American Psychiatric Press, Inc. 5. Dow Jones Newswire .2005(21 April). FDA Requests Reviews of Epilepsy Drugs-Paper. The Wall Street Journal Online. WSJ.com 6. Murray, Lori, Senior Ed. (2004) PDR 58 Edition 2004: Physicians’ Desk Reference. Montvale, NJ, Thompson PDR. Competing interests: None declared |
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Brian P Hallahan, Lecturer in Psychiatry Beaumont Hospital, Dublin
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Sir First of all this was a very interesting study. A number of issues deserve mention however. As Andrew Al-Adwani noted a diagnosis of epilepsy precludes a diagnosis of schizophrenia according to ICD-10 diagnostic criteria. ICD-10 states that "Schizophrenia should not be diagnosed in the presence of overt brain disease or during states of drug intoxication or withdrawal. Similar disorders developing in the presence of epilepsy or other brain disease should be coded under F06.2 and those induced by drugs under F1x.5." We are unaware how many of the individuals with epilepsy in this large cohort had ictal or post-ictal psychosis and if these individuals were diagnosed as Schizophrenia or Schizophrenia-like psychosis. Understandably this was beyond the remit of Qin and colleagues study. The authors noted that there was an increased risk of schizophrenia for those with a personal history of epilepsy and the risk was stronger among people with no family history of psychosis. From their results presented in Table 3. this does not appear to be so. For those with no family history of psychosis, and a personal history of epilepsy the relative risk is 2.61 (95%CI 2.29-2.99). This is not markedly different to those with a family history of schizophrenia - the relative risk is 2.60 (95%CI 1.78 - 3.80). Individuals with only a family history of epilepsy and no psychiatric family history the relative risk is 1.17 (95%CI 1.05- 1.31) compared with 0.96 (95%CI 0.72-1.29) for those individuals with a family history of epilepsy . I feel that the authors can make this statement for those patients with a family history of epilepsy. Competing interests: None declared |
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