Abstracts

Hallucinations are commonly believed to reflect temporal lobe dysfunction. In contrast, disturbances of the frontal lobe are associated with altered motor activity, behavior, planning and organization. We report a boy who presented in an acute psychotic state characterized by formed vivid visual and auditory hallucinations due to frontal lobe partial status epilepticus. Case report. An 8 year old right handed boy presented with new onset hallucinations. He reported being scared by visions of people and animated characters. He initially saw familiar faces talking to him which later commanded him to kill his mother and himself. His sleeping was disturbed and he became impulsive and hyperactive. There was no history of prior psychiatric illness and he was on no medications. He had one generalized seizure at age nine months. There were no family members with psychiatric illness.
His physical and elementary neurological examinations were unremarkable. Neurology consultation was requested because of vague complaints of headaches. EEG revealed frequent electrographic discharges from the right frontal lobe. Video-EEG monitoring demonstrated stereotyped seizures characterized by motor restlessness and gestural automatisms. Electrographic seizures were characterized by rhythmical spike-wave activity maximal at the FP2 and F8 electrodes. MR imaging revealed loss of gray-white matter arborization in the right orbital frontal and inferior frontal gyrus consistent with cortical dysplasia. Ictal SPECT revealed hyperperfusion corresponding to the structural lesion. Resection of the lesion and its surround tailored to ECoG data led to secession of seizures; his impulsive behavior normalized and his psychotic state ameliorated. Histologic tissue examination revealed Taylor type cortical dysplasia without balloon cells. This case demonstrates conclusively that seizures consisting exclusively of formed visual and auditory hallucinations can begin in the frontal lobes. We hypothesize that electrographic discharges originating from epileptogenic orbitofrontal regions propagated to temporo-limbic structures via the uncinate fasiculus to trigger complex hallucinations. Alternatively, propagation pathways may have involved aberrant neural networks known to be associated with cortical malformation.