Tumefactive multiple sclerosis (TMS) is a rare variant of multiple sclerosis (MS), mimicking features of infectious, inflammatory, neoplastic, and vascular neurological phenomena1-3. TMS can present a..
Tumefactive multiple sclerosis (TMS) is a rare variant of multiple sclerosis (MS), mimicking features of infectious, inflammatory, neoplastic, and vascular neurological phenomena1-3. TMS can present asymptomatically, as well as with higher cortical, motor, sensory, cerebellar, and brainstem symptoms4-6. However, there have not been reported TMS cases presenting with psychiatric features. We describe the case of a 42-year-old woman with a chart reported history of schizoaffective disorder who was first admitted for worsening aggression in the context of divalproex and haloperidol non-adherence. She was not psychotic on initial encounter; hallucinations and paranoia last occurred three years prior to admission. She seemed to have improved on divalproex alone and was discharged. The patient was later re-admitted, this time appearing acutely psychotic and aggressive. She demonstrated predominately positive psychotic symptoms, without evident medical abnormalities or concomitant substance intoxication. There was no improvement in symptoms upon re-initiation of divalproex and trials of olanzapine and paliperidone. Due to concern for catatonia, aripiprazole was initiated. Interval development of focal deficits prompted medical hospital admission. Imaging revealed an enhancing, diffusion restricted mass at the left basal ganglia and frontal lobe, which was biopsied. Pathology was consistent with TMS. Primary malignancy, seizures, and infections were ruled out, and following a short course of methylprednisolone, vasogenic edema convalesced. Psychotic behavior progressively improved after administration of high-dose prednisone and re-initiation of divaloproex, and aripiprazole. To our knowledge, this is the first case study to demonstrate psychotic features and aggression as a possible manifestation of TMS. As psychiatric illnesses may occur in the prodromal period or at onset of MS7-8, this patient’s presentation may have been consistent with flares of a unique demyelinating process.