Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage, however the relationship between radiological arterial spasm (seen on angiography) and clinical neurological deterioration is nuanced and uncertain.
Prinzmetal angina, Buerger's disease, contrast mediated selective renal vasospasm, hypercoagulability and cryoglobulinemia likely represent just a few of the known pieces of this puzzling phenomena.
[7] In a case study in 2000, following surgery for head trauma, a patient developed mild hypothermia, a typical defense mechanism the brain uses to protect itself after injury.
This can be done in several ways, the most important being lifestyle modifications—decreasing low-density lipoprotein (LDL), quitting smoking, physical activity, and control for other risk factors including diabetes, obesity, and hypertension.
Pharmacological options for reducing the severity and occurrence of ischemic episodes include the organic nitrates, which are rapidly metabolized to release nitric oxide in many tissues,[9] and are classified as having either long-acting (i.e. isosorbide dinitrate) or short-acting (i.e. nitroglycerin) durations of action.
The reduction of these latter three factors decreases the contractile force that the myocardium must exert in order to achieve the same level of cardiac output.
Beta-receptor antagonists do not cause vasodilation, but like L-type calcium channel blockers, they do reduce the heart's demand for oxygen.
Tolerance may also develop over time due compensatory response of the body, as well as depletion of -SH groups of glutathione which are essential for the metabolism of the drugs to their active forms.
What you could see upon taking both medications at the same time, as caused by the much higher induction of relaxation of smooth muscle cells, include a severe drop in blood pressure.
Since vasospasms can be caused by atherosclerosis and contribute to the severity of ischemia there are some surgical options which can restore circulation to these ischemic areas.