Bilateral Basal Ganglia Infarction from Intranasal Use of Cocaine and Heroin.

Oscar Cisneros MD, Razia Rehmani MD

Key Points:

  • Cocaine is an alkaloid extracted from leaves that can be chewed or be prepared in concentrated forms, the most common of which is cocaine hydrochloride [1,2].
  • Cerebral ischemic infarcts are a known complication of cocaine use and less commonly Heroin use.
  • This complication is rare and has been reported in the past with cocaine and concomitant use of other drugs such as heroin and amphetamines.
  • Several studies have demonstrated the association between cerebrovascular disease and the use of cocaine [3-10].
  • In the CNS, cocaine can cause a variety of complications such as stroke, vasculitis, seizures, cognitive impairment, parenchymal and subarachnoid hemorrhage, and toxic encephalopathy [1-5,11-15].
  • Cocaine use, even in first-time users, can cause a wide variety of pathologies. Many intracranial lesions have been described.



Bilateral lesions in ischemic infarcts of the basal ganglia are rare. Conditions known to be associated with bilateral basal ganglia infarct include carbon monoxide poisoning, methanol intoxication, diffuse hypoxic or ischemic injury from cardiorespiratory arrest, hypovolemia due to trauma, bibasilar artery occlusion, and intravenous heroin use [9].

The mechanisms by which cocaine produces cerebrovascular damage are multifaceted [4]. Various mechanisms are believed to contribute to the increased risk of ischemic stroke associated with cocaine. Cerebral vasospasm secondary to cocaine ingestion may affect large cranial arteries as well as the cortical microvasculature. Cocaine also increases the risk of vascular thrombosis by potentiating platelet aggregation [4,5,10,12]. The mechanism by which heroin may cause bilateral basal infarctions is through hypoxia from hypoventilation and hypotension [9]. MRI imaging demonstrated high fluid attenuation inversion recovery (FLAIR) signal changes bilaterally in the basal ganglia, globus pallidus, and internal capsule, as can be seen in Figures 1A1D. None of these changes were appreciable on the CT scan of the brain as can be seen in Figure 2.

Recently newer imaging modalities have emerged that can demonstrate functional status in addition to structural lesions, unlike CT or MRI that only demonstrate structural lesions. However these newer, functional neuroimaging techniques such as single photon emission computed tomography (SPECT) and positron emission tomography (PET) may demonstrate significant changes in brain functioning even in the absence of structural lesions [1,9,13]. In a study involving patients with chronic cocaine use, MRI data demonstrated that these patients (without clinically apparent cerebrovascular symptoms or major risk factors) suffered from accelerated cerebrovascular damage when compared to age-matched normal control subjects. The lesions described in this study, however, were more common in the white matter of the cerebral hemispheres and insular region [10]. A dynamic susceptibility contrast MRI study also demonstrated that global cerebral blood volume (CBV) reduction is observed following intravenous (IV) cocaine administration. The study failed to show dose-effect relationship likely due to single time point measurement CBV and cocaine dosage [7]. Diffuse vasoconstriction or decrease in CBV is clearly associated with cerebrovascular events in animals and humans. There is one reported case of a young woman who developed vasculitis of the small arteries of the deep white matter and basal ganglia bilaterally. The cause was later confirmed by biopsy and is the only case to our knowledge of vasculitis due to cocaine [3].



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Oscar Cisneros, MD

PGY 2 Internal Medicine Resident
St Barnabas Health System
Bronx, NY

Razia Rehmani, MD

Chief of Neuroradiology & Musculoskeletal Imaging
Diagnostic Radiology
St Barnabas Health System
Bronx, New York