Case Report Amphetamine-Associated Ischemic Stroke: Clinical Presentation and Proposed Pathogenesis Deidre Anne De Silva, MBBS, MRCP, Meng Cheong Wong, MBBS, MRCP, FRCP, FAMS, Moi Pin Lee, RBT, Christopher Li-Hsian Chen, BMBCh, MRCP, FRCP, FAMS, and Hui Meng Chang, MBBS, MRCP, FAMS We report a young lady with acute left middle cerebral artery infarction after acute intake of amphetamine. This is the first case report of amphetamine-induced ischemic stroke with serial angiography and transcranial color-coded Doppler studies. The temporal sequence of stenosis of at least 3 weeks with subsequent complete resolution by 3 months and a “beaded” appearance on angiography support vasculitis or vasospasm as the pathogenesis of ischemic stroke in this patient. The presence of microembolic signals supports acute thrombosis at the site of vasculitis/vasospasm with distal embolism. Key Words: Stroke—amphetamine—microembolic signals—transcranial color-coded Doppler. © 2007 by National Stroke Association Case Report A 30-year-old woman presented with right-sided weakness after an alcohol binge. She reported no significant past medical history and that she did not smoke, rarely drank alcohol, and had never used illicit drugs. Examination revealed global aphasia, right neglect, and right hemiparesis. She was afebrile, her heart rate was 68 bpm, and her blood pressure was 130/60 mm Hg. Brain computed tomography (CT) scan on admission showed a left parietal hypodensity consistent with left middle cerebral artery (MCA) infarction. She was given aspirin 100 mg daily. From the Singapore General Hospital, National Neuroscience Institute, Singapore. Received December 13, 2006; revised March 31, 2007; accepted April 18, 2007. Address reprint requests to Deidre Anne De Silva, MBBS, MRCP, Department of Neurology, Block 6 Level 9, Singapore General Hospital, Singapore 169608. E-mail: gnrdsd@sgh.com.sg 1052-3057/$—see front matter © 2007 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2007.04.001 Full blood count, renal panel, liver panel, coagulation profile, autoimmune screen (erythrocyte sedimentation rate, complement 3, complement 4, antinuclear antibody, and anti– double-stranded DNA), prothrombotic screen (protein C, protein S, antithrombin III, anticardiolipin IgG, and anticardiolipin IgM), lipid profile, chest X-ray, electrocardiogram, and transthoracic echocardiograph were normal. Ultrasound of the extracranial carotid arteries revealed no significant stenosis. Two days after symptom onset, transcranial colorcoded Doppler (TCCD) studies demonstrated elevated mean velocities of the left MCA (193 cm/s), left terminal internal carotid artery (tICA) (82 cm/s), right tICA (102 cm/s), right verterbral artery (VA) (99 cm/s), and basilar artery (BA) (100 cm/s). Three microembolic signals were detected over 30 minutes in the distal left MCA. Brain magnetic resonance angiography (MRA) showed irregularity of the left MCA (M1 and lower M2) (Figure 1). Urine toxicologic analysis demonstrated amphetamine metabolites. On further questioning, the patient admitted that she had ingested Ecstasy the night before presentation. Journal of Stroke and Cerebrovascular Diseases, Vol. 16, No. 4 (July-August), 2007: pp 185-186 185 D. DE SILVA ET AL. 186 Figure 1. Angiography images. (A) Brain MRA on day 2 of admission showing irregularity of the left distal MCA (M1 and lower M2). (B) 4VA done 2 weeks after symptom onset showing focal beading and outpouching of the left MCA (M1) with pruning of the vessels that it supplies. Sequential investigations support amphetamine-induced vasculitis or vasospasm as the pathogenesis for ischemic stroke in our patient. This is evidenced by persistent left MCA stenosis for the first 3 weeks that resolved completely by 3 months, along with visualization of beading by both MRA and 4VA techniques. The presence of microembolic signals suggests acute thrombosis at the site of vasculitis/vasospasm with distal artery-to-artery embolism. Elevated mean velocities on TCCD of the other vessels that later normalized may have been due to a generalized vasculitic process or to compensatory increased collateral flow. Illicit drug use should be considered in young patients experiencing ischemic stroke. Serial TCCD and angiographic findings support vasculitis or vasospasm as the likely pathogenesis of amphetamine-induced stroke in this patient. References Four-vessel catheter angiography (4VA) performed 2 weeks after onset of symptoms revealed focal beading and outpouching of the left MCA with pruning of its distal branches (Figure 1). TCCD done 3 weeks after symptom onset revealed persistently elevated mean velocities in the left MCA (198 cm/s), left tICA (100 cm/s), and right tICA (102 cm/s). Velocities of the right VA (76 cm/s) and BA (78 cm/s) had normalized. Repeat TCCD studies done 3 months after onset were completely normal. Amphetamines and amphetamine-like compounds are common causes of stroke in the young.1-3 Various routes of pathogenesis for ischemic stroke due to amphetamines have been proposed, including vasculitis and vasospasm.4-7 1. Kaku DA, Lowenstein DH. Emergence of recreational drug abuse as a major risk factor for stroke in young adults. Ann Intern Med 1990;113:821-827. 2. Petitti DB, Sidney S, Quesenberry C, et al. Stroke and cocaine or amphetamine use. Epidemiology 1998;9:596-600. 3. Klonoff DC, Andrews BT, Obana WG. Stroke associated with cocaine use. Arch Neurol 1989;46:989-993. 4. Heye N, Hankey G. Amphetamine-associated stroke. Cerebrovasc Dis 1996;6:149-155. 5. Kessler JT, Jortner BS, Adapon BD. Cerebral vasculitis in a drug abuser. J Clin Psychiatry 1978;39:559-564. 6. Krendel DA, Ditter SM, Frankel MR, et al. Biopsy-proven cerebral vasculitis associated with cocaine abuse. Neurology 1990;40:109. 7. Wang AM, Suojaren JN, Colcucci VM, et al. Cocaine and methamphetamine-induced acute cerebral vasospasm: an angiographic study in rabbits. Am J Neuroradiol 1990;11: 1141-1146.