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).
Sudden headache is the cardinal feature, but patients might not report the mode of onset, usually with vomiting, syncope (apoplexy), neck pain (meningismus), and photophobia. If there is LOC, patient may subsequently recover consciousness“. Focal cranial nerve deﬁcits may occur (e.g. third nerve palsy from aneurysmal compression, causing diplopia and/or ptosis), Low back pain may develope due to irritation of lumbar nerve roots by dependent blood.
In patients with a normal level of consciousness without focal neurological deficits the presence of neck stiffness is helpful but not pathognomic for the diagnosis of SAH. Moreover, the absence of neck stiffness does not rule out SAH, especially when evaluated ≤6h after symptom onset 3).
The most common symptom, present in up to 97% ofcases. Usually severe (classic description: “the worst headache of lny life”) and sudden in onset. They may clear and the patient may not seek medical attention (referred to as a sentinel hemorrhage or headache, or warning headache; they occur in 30-60% of patients presenting with SAH. If severe or accompanied by reduced level of consciousness, most patients present for medical evaluation. Patients with HA due to minor hemorrhages will have blood on CT or LP.
However, warning headaches may also occur without SAH and may be due to aneurysmal enlargement or to hemorrhage conﬁned within the aneurysmal wall”.Warning H/A are usually sudden in onset, severe, and clear within 1 day.
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.