Passivity Phenomena in Nocturnal Frontal-Lobe Epilepsy

This is the case of a left-handed 34-year-old man with a negative family history for epilepsy and psychosis. At the age of 7, he started having seizure episodes, during which he looked frightened, screamed, bit his arm, kicked, and became rigid, while he was fully conscious and aware. His seizures occurred mainly at night, sometimes in clusters lasting for as many as 8 hours. Since no underlying cause had been demonstrated, the final diagnosis was cryptogenic NFLE. His seizures were never adequately controlled by any of a number of antiepileptic medications and vagus nerve stimulation. During his last visit to our clinic, the patient reported that during the last 2 years he experienced the existence of “a malicious person” who controlled his movements and thoughts during the seizures. Although the patient did not perceive this existence with his senses, sometimes he communicated verbally with that person in the form of his own thoughts. When seizure-free, he did not have any concern about this phenomenon. He had no explanation for this experience, and he readily accepted that it is a symptom of his illness. The psychiatric examination revealed no other psychopathological findings. An all-night video-EEG showed sharp and slow waves mostly at the left anterior frontal electrode and less at the right frontal electrode, as well as small, bilateral spikes, mainly in the left parietal electrodes. Recent MRI and positron emission tomography (PET) scans were both normal. A comprehensive neuropsychological assessment revealed deficits in perceptual organization, reasoning, sustained attention, response time variability, response inhibition, and social cognition, while his memory and executive functions were normal and his intelligence low-average.

Our patient's experiences seem to be typical instance of passivity phenomena, specifically delusions of alien control and thought-insertion. The pattern of his cognitive deficits, together with his parietal epileptic activity may be supportive of the assumption that there is involvement of extrafrontal brain areas in some cases of NFLE,³ probably parietal areas in our case. On the other hand, this fronto-parietal pattern of neuropsychological dysfunction might be related to the neural substrate underlying the passivity experiences, according to recent neuropsychological and functional neuroimaging data.⁴ Finally, left-handedness might also be related to his passivity symptoms in the light of recent evidence suggesting reduced cerebral asymmetry as an abnormality underpinning FRS.⁵