Abstract 087: Cocaine‐Induced Acute Spinal Cord Ischemia Syndrome

Abstract

Introduction Acute spinal cord ischemia syndrome (ASCIS) is a rare disease that is thought to comprise roughly only 1.2% of all strokes [1, 2]. These strokes primarily occur in the anterior spinal cord artery (ASA) and/or the posterior spinal cord artery (PCA) territory and can have widely variable clinical presentation. The use of recreational cocaine in young adults is well known to be responsible for acute ischemic and hemorrhagic strokes in individuals who lack other vascular risk factors. What is significantly rarer with few reported cases, however, is cocaine‐related ASCIS as the etiology of non‐traumatic acute spinal cord myelopathy [3‐7]. Methods N/A Results A 40‐year‐old female with a history of type I Diabetes mellitus, bipolar disorder, and polysubstance abuse presented with acute‐onset bilateral lower limb weakness, sensory loss, neck pain, and bladder incontinence. On admission, she reported using intravenous crack cocaine in the evening before admission and experiencing a fall in the bathroom a few hours after. She was unable to move her lower limbs following this fall. On examination, there was flaccid weakness in both lower extremities with decreased pinprick sensation below the T4 level and absent sensation below the thighs on both sides. She had no trauma preceding her symptoms and denied any recent vaccinations or travel history. An urgent CT (computed tomography) scan of the cervical, thoracic, and lumbar spine ruled out any obvious traumatic injury. Her urine drug screen was positive for cocaine, opiate, cannabinoid, and benzodiazepine. MRI (Magnetic Resonance Imaging) of the brain without contrast was unremarkable. MRI of the spine with contrast demonstrated two areas of T2 hyperintensities from C5‐C6 and T4 to the conus with cord expansion. The lesion in the thoracic spinal cord showed contrast enhancement and spared the dorsal column. Lumbar puncture was traumatic and showed elevated protein (>300 mg/dl) as well as elevated glucose (186 mg/dl). CSF studies, including meningitis/encephalitis panel, gram stain and culture, flow cytometry, cytology, and oligoclonal bands were negative. Serum autoimmune myelopathy panel, serum Aquaporin‐4 antibodies and MOG (Myelin Oligodendrocyte Glycoprotein) antibodies were negative. The other etiologies of non‐traumatic myelopathy, including HIV, Treponema pallidum, and HTLV‐I/II antibodies, were negative. A diagnostic spinal angiogram was completed with no evidence of arteriovenous fistula or aortic dissection. She completed five days of plasma exchange without any improvement and was transferred to an acute rehabilitation facility. At four months follow‐up, she continues to be flaccid in her lower limbs and requires a urinary catheter leading to frequent urinary tract infections. Conclusion While cocaine‐related cerebrovascular events are well documented, very few cases of cocaine‐related ASCIS have been described. The mechanism is thought to be multifactorial due vasospasm, cerebral vasculitis, vascular thrombosis, cardioembolism from cocaine‐induced myocardial infarction or cardiomyopathy, and hypertensive surges [9]. Due to the scarcity of these events, the patient outcomes are unclear. Other studies on outcomes of spinal cord ischemia have shown that ASIA Impairment Scale (AIS) score, lesion level, and patient age were the strongest predictors of neurologic and functional outcomes, whereas etiology of the ischemia had no effect on outcomes [10].