Stroke or stroke mimic? Paranoid psychosis with misidentification delusions complicating right but not left hemisphere attacks in a case of familial hemiplegic migraine

Abstract

Background: Familial hemiplegic migraine (FHM) is a stroke mimic which is problematic to differentiate from stroke. We present a rare case of psychosis after FHM and the first with a neuropsychological assessment that sheds light both on this condition and neuropathological theories of psychosis. Method presentation: A 68 year old right-handed male with a history of hypertension, diabetes and smoking had suffered migraine since adolescence, accompanied by right (never left) hemiparesis and dysphasia which usually resolved in 24 hours; his son also suffered FHM. He had no previous psychiatric history. On this occasion after 3 days headache he developed, for the first time, left hemiparesis with power 0/5, hyper-reflexia and extensor plantar response. On day 3 after recovery of power he developed a florid psychosis. He claimed he had been abducted by Mafia, one with a mask of his wife's face. He saw faces on toilet paper, strangers on the ward, thought monitors were watching him and that ceiling sprinklers could spray acid. The symptoms persisted until responding rapidly to quetiapine started on day 10. Results: He scored highly on the Psychotic Symptoms Rating Scale (PSYRATS) and low (2SD below predicted) on Performance IQ, and the Perceptual Organisation and Processing Speed Indices of the WAIS-III while Verbal IQ, Comprehension and Working Memory Indices were normal. Delirium and infection screens, CT and MRI scans (day 7) were normal Discussion: FHM can produce temporary but profound neuropsychological changes. This patient provides a natural study contrasting right and left hemisphere dysfunction and supporting the aetiological role of the right hemisphere in psychosis, a conclusion previously drawn largely from stroke and brain injury patients. The normal MRI at 7 days is consistent with recently reported rapid resolution of cerebral oedema in a similar case. Spreading cortical depression or ion channel dysfunction rather than hypoperfusion may be the mechanism.