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Table of Contents    
LETTER TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 3  |  Page : 826-827

Methamphetamine-induced internal carotid artery vasospasm: A rapidly fatal stroke


1 Department of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
2 Department of Radiology, Ampang Hospital, Selangor, Malaysia

Date of Web Publication15-May-2018

Correspondence Address:
Dr. Chen Fei Ng
Department of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur
Malaysia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.232337

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How to cite this article:
Ng CF, Chong CY. Methamphetamine-induced internal carotid artery vasospasm: A rapidly fatal stroke. Neurol India 2018;66:826-7

How to cite this URL:
Ng CF, Chong CY. Methamphetamine-induced internal carotid artery vasospasm: A rapidly fatal stroke. Neurol India [serial online] 2018 [cited 2018 Nov 18];66:826-7. Available from: http://www.neurologyindia.com/text.asp?2018/66/3/826/232337




Sir,

Amphetamine has been known to cause vascular events including stroke. Methamphetamine, the most common illicitly abused type of amphetamine, is a potent sympathomimetic drug that can result in stroke with heterogeneous clinical presentations. Different pathophysiological mechanisms such as accelerated atherosclerosis, cerebral vasculitis, and cerebral vasospasm have been suggested; however, the mechanism of stroke remains unclear in a significant fraction of cases.[1]

A 33-year old young man presented with sudden onset of reduced consciousness and right-sided body weakness for 5 h. There was no fever or witnessed seizure. On further questioning, his friend revealed that he was inhaling methamphetamine just before the onset of the symptoms. This was his first time that he had used methamphetamine and there was no previous history of illicit drug abuse. There was no significant medical history of note. He did not smoke or consume alcohol. On examination, his Glasgow Coma Scale was E3V1M4 (8/15). The blood pressure was 120/70 mmHg, heart rate was 80 beats/minute, and he was afebrile. There were global aphasia, right hemianopia, right-sided neglect, and right-sided hemiplegia. Deep tendon reflexes of the right sided limbs were brisk, and there was presence of right ankle clonus. The initial National Institutes of Health Stroke Scale (NIHSS) score was 30.

Blood investigations revealed a hemoglobin level of 11.9 g/dL, a total white blood cell count of 10.6 × 109/L, and a platelet count of 450 × 109/L. Renal and liver panels, coagulation profile, and infective screening for hepatitis B, hepatitis C, and retrovirus were normal. Urine toxicology screen was positive for methamphetamine but negative for cocaine and opiates. Electrocardiography revealed a sinus rhythm, with a heart rate of 80 beats/minute. Non-contrast computed tomography (CT) of the brain showed hypodensities in the left anterior circulation involving the whole anterior and middle cerebral artery territories [Figure 1]a. He was not thrombolysed and was started on oral aspirin 100 mg daily.
Figure 1: Axial view of non-contrast CT scan of the brain. (a) Mild hypodensities were seen in the left anterior and middle cerebral artery territories. (b) A repeat imaging at 24 h showed the established infarction associated with the presence of cerebral edema, midline shift, and obstructive hydrocephalus

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Reassessment on the next day showed non-reactive pupils and absence of brain stem reflexes. A repeat CT scan of the brain done at 24 h of admission showed an established infarction with cerebral edema and obstructive hydrocephalus [Figure 1]b. Unfortunately, the patient expired shortly after this imaging.

Amphetamine is the parent compound of its own structural class, which includes a wide range of psychoactive derivatives, such as 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) and methamphetamine. Methamphetamine can be abused in oral, inhaled, smoked, or intravenous form, and it is often referred to as “ice,” “speed,” “crystal,” or “crank.” It causes an increase in the synapse of monoamine neurotransmitters including dopamine, serotonin, and noradrenaline resulting in a cascade of mechanisms. The effect of methamphetamine use is largely mediated through the dopaminergic system. Cerebrovascular complications, especially the occurrence of stroke, have been the leading causes of morbidity and mortality. An earlier study has shown that amphetamine abuse was associated with hemorrhagic stroke but not with ischemic stroke.[2] In another retrospective study, methamphetamine use was associated with ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. The majority of strokes were located in the anterior circulation.[3]

The pathophysiological mechanisms of ischemic stroke are multifactorial. Chronic exposure to methamphetamine may lead to vessel injury through repeated episodes of hypertension, which subsequently leads to microinfarction in the vasa vasorum of medium-sized vessels such as the carotid artery, resulting in accelerated atherosclerosis. However, smaller intracranial vessels such as anterior cerebral artery, middle cerebral artery, and basilar artery, which have a less developed vasa vasorum, would not undergo the same damage, but may be injured by other mechanisms.[3]

Cerebral vasculitis is another important pathogenesis found in hemorrhagic or ischemic stroke in chronic methamphetamine abusers. Radiological and histological findings of vasculitis suggest that methamphetamine has a direct toxic or immunological effect on cerebral vessels. Histologically, the cerebral vessels of patients with methamphetamine addiction have shown necrotic lesions in small and large cerebral arteries, with moderate to extensive necrosis of the tunica media with minimal inflammatory cell infiltration.[1] The evidence of vasculitic changes associated with methamphetamine usage has suggested that the use of immunonsuppressants might be beneficial. However, there is no large study to support its use.

The increased level of catecholamine in patients using methamphetamine can lead to coronary vasoconstriction and myocardial necrosis. It is thought that the vasoconstrictive effects of methamphetamine would also result in cerebral vasospasm, leading to ischemic stroke.[4],[5] In chronic methamphetamine abusers, cerebral vasospasm as a cause of acute ischemic stroke may be in conjunction with other mechanisms such as accelerated atherosclerosis and cerebral vasculitis.

There are variable neurovascular pathologies responsible for the ischemic stroke associated with the use of methamphetamine. Therefore, the definitive treatment of acute ischemic stroke secondary to methamphetamine abuse differs in comparison to that offered when stroke occurs due to thromboembolism. Intravenous thrombolysis and intra-arterial treatment will potentially result in lethal intracranial hemorrhage if cerebral vasospasm or cerebral vasculitis is the cause of stroke. The patient in this case was a young man with no other risk factors for ischemic stroke. In view of his first exposure to methamphetamine, it is postulated that acute severe internal carotid artery vasospasm would most likely be the cause of stroke. The patient succumbed to the massive stroke that he had, within 30 h from the onset of the symptoms. The rapid and fatal progression of stroke reported here is uncommon in methamphetamine abusers.

Ischemic stroke is associated with methamphetamine abuse and there are a few possible pathogenetic mechanisms. As stroke under these circumstances is not always associated with thromboembolism, urine toxicology should be done in doubtful cases to detect methamphetamine abuse, especially in young adults, before intravenous thrombolysis is planned. An earlier neurosurgical referral for a decompressive craniectomy in the presence of stroke should be considered as a massive stroke can be rapidly fatal.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Fonseca AC, Ferro JM. Drug abuse and stroke. Curr Neurol Neurosci Rep 2013;13:325.  Back to cited text no. 1
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2.
Westover AN, McBride S, Haley RW. Stroke in young adults who abuse amphetamines or cocaine: A population-based study of hospitalized patients. Arch Gen Psychiatry 2007;64:495-502.  Back to cited text no. 2
[PUBMED]    
3.
Ho EL, Josephson SA, Lee HS, Smith WS. Cerebrovascular complications of methamphetamine abuse. Neurocrit Care 2009;10:295-305.  Back to cited text no. 3
[PUBMED]    
4.
Neiman J, Haapaniemi HM, Hillbom M. Neurological complications of drug abuse: Pathophysiological mechanisms. Eur Neurol J 2000;7:595-606.  Back to cited text no. 4
    
5.
Wang AM, Suojanen JN, Colucci VM, Rumbaugh CL, Hollenberg NK. Cocaine-and methamphetamine-induced acute cerebral vasospasm: An angiographic study in rabbits. Am J Neuroradiol 1990;11:1141-6.  Back to cited text no. 5
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