The Chronic Hallucinatory‐Paranoid State of Symptomatic Localization‐Related Epilepsy Studied by CCTV/EEG Monitoring
Authors: Kudo Tatsuya , Nomori Yasuyo , Kageyama Michiyo , And Kouichi Hamada. , Yagi Kazuichi 
Published: August 2009

Purpose: Because an epileptogenic zone is considered an important factor in the genesis of the hallucinatory–paranoid state of symptomatic localization‐related epilepsy, the epileptogenic zones of patients with chronic hallucinatory‐paranoid states were studied. Methods: The 10 patients (P1‐P10) studied were right‐handed and had both symptomatic localization‐related epilepsy and chronic hallucinatory‐paranoid states, without a family history of either psychosis or epilepsy. Their average age was 30.3 years at examination, 11.5 years at the onset of epilepsy, and 20.2 years at the onset of psychosis. The duration of the follow‐up was 7.6 years the localizations of epileptogenic zones were investigated by seizure manifestations, and the findings from interictal and ictal EEG, computed tomography (CT), magnetic resonance imaging (MRI), single‐proton‐emission CT (SPECT), and electromyogram (EMG). Results: The patients had auditory hallucinations of voices speaking directly to them or in conversation with other voices, and also had delusions of reference and persecution and delusional perception and mood (“Wahnstimmung”). Four patients had a prefrontal syndrome, which appeared and deteroirated before the onset of psychosis, and showed attention deficits, hyperreactivity, puerilism, disinhibition of impulsive behavior, irritability, and paranoid tendencies (P1, P2, P3, and P4) in addition to euphoria (P1, P2, and P4) and moria (P1 and P2). PS had memory disturbances, anomia, and irritability, and both P6 and P10 had a state indistinguishable from the residual phase of schizophrenia, showing autism, bizarre behaviors, blunted affect, poverty of content of thought, and lack of volition, which progressed after the onset of psychosis. P1, P2, P3, P4, and P8 had seizures of frontal origin such as tonic posturing and complex gestural automatism. P5, P6, P7, P9, and P10 showed seizures of the temporal lobe origin such as au‐tonomic signs, impairment of consciousness, and motionless staring. Interictal epileptogenic discharges were observed bilaterally in the frontal areas of P1, P2, P3, and P4, in the right or left temporal areas or both of P5, P6, P7, and P8, in the right of left frontotemporal areas of P9, and bilaterally in the temporofrontal or occipital areas of P10. The onset of ictal discharges seemed to be at the left frontal area of PI and P2, the central area of P3, the right temporal area of P6. the right or left frontotemporal areas of P9, and the right hemisphere or the left occipital area of P10. Organic lesions were observed in the left lateral (P1), left medial (P2), and medial (P4) parts of prefrontal lobe, in the right (P6 and P9) and left (P7) temporal lobes, and in multiple lobes (P10) consisting of the left temporal and the occipital lobes bilaterally. The epileptogenic zones were suggested to he in the prefrontal lobe of P1, P2, P3, and P4, the temporal lobe of P5, P6, and P7, either the temporal or the frontal lobe or the area extending over the temporal and frontal lobes of P8 and P9, and the temporal lobe or the area extending temporal to the occipital area of P10. Conclusions: The results suggest that the frontal and temporal lobes participate in the genesis of the seizures of patients with chronic hallucinatory–paranoid states. The hallucinatory–paranoid state is shared in common by patients with epileptogenic zones of both the temporal and frontal lobes, whereas changes in behavior and personality differ depending on whether the site of epileptogenic zones is in the temporal or frontal lobes.