Nimodipine is a dihydropyridine calcium channel antagonist that blocks the flux of extracellular
calcium through L-type, voltage-gated calcium channels. While nimodipine is FDAapproved
for the prevention and treatment of neurological deficits in patients with aneurysmal subarachnoid
hemorrhage (aSAH), it affects myriad cell types throughout the body, and thus, likely has
more complex mechanisms of action than simple inhibition of cerebral vasoconstriction. Newer
understanding of the pathophysiology of delayed ischemic injury after a variety of acute neurologic
injuries including aSAH, traumatic brain injury (TBI) and ischemic stroke, coupled with advances in
the drug delivery method for nimodipine, have reignited interest in refining its potential therapeutic use.
In this context, this review seeks to establish a firm understanding of current data on nimodipine’s
role in the mechanisms of delayed injury in aSAH, TBI, and ischemic stroke, and assess the extensive
clinical data evaluating its use in these conditions. In addition, we will review pivotal trials using
locally administered, sustained release nimodipine and discuss why such an approach has evaded
demonstration of efficacy, while seemingly having the potential to significantly improve clinical care.