Vertebral Artery Dissection Related to Amphetamine Abuse – A Case Report

Abstract

We report the case of a 37-year-old male patient with chronic amphetamine abuse who presented with vertebral artery dissection. Prior to presentation, he had increased the consumption of amphetamine from 5 times a year to once every week and had used amphetamine on the day of presentation. He attended with neck pain, vertigo and coordinating difficulties of his left arm. Computed tomography angiogram of the neck vessels showed a left vertebral stenosis and cerebral magnetic resonance imaging showed a left vertebral pseudolumen and a medullary stroke. Cervical artery dissection is a major cause of stroke in the young. To the authors’ knowledge, this is the second reported case of vertebral artery dissection in a patient with amphetamine abuse. Amphetamine might contribute to an increased risk of vertebral artery dissection through its vasculopathic properties although more data are needed to establish a causal relationship.

Introduction

Cervical artery dissection (CAD) is a major cause of stroke in the young.¹ Amphetamine is related to an increased risk of stroke through its presumed vasculopathic properties.² Evidence suggesting a causal relationship between amphetamine abuse and vertebral artery dissection (VAD) is limited. We present the case of a patient who developed VAD in close temporal relation to amphetamine abuse.

Case Report

A 37-year-old male patient previously known with abuse of amphetamine and cannabis presented to the emergency department with acute left-sided neck pain and vertigo with no exacerbating factors. He also complained of a mild cough but had no history of neck trauma. A month prior to his admission, he had increased the consumption of amphetamine from 5 times a year to once a week and admitted to have taken amphetamine on the day of presentation. He had no neurological deficits and was discharged home. No toxicology screen was performed. The following day, he re-attended with worsening vertigo, nausea and vomiting, left facial numbness and coordinating difficulties of his left arm. General examination was unremarkable. Neurological examination showed a mild left arm ataxia but was otherwise normal. Routine blood tests were unremarkable. Computed tomography angiogram of the neck vessels showed a stenosis at the left V3 segment. Cerebral magnetic resonance imaging (MRI) revealed a left vertebral pseudolumen and a diffusion restriction in the left posterolateral medulla oblongata (Figure 1). Treatment with dual platelet therapy was instituted. A repeat computed tomography (CT) angiogram after 3 months showed resolution of the left vertebral intramural haematoma.

Figure 1.

(Left): CT angiogram with 3-dimensional reconstruction shows a left vertebral stenosis (arrow). (Middle): Axial T2-weighted MRI shows left vertebral hyperintense pseudolumen (arrow). (Right): Cerebral DWI shows a diffusion restriction in the left posterolateral medulla. CT indicates computed tomography; MRI, magnetic resonance imaging; DWI, diffusion-weighted imaging.

Discussion

Several risk factors for CAD has been hypothesised including congenital (connective tissue disorders, hyperhomocysteinemia), neck manipulation (blunt neck trauma, chiropractor manipulation, coughing, skiing, child birth) and other medical disorders (infection, migraine).³ In this case, the patient had no connective tissue disorder or history of neck manipulation, but he did complain of a cough. Interestingly, he had increased the consumption of amphetamine significantly and had used amphetamine on the day of presentation. Although coughing is a possible cause for VAD in this case, amphetamine abuse could be a contributing factor. Dissection of the aorta, coronary arteries and the internal carotid artery has been reported in relation to amphetamine abuse.^4-6 One case report described VAD in a patient with amphetamine abuse.⁷ The vasculopathic properties of amphetamine remains to be fully elucidated. Several mechanisms have been described including vasculitis and vasospasm.^8,9 The sparsity of cases relating VAD to amphetamine could be partly due to reporting bias. First, doctors who are unaware of a potential relationship between VAD and amphetamine abuse are less prone to ask about illicit drug use. Second, patients demonstrate high false negative rates in self-reported substance abuse when abuse is verified by biochemical testing.¹⁰

Conclusions

This is the second reported case of VAD in a patient with amphetamine abuse. Although amphetamine might contribute to an increased risk of VAD, more data are needed to establish a causal relationship.