Calcium Channel Blockers

As noted previously, accumulation of intracellular calcium is a major player in secondary injury after CNS injury or stroke. One of the mechanisms for the postinsult calcium overload involves depolarization-induced entry via voltage-dependent L-type channels. Accordingly, the first neuroprotective approach to be tested in phase III clinical trials in TBI or stroke was the competitive L-type calcium channel blocker nimodipine, which entered clinical trials in the late 1970s. In two separate phase III, multicenter TBI (moderate and severe) trials17 and a single stroke trial,16 no overall benefit was revealed with nimodipine treatment. However, retrospective analysis of the TBI trials revealed that nimodipine may improve outcome in patients with traumatic SAH (tSAH). This was not an insignificant finding, as about half of all patients with severe TBI have tSAH as part of the pathophysiology. Furthermore, nimodipine produces a slight, but significant, increase in survival in aneurysmal SAH patients, and has been approved in most countries for the treatment of that condition. Indeed, nimodipine represents the first agent to be approved for neuroprotective use, even though much of its effect is probably mediated via protection of the microvasculature and vasodilatation-mediated improvements in cerebral blood flow. Due to a manifestation of its microvascular vasodilatation, the compound must be used with care, because it can lower arterial and cerebral perfusion pressures that can exacerbate posttraumatic, postiischemic, or post-SAH secondary brain injury.

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