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Kenneth R. Alper, M.D.; Orrin Devinsky, M.D.; Laura Boylan, M.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2002;14:465-a-466. doi:10.1176/appi.neuropsych.14.4.465-a
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SIR: Dr. Fong notes our finding of a high prevalence of mood disorder among the first- and second-degree relatives of patients with postictal psychosis (PIP) and suggests that it would be interesting to know the relationship between seizure cluster characteristics in patients with PIP and presence of mood disorder among their first- or second-degree relatives. We agree that such an approach would be useful in exploring the underlying hypothesis of an abnormality of modulation of excitatory neurotransmitter in familial mood disorders, which could be associated with a greater tendency toward seizure clustering or multiple seizure foci, which could in turn facilitate or permit the development of psychosis in epilepsy.

The expected outcome of a study based on the above hypothesis would be a positive association of an increased tendency toward seizure clustering and multifocality with a family history of mood disorder. Important methodological aspects of such a study would include obtaining structured family psychiatric history data from family members themselves, as well as patients, and using an appropriate quantitative definition of the tendency toward seizure clustering. Such a study might optimally involve more than one center, and we would welcome further communication from Dr. Fong and colleagues from other epilepsy centers with an interest in this possibility.

Dr. Fong also notes a prior finding of regional hyperperfusion in patients with PIP and suggests that this may be related to prior reports of reduced activity of 5-HT (serotonin), GABA, and GABA-synthesizing enzyme as state markers in depression, and of low plasma GABA level as a trait marker in depressed patients independent of mood state. PIP may be related to combined hyperfunction and hypofunction in CNS during recovery from a seizure cluster. A common formulation regarding PIP combines some form of cortical inhibition and subcortical disinhibition. The condition of PIP often appears to take root in a "soil" of associated neurologic risk factors such as bilateral CNS dysfunction (e.g., head trauma, encephalitis, multifocal EEG abnormalities). A cluster of seizures then further depresses CNS function, and in the recovery phase, some aspects enter a hyperactive state and others are depressed, with PIP as a resulting clinical manifestation. On the basis of findings in our study, family history of mood disorder appears to exert a permissive or facilitatory influence on the development of PIP or to "fertilize the soil."

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