Vitamin D as a modifiable risk factor, predictor, and theoretical therapeutic agent for vasospasm in spontaneous subarachnoid hemorrhage.

Abstract

Delayed deterioration associated with cerebral vasospasm (CVS) is a feared complication after spontaneous subarachnoid hemorrhage (SAH) and is one of the leading causes of death in patients with intracranial hemorrhage. The pathophysiology of vasospasm is complex and not fully understood, involving multiple inflammatory pathways in addition to vasoconstriction induced ischemia. Current treatment with anti-inflammatory or vasodilatory medications has been met with limited success and has not led to a decrease in vasospastic associated mortality prompting continued investigation of potential treatment options. The active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-VitD3), is a hormone with downstream effects that induce anti-inflammatory pathways, promote nitric oxide (NO) induced vasodilation, and lead to neuroprotective-gene expression, which may be useful in mitigating the vascular pathogenesis associated with CVS. A high prevalence of vitamin D deficiency has been identified in patients admitted with SAH. Low vitamin D levels in patients, as determined by time of year, has also been correlated to an increased incidence and severity of CVS. Further, the therapeutic usefulness of 1,25-VitD3 has been demonstrated in animal models leading to a decreased incidence of CVS but has yet to be thoroughly investigated in human studies. In this review, we will discuss the findings that suggest the potential of utilizing vitamin D as a predictive indicator, method of prevention, and or treatment option for CVS in patients following spontaneous SAH.