The neurovascular complications of cocaine

The use of cocaine can lead to a variety of neurologic complications, including cerebral vasoconstriction, ischemia, aneurysm formation, and aneurysm rupture. A previous study has shown that cocaine use is associated with an increased risk of subarachnoid hemorrhage (SAH). This study conducted a systematic review and meta-analysis of observational studies to assess the association between cocaine use and the risk of poor neurological outcomes and mortality in patients with SAH.

A systematic review and meta-analysis were performed following the meta-analysis of observational studies in epidemiology (MOOSE) declaration for systematic reviews and the Cochrane Manual of Systematic Reviews and Meta-Analyses guidelines. Randomized controlled trials (RCTs), nonrandomized clinical trials, and prospective and retrospective cohort studies that reported data about adults who suffered Aneurysmal Subarachnoid Hemorrhage (aSAH) after having consumed cocaine recreationally were included. Variables such as mortality, vasospasm, seizures, re-bleeding, and complications were analyzed.

After a thorough selection process, 14 studies involving 116,141 patients, of which 2227 had a history of cocaine consumption, were included in the analysis. There was a significant increase in overall unfavorable outcomes in aSAH patients with a history of cocaine use (OR 5.51 CI 95% [4.26–7.13] P = <0.0001; I2 = 78%), with higher mortality and poor neurologic outcomes. There were no significant differences in the risk of hydrocephalus, seizures, or re-bleeding. Cocaine use was found to increase the risk of vasospasm and overall complications.

This study insinuates that cocaine use is associated with worse clinical outcomes in aSAH patients. Despite the cocaine users did not exhibit a higher risk of certain complications such as hydrocephalus and seizures, they had an increased risk of vasospasm and overall complications. These findings highlight the importance of addressing the issue of cocaine consumption as a primary preventive measure to decrease the incidence of aSAH and improve patient outcomes.

The pathophysiology of saccular aneurysm rupture (berry aneurysm) secondary to cocaine and methamphetamine use has been classically attributed to their effects on cerebrovasculature. We conducted a literature review to determine the contribution of cocaine and methamphetamines to aneurysm formation and subarachnoid hemorrhage (SAH). Our literature search revealed the contribution to berry aneurysm by both cocaine and methamphetamines is multifactorial and includes: hemodynamic compromise, hypertensive effects, inflammation, wall stress and hypoperfusion of cerebral vasculature. The pathophysiological mechanisms by which these drugs contribute to saccular aneurysm and SAH is reviewed. We further discuss current grading scales used to measure the severity and extent of SAH in cocaine and methamphetamine users. Additionally, conflicting data regarding the specific role of cocaine and methamphetamines was retrieved. Although questions remain regarding the exact role of cocaine and methamphetamines, the evidence suggests that they do increase the probability of saccular aneurysm formation, rupture and poor patient prognosis.

A number of recreationally used drugs, licit and illicit, have been linked to ischemic and hemorrhagic stroke. In some cases, for example, ethanol and tobacco, epidemiologic data convincingly identify the agents as risk factors without implying direct temporal causality. In the case of psychostimulant drugs-including methamphetamine, 3,4-methylenedioxymetamphetamine ("ecstasy"), cathinone derivatives ("bath salts"), and cocaine, as well as cannabis products-linkage is based on case reports and limited epidemiologic data, but temporal association of use, plus biological plausibility, suggest direct causality. Recreational drug use should be considered in any patient with a stroke, regardless of age.

Cocaine is a known vasoactive drug associated with poor clinical outcomes and high in-hospital mortality related to aneurysmal subarachnoid hemorrhage; however, the association of prior cocaine use with the incidence of vasospasm and delayed cerebral ischemia remains controversial. We report a case of a 42-year-old male with a history of active cocaine use who presented with a severe headache. Imaging demonstrated diffuse cisternal subarachnoid hemorrhage due to a ruptured basilar apex aneurysm, which was successfully treated with endovascular coil embolization. Despite expedited endovascular treatment and an initially benign clinical course, he suffered from delayed cerebral ischemia resulting in cortical blindness due to bilateral posterior cerebral artery vasospasm secondary to repeat cocaine use weeks after his initial ictus. To our knowledge, the present case is the first to describe delayed cerebral ischemia resulting in a severe neurologic deficit due to repeat cocaine use weeks subsequent to aneurysm rupture. We review the current literature on the association of cocaine use with the incidence of vasospasm and delayed cerebral ischemia as well as the effects of cocaine on the cerebrovasculature.

Neuropsychiatric disorders caused by toxic substances pose a great diagnostic challenge due to the large variety of changes caused in the central and peripheral nervous system. The pathogenetic mechanisms at work are multifaceted and partly not solved.

In human drug abusers (cannabis, opiates, cocaine, amphetamines, methamphetamine and “designer drugs”), a broad spectrum of central nervous system alterations are observed including infarction, intracerebral and subarachnoidal hemorrhage, hypoxic-ischemic leukoencephalopathy, infections, neuronal loss, specific astroglial and microglial reaction patterns, and vascular changes, including the endothelial cell as well as the basal lamina.