Spontaneous subarachnoid hemorrhage should be stratified into:
following cocaine abuse
alcohol consumption: controversial
diurnal variations in blood pressure
pregnancy and parturition
slight increased risk during lumbar puncture and/or cerebral angiography in patient with cerebral aneurysm
slight increased risk with advancing age
conditions with an increased incidence of cerebral aneurysms
An adverse lipid profile seems to elevate SAH risk similar to its effect in other cardiovascular diseases, especially in men. Whether SAH incidence diminishes with increasing statin use remains to be studied 1).
The extent and nature of impairment in autoregulation accurately predicts neurologic complications on an individual patient level, and suggests potentially differential impairments in underlying physiologic mechanisms. A better understanding of these can lead to targeted interventions to mitigate neurologic morbidity 2).
Differential diagnosis of severe, acute, paroxysmal headache (25% will have SAH):
subarachhnoid hemorrhage. AKA “warning headache” or sentinel H/A
benign “thunderclap headaches” (BTH) or crash migraine“, severe global headaches of abrupt onset that reach maximal intensity in < 1 minute, accompanied by vomiting in e 50%. They may recur, and are presumably a form of vascular headache, some may have transient focal symptoms. There are no clinical criteria that can reliably differentiate these from SAH. There is no suharachnoid blood on CT and LP, which should probably be performed on at least the first presentation to R/O SAH. Earlier recommendations to angiogram these individuals have since been tempered by experience.
reversible cerebral vasoconstrictive syndrome (RCVS) (AKA benign cerebral angiopathy or vasculitis) severe H/A with paroxysmal onset, ± neurological deicit.