A 29-year-old female presented with acute onset bilateral flaccid paraplegia and areflexia as well as T10 sensory level. She denied any prodromal symptoms, recent illness, injuries, or prior episodes. Her past medical history was significant for IV heroin use over several years with no recent periods of abstinence. Her last use of heroin was the evening prior to onset of paralysis. Imaging was notable for a longitudinal (T2-T10) T2 hyperintense signal abnormality with enhancement affecting the central cord from T2-T5 and T8-T10, but more extensive holocord involvement from T5-T7. CSF studies demonstrated 25 nucleated cells (85% neutrophils), 10 RBCs, normal glucose and protein of 55 mg/dL. The patient had presumed inflammatory myelitis.  Extensive autoimmune and infectious workup were negative in both CSF and serum. Etiology of her presentation was suspected to be secondary to her heroin use. She was treated with five days of IV methylprednisolone with minimal improvement of her strength, sensation, and areflexia one month after presentation. Interval imaging of her cord demonstrated improvement with cord signal abnormality limited to T6-T7.

This case examines a 29-year-old female with heroin-associated myelitis. Inflammatory cells in the CSF have only been documented in one case report previously. This case also occurred without a period of abstinence from heroin. Based on the current literature, both of these features are atypical for heroin myelopathy.