We report the case of a young man with an acute infarction of the left putamen and caudate nucleus, whose symptoms appeared six hours after intranasal use of approximately 0.5 g of cocaine hydrochloride. It seems probable that in this patient cocaine consumption played a role in the development of stroke

Andresen, Jennie

Estrada, Carlos A.

Hidalgo, Walter N.

Meza, Iliana

Montalvo, Justo A.

English

Henry Ford Health System Scholarly Commons

Henry Ford Hospital Medical Journal Volume 37 Number 1 Article 15 3-1989 Cerebral Infarction Associated with Cocaine Use Iliana Meza Carlos A. Estrada Justo A. Montalvo Walter N. Hidalgo Jennie Andresen Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal  Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Meza, Iliana; Estrada, Carlos A.; Montalvo, Justo A.; Hidalgo, Walter N.; and Andresen, Jennie (1989) "Cerebral Infarction Associated with Cocaine Use," Henry Ford Hospital Medical Journal : Vol. 37 : No. 1 , 50-51. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol37/iss1/15 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Cerebral Infarction Associated with Cocaine Use Iliana Meza, MD,* Carlos A. Estrada, MD,t Justo A. Montalvo, MD,* Walter N. Hidalgo, MD,* and Jennie Andresen, MD* We report the case of a young man with an acute infarction of the left putamen and caudate nucleus, whose symptoms appeared six hours after intranasal use of approximately 0.5 g of cocaine hydrochloride. It seems probable that in this patient cocaine consumption played a role in the development of stroke. (HenryFordHospMedJ 1989;37:50-1) The clinical picture of cocaine intoxication is well known (1). However, medical complications from its abuse have only recentiy been reported (1,2). These include acute myocardial in-farction, cardiac arrhythmias, and central nervous system in-volvement (1-8). We report the case of a young adult man with cerebral infarction following cocaine snorting. Case Report A 31-year-old male normotensive chronic cocaine user was admitted with a history of dysarthria, tonic-clonic motor seizures of the right up-per limb, and right-sided hemiparesis appearing six hours after intra-nasal use of approximately 0.5 g of cocaine hydrochloride and heavy alcohol consumption (witnessed by his wife). He did not complain of headache. The patient's history included a similar hemiparesis episode six months earlier which resolved spontaneously in 20 minutes. This deficit, which also followed cocaine snorting, was without seizures. There was no history of intravenous drug abuse. He suffers from chronic asthma but was taking no medications. His father died from acute myocardial infarction at age 55, and a coronary bypass graft was performed on his brother at age 46. There was no family history of cere-brovascular disease or homocystinuria. On physical examination his blood pressure was 130/90 mm Hg (supine), heart rate was 78 beats/min, and temperature 37°C (98.6°F). General physical examination was normal. He was alert and oriented but had slurred speech. Right-sided flaccid hemiparesis was present, with brachial predominance. He also had paresis of the right 6th and 7th (central type) cranial nerves, and hyperreflexia was present on the right side. The funduscopic examination was normal. Laboratory studies revealed a hematocrit of 0.50, WBC count of 9.9 x lO'/L, erythrocyte sedimentation rate of 2 mm/h, blood glucose level of 5.5 mmol/L (100 mg/dL), and serum creatinine of 88.4 |xmol/L (I mg/dL). Semm cholesterol was 5.82 mmol/L (225 mg/dL), and semm triglycerides were 0.34 mmol/L (30 mg/dL). Chest x-ray and elec-trocardiogram were normal. Computed tomography (CT) of the head (Figure) showed an acute infarct of the left putamen and head of the caudate nucleus surrounded by edema. The patient was treated with phenytoin sodium, steroids, and aspirin. His neurologic status im-proved substantially except for right upper limb motor activity, and he was discharged five days later No urine dmg screen for cocaine or other drugs was done. The patient refused further workup such as lumbar puncture or cerebral angiography. Comments Neuropsychiatric effects of cocaine use include euphoria, hy-porexia, increased creativity and physical performance, para-noid ideation, tremors, and seizures (1). However, in recent years, acute cerebrovascular events have been reported to occur in association with cocaine use (2-8). We have identified in the English literature seven published cases of cerebral infarction associated with cocaine use. Chas-noff et al (4) described a newbom infant whose mother had used cocaine intranasally for three days before delivery; on the day of delivery she used approximately 1 g of cocaine. This infant had an acute infarction in the distribution of the left middle cerebral artery. A second patient had snorted cocaine one day prior to developing a cerebral infarct (5). A third patient smoked two vials of "crack" four hours before the stroke (6). A fourth pa-tient injected himself intramuscularly with cocaine one to two hours before the cerebrovascular event (7); in this patient, nei-ther CT nor angiography was performed. Three recently re-ported patients had cerebral infarction also documented by CT and angiography; two had used cocaine intranasally (3,8), and one had smoked "crack" (2). Possible mechanisms of cerebral infarction in our patient in-clude vasospasm and intracerebral thrombosis (2), as proposed Submitted for publication: August 11. 1988. Accepted for publication: November 30. 1988. ^Department of Neurology. Guillermo Almenara Hospital and Federico Villarreal Uni-versity. Lima. Pern. tDepartment of Intemal Medicine. Henry Ford Hospital. ^Department of Pediatrics. Children's Hospital of Michigan. Address correspondence to Dr Esn-ada, Department of Intemal Medicine, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, Ml 48202. 50 Henry Ford Hosp Med J—Vol 37, No 1, 1989 Stroke and Cocaine Abuse—Meza et a! for young patients who develop an acute myocardial infarction with no identifiable cardiovascular disease (1). This patient may also have an increased risk for vascular disease in view of his family history. Ethanol consumption may also be associated with an increased risk of cerebral infarction in young adults (9). Other possible causes of stroke in this patient such as a minor aneurysmal leak or homocystinuria are unlikely. Strokes due to mpture of the minor aneurysms located in the patient's area of neurologic defect are usually associated with hypertension (10). Moreover, cerebral infarction associated with aneurysms results from posthemorrhage vasospasm of the arteries, and symptoms usually appear four to 14 days after the hemorrhage (11). The patient had neither hemorrhage nor history of hypertension. The clinical picture of homocystinuria includes mental retardation, osteoporosis, failure to thrive, severe myopia, glaucoma, malar flush, marfanoid appearance, and recurrent thrombotic events (12,13). Our patient had none of these characteristics. The clinical findings deserve further comment, given the lo-cation of the lesion on the CT scan. Paresis of the 6th cranial nerve is sometimes a false localizing sign due to a transient in-crease of intracranial pressure (14), but its etiology may remain unknown in up to 30% of the cases (15). Also, the presentation with seizures is a known, but rare, clinical finding in subcortical lesions. The mechanism of such events is unclear (16,17). Stroke associated with cocaine use is a clinical entity that is being reported with increased frequency. It is uncertain if cocaine causes or precipitates stroke. The history of a transient ischemic attack and subsequent documented infarct following nasal cocaine intake in this patient supports a causal relationship between cocaine use and cerebral infarction. Figure—Contrast CT scan showing decreased density in the head ofthe caudate nucleus and putamen of the left side. Frontal horn of left lateral ventricle is partially occluded (L = left, R = right). References 1. Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-500. 2. Levine SR, Washington JM, Jefferson MF, et al. "Crack" cocaine-associ-ated stroke. Neurology 1987;37:1849-53. 3. Lowenstein DH, Massa SM, Rowbotham MC, Collins SD, McKinney HE, Simon RP. Acute neurologic and psychiatric complications associated with cocaine abuse. Am J Med 1987;83:841-6. 4. Chasnoff IJ, Bussey ME, Savich R, Stack CM. Perinatal cerebral infarc-tion and maternal cocaine use. J Pediatr 1986;108:456-9. 5. Schwartz EA, Cohen JA. Subarachnoid hemorrhage precipitated by cocaine snorting (Letter). Arch Neurol 1984;4I:705. 6. Golbe LI , Merkin MD. Cerebral infarction in a user of free-base cocaine ("crack"). Neurology 1986;36:1602-4. 7. Brust JCM, Richter RW. Stroke associated with cocaine abuse—? NY StateJ Med 1977;77:1473-5. 8. Kaye BR, Fainstat M. Cerebral vasculitis associated with cocaine abuse. JAMA 1987;258:2104-6. 9. Hillbom M, Kaste M. Ethanol intoxication: A risk factor for ischemic brain infarction in adolescents and young adults. Stroke I981;12;422-5. 10. Adams J, ed. Greenfield's neuropathology. 4th ed. New York: John Wiley and Sons, 1984:172-6. 11. Braunwald E, et al, eds. Harrison's principles of intemal medicine. Uth ed. New York: McGraw Hill Book Co, 1987:1956. 12. Sianbury JB. The metabolic basis of inherited diseases. 5th ed. New York: McGraw Hill Book Co, 1983:492. 13. Behrman RE, ed. Nelson textbook of pediatrics. Bth ed. Philadelphia: WB Saunders Co, 1987:285-6. 14. Walton J. Brain's diseases of the nervous system. 9th ed. Oxford: Oxford United Press, 1985:107. 15. Rowland LP. Merritt's textbook of neurology. 7th ed. Philadelphia: Lea Febiger, 1984:318-9. 16. Rowland LP. Merritt's textbook of neurology. 7th ed. Philadelphia: Lea Febiger, 1984:221. 17. Adams R. Principles of neurology. 3rd ed. New York: McGraw Hill, Inc, 1985:615. Henry Ford Hosp Med J—Vol 37. No 1, 1989 Stroke and Cocaine Abuse—Meza ct al 51 

Cerebral Infarction Associated with Cocaine Use

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Cerebral Infarction Associated with Cocaine Use

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