A 49 year old female with a history of Depression and Multiple sclerosis (MS) presented with acute psychosis in the setting of recent polysubstance abuse. The patient endorsed both visual and auditory hallucinations; stating she saw bugs and could hear her dead father calling her. In addition, the patient was convinced that her ex-husband was attempting to steal her adult daughter. The patient’s only other known psychotic episode occurred 10 years prior and was attributed to steroids administered for an MS flare.
On initial evaluation in the ED the patient was found to have a toxicology screen positive for Cocaine, Cannabinoids, Benzodiazepines. A head CT scan revealed a new hypodense lesion in the left frontal lobe. The psychosis was originally attributed to recent cocaine use, however the patient’s delusions persisted. An MRI revealed 5 ring lesions in the left cerebral hemisphere that were consistent with acute plaques of demyelination (figure 1). The patient was started on IVIG for 5 days. Her hallucinations and delusions dissipated shortly after IVIG therapy, however the patient did not return to her cognitive baseline during hospitalization. The patient was discharged to a cognitive rehabilitation program with plans for outpatient neurology follow-up.
Discussion:
Multiple sclerosis is a chronic inflammatory disease of the central nervous system, causing both motor and sensory impairment by progressive demyelinization. The neurological manifestations of MS are well known, but involvement of psychiatric presentations are relatively limited.
Our patient had one episode of steroid induced psychosis upon initial diagnosis 10 years prior to admission, however, her presentation could be confounded by her co-ingestants including cocaine, alcohol and benzodiazepines. Brief psychotic episodes – mainly comprising religious or persecutory delusions and hallucinations – have been associated with MS. Psychosis in MS distinctly differs from schizophrenia as it has a later age at onset, quicker resolution, fewer relapses, better response to treatment and a better prognosis. Our patient’s frontotemporal involvement as revealed on MRI could explain her cognitive dysfunction.
Our patient had gone over 10 years without an MS flare. One month prior to admission, she was evaluated by her neurologist who performed an MRI which revealed no active plaques. We suspected that the patient was non-compliant with her Fingolimid, which led to a severe MS exacerbation with cognitive and psychotic features.
Conclusions: As in this case, psychosis caused by active MS exacerbation should be considered when certain territories are involved and after alternate etiologies have been entertained.