Postictal psychosis in partial epilepsy: A case–control study
- 14 May 2008
- journal article
- research article
- Published by Wiley in Annals of Neurology
- Vol. 63 (5) , 602-610
- https://doi.org/10.1002/ana.21341
Abstract
Objective: Divergent findings among prior studies on correlates of risk for postictal psychosis (PIP) suggest the value of a controlled study involving a relatively large number of patients.Methods: The study population consisted of a consecutive series of 59 patients with partial epilepsy and a history of PIP, and 94 control patients with partial epilepsy and no history of PIP evaluated as inpatients with video‐electroencephalography. The groups did not differ significantly regarding demographic features. Exact tests yielded a subset of variables and a tentative interpretation that were evaluated further utilizing principal components analysis and logistic regression.Results: PIP was associated with extratemporal versus temporal (p= 0.036) or undetermined (p= 0.001) localization of seizure onset, bilateral interictal epileptiform activity (p= 0.017), secondary generalization (p= 0.049), and history of encephalitis (p= 0.018). Interictal slow activity was more frequently absent in control patients (p= 0.045). PIP was associated with family histories of psychiatric disorders (p= 0.007) and epilepsy (p= 0.042), which themselves were significantly intercorrelated (r= 0.225;p= 0.006). Age of onset or duration of epilepsy and lateralized electroencephalographic or magnetic resonance imaging asymmetries did not differ significantly between control and PIP groups. The analysis indicated four underlying domains of risk for PIP: ambiguous/extratemporal localization, family neuropsychiatric history, abnormal interictal electroencephalographic activity, and encephalitis. Each unit increase on a simple additive scale composed of 9 dichotomous independent variables multiplied the odds ratio for PIP by 1.71 (95% confidence interval, 1.36–2.15;p< 0.0001).Interpretation: PIP in partial epilepsy is associated with relatively broadly and bilaterally distributed epileptogenic networks, genetic determinants of psychiatric disorders and seizures, and encephalitis. Ann Neurol 2008;63:602–610Keywords
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