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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.