SAH: refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20% of all strokes.
- High morbidity and mortality, usually associated with head trauma
- Associated with aneurysm and avm rupture
- Aneurysms usually occur at the branching sites on the large cerebral arteries of the circle of Willis. The early precursors of aneurysms are small outpouchings through defects in the media of the arteries. These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations.
- calcium channel blocker
- shown to reduce the incidence of ischemic neurological deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. Although the mechanism is unproved, it appears that nimodipine may prevent the ischemic complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged neurons.
a. General: dihydropyridipine CCB, used to treat cerebral vasospasm 2/2 to SAH
b. MOA: works on L type Ca channels, no one actually knows how it prevents vasospasm
Theory: may prevent the ischemic complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged neurons
i. It is selective for cerebral vasculature
ii. Given within 4 days of SAH and cont’d for 3 weeks
i. Absorption: given orally, peak [ ]plasma takes 1.5 hrs
ii. Metabolism: 1st pass metabolism by the liver, CYP450
iii. Excretion: urine
e. Side Effects: flushing, thrombocytopenia, CHF, DVT