Illicit Sympathomimetic Drug Abuse in Demyelinating Diseases

Rose Jeppesen,Michael Stormly Hansen,Christoffer Frederik Bang Jensen,Shanu Faerch Roemer

doi:10.18314/abne.v1i1.1049

Abstract

Multiple Sclerosis (MS) is an inflammatory demyelinating disease characterized by progressive motor deficits. Behavioral problems have previously been linked to the use of illicit drugs such as cocaine and amphetamine. We present 4 patients with frequent abuse of illicit sympathomimetics who presented with symptomatic White Matter Lesions (WML). Three patients had positive Oligoclonal Bands (OCB), one patient without OCB revealed marked pleocytosis. In this case-series we present clinical and radiological features and discuss possible mechanisms underlying substance abuse in patients with demyelinating lesions. Previous case reports in illicit sympathomimetic substance abusers highlight leukoencephalopathy rather than focally demyelinating WML. We hypothesize a two hit model with drug abuse exacerbating an unknown underlying diagnosis of MS.

Highlights

Cognitive dysfunction is a frequent feature and may correlate to cortical lesions evident at disease onset and progression [2]. Focus on these debilitating features of the disease has increased in the later years, while research in to possible behavioral problems is still scarce
Patients diagnosed with pediatric Multiple Sclerosis (MS) have demonstrated co-morbid psychiatric diagnosis with anxiety disorders, Attention Deficit Hyperactive Disorder (ADHD) and mood disorders associated with cognitive impairment [3]
In adult patients diagnosed with MS, more than 14% expressed suicidal ideation such as thoughts of selfharm or being better off dead [4]

Summary

Introduction

A VEP performed 14 months after first presentation, revealed bilateral prolonged latencies supportive of optic nerve abnormalities.In retrospect, the patient admitted to abuse of cocaine and amphetamine including time at first presentation. Spinal tap revealed mild pleocytosis 7 and positive OCB, protein and glucose were normal. Case 3: MRI pt3, at presentation (T2) Case 4 monophasic course, a radiological diagnosis of ADEM was proposed despite lack of contrast-enhancement, and the patient was treated with high-dose IV corticosteroids.

Results

Conclusion