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Cocaine-Induced Bilateral Basal Ganglia Infarction in a Patient With ST-Elevation Myocardial Infarction: A Case
Marisol Trejos1, Solomon Nittala1, Kester Nedd1
1Neurology, Larkin Community Hospital Palm Springs Campus, Hialeah, USA.
Abstract:
Cocaine is an alkaloid-based extract made into cocaine hydrochloride, a substance found to influence the central nervous system to a higher degree when smoked and linked to numerous neurological ailments such as stroke, hemorrhage, seizures, and other cognitive impairments. We present the unique case of a 60-year-old male with unknown past medical history presenting initially with an acute ST-elevation myocardial infarction (STEMI) and a concurrent cardiocerebral infarction (more specifically in the bilateral globus pallidus stroke), with toxicology positive for cocaine intoxication. Lesions in the bilateral basal ganglia are usually correlated to carbon monoxide poisoning, cardiorespiratory arrest, hypovolemia, trauma, heroin usage, and methanol intoxication. However, in extremely rare instances, cocaine usage can lead to cerebral vasospasm causing infarction. Vascular thrombosis can be caused by platelet aggregation potentiated by cocaine. This unique presentation of bilateral basal ganglia with the comorbidity of a STEMI in association with cocaine intoxication encourages further research toward the usage of innovative imaging techniques such as positron emission tomography and single-photon emission computed tomography to facilitate viewing lesions associated with cerebral blood volume flow in cases where substance intoxication play a preeminent factor.
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