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Postictal psychosis is a known complication of complex partial seizure in particular temporal lobe epilepsy. It usually runs a benign and self limiting course. A postictal phenomenon with focal cerebral hypofunction (similar to Todd's palsy), rather than ongoing seizure activity, has been postulated.1 2 Surface EEG is either normal or showing non-specific slow waves.3 Hence, antipsychotic medications are prescribed instead of antiepileptic drugs. Until recently, the pathogenic mechanisms have remained unknown. In this communication, we report on two patients with postictal psychosis, during which a cerebral SPECT study showed a hyperperfusion signal over the right temporal lobe and contralateral basal ganglion. As hyperperfusion in ictal cerebral SPECT is closely linked to epileptic activities,4 our findings support a contrary explanation for postictal psychosis.
Prolonged video-EEG telemetry study was performed in patients who underwent presurgical evaluation for epilepsy surgery. Antiepileptic drugs were withdrawn to facilitate seizure recording. A diagnosis of temporal lobe epilepsy was based on analysis of the electroclinical events and, if applicable, postoperative outcome after anterior temporal lobectomy. Psychosis was diagnosed according to the fourth edition of the diagnostics and statistical manual of mental disorders (DSM-IV) criteria of brief psychotic disorders without marked stressor. HMPAO-SPECT was performed during the psychotic period, which ranged from 2–4 days after the last seizure. Interictal cerebral SPECT, brain MRI, and a Wada test were performed as part of presurgical evaluation.
Patient 1 was a 34 year old Chinese woman with complex partial seizures since the age of 18. Her seizure control was suboptimal on a combination of antiepileptic drugs. Brain MRI showed a small hippocampus on the right. Interictal EEG showed bilateral temporal sharp waves and ictal recordings confirmed a right temporal epileptogenic focus. A Wada test confirmed right hippocampal memory dysfunction. Six hours after her last secondary generalised tonic-clonic seizure after video-EEG telemetry, she began to develop emotional lability, talking nonsense, motor restlessness, and auditory hallucination. A cerebral SPECT study was performed at day 4 after her last seizure. Her psychotic features persisted although she was taking antipsychotic medication (pimozide). Cerebral SPECT showed a clear hyperperfusion signal over the right lateral temporal neocortex and contralateral basal ganglion. An interictal cerebral SPECT study was repeated at 4 weeks after postictal psychosis which showed a complete resolution of hyperperfusion signal in the right temporal lobe and basal ganglia. Anterior temporal lobectomy was performed and she became seizure free after surgery.
Patient 2 was a 44 year old man with intractable complex partial seizures since the age of 30. His seizures were intractable to multiple antiepileptic drugs. Brain MRI showed left hippocampal sclerosis. Interictal cerebral SPECT showed a relative hypoperfusion area over the left hemisphere. Interictal surface EEG was non-lateralising but ictal EEG disclosed a right hemispheric onset. On withdrawal of antiepileptic drugs, seven complex partial seizures with secondary generalised tonic clonic seizures were recorded within a period of 72 hours. His usual antiepileptic drugs were then restarted. Thirty hours after his last secondary generalised tonic-clonic seizure; he began to develop emotional lability, talking nonsense, restlessness, auditory hallucination, persecutory delusion, and delusion of superstition. Cerebral SPECT study, performed 2 days later while his psychotic features persisted, showed two relative hyperperfused areas over the right temporal neocortex and contralateral basal ganglion in addition to the original hypoperfused area over the left hemisphere. An antipsychotic agent (thioridazine) was started after the cerebral SPECT. His psychotic symptoms resolved 2 weeks later with full recovery.
Cerebral SPECT performed during the interictal period (IP) and during postictal psychosis (PP) were analysed visually and areas of hyperperfusion were identified. Quantitaive data at regions of interest (ROIs) were measured on coronal and axial slides containing basal ganglia (BG), mesial (MT), and lateral (LT) temporal lobe structures. Asymmetry index (ASI) was calculated as ((ROI focus−ROI contralateral)/ROI focus+ROI contralateral))×200%. We set an arbitrary change of ASI >100% to be significant. As there were only two patients, statistical testing was not performed.
Both patients showed postictal psychosis and had a regional increase in rCBF over the right temporal neocortex and the left basal ganglion compared with their interictal study (figure). Quantitative analysis for patient 1 showed changes of ASI during IP and PP over right MT was +75% (-6.64476 to -1.65289); over the right LT was +1167.8% (1.07527 to 12.55764); and over the left BG was +206.8% (-2.07373 to 2.21574). Quantitative analysis for patient 2 showed changes of ASI during IP and PP over right MT was −3.8% (13.14217 to 12.64158); over right LT was +178.6% (10.4696 to 18.70027); and over left BG was +155.9% (−5.85556 to 3.27522).
Postictal psychosis is a distinct clinical event associated with temporal lobe epilepsy.1 The diagnosis of postictal psychosis requires a close temporal relation between bouts of complex partial seizures and the onset of psychosis. The psychosis usually develops after a cluster of complex partial seizures precipitated by abrupt withdrawal of antiepileptic drugs.1 The cluster occurs in patients with poor drug compliance or during video EEG telemetry studies when antiepileptic drugs are withdrawn purposefully. The clinical course of postictal psychosis is usually benign and predictable.1 5 In our patients, the duration of psychotic disturbances lasted from 10 to 14 days, which is in keeping with the good prognosis. Antipsychotic drugs, such as haloperidol and fluphenazin are usually prescribed.1
The underlying mechanism of postictal psychosis is unknown. Postictal cerebral hypofunction has been postulated as an analogue to Todd's paralysis after seizure.1 2 However, the presence of increased rCBF during postictal psychosis, may suggest an alternative explanation as ictal SPECT has been shown to be highly sensitive and specific in demonstrating seizure foci.4
To conclude, our results are contradictory to the hypofunction theory of Todd's paralysis in postictal psychosis. We think that these hyperperfusion areas are responsible for the postictal psychosis. Further serial studies with cerebral SPECT or PET may enhance our understanding on the mechanism of postictal psychosis.
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