Acute ischaemia after subarachnoid haemorrhage, relationship with early brain injury and impact on outcome: a prospective quantitative MRI study

Abstract

Early ischaemia is related to poor acute neurological status after SAH and predicts future ischaemia and worse functional outcomes. Treatments addressing acute ischaemia should be evaluated for their effect on outcome.

Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage

“…We observed a higher than expected incidence of infarction in this cohort, however, given the small sample size, no conclusions may be drawn regarding a causal relationship. A recent prospective single center study obtained early MRI (0-3 days) in patients with aneurysmal subarachnoid hemorrhage and found early ischemia in 66 % of patients [35]. Nearly half of these patients underwent MRI prior to angiography.…”

“…Nearly half of these patients underwent MRI prior to angiography. While the etiology of cytotoxic edema identified on MRI early in the course of the disease is not well understood, hypotheses include reduced cerebral perfusion pressure in the setting of rapid elevations in intracranial pressures [36,37] as well as platelet activation secondary to endothelial damage and collagen matrix exposure [35]. Perhaps hyperacute vasospasm might be another contributor to early ischemia.…”

Early Prediction of Delayed Ischemia and Functional Outcome in Acute Subarachnoid Hemorrhage

“…The cerebellum is particularly vulnerable to several types of insults. Involvement of the cerebellum in ischemic lesions secondary to DCI has been described in a few studies, [34][35][36] affecting ≤20% of patients. 37 Because DTI parameters have increased sensitivity to microstructural changes 29 they might be able to demonstrate injury, not visible in conventional MRI sequences.…”

“…Accordingly, acute ischemia after SAH is detectable in MRI studies using DWI and is proportional to neurological impairment on admission 12,34 and functional outcome in the long term. 35 Besides, increased ADC values were described at a subacute stage of SAH, thought to be caused by vasogenic edema. Pathophysiological mechanisms involved in increased ADC in the subacute phase of SAH are probably multifactorial and include altered cerebral autoregulation, effects of treatment (hypervolemia), and disruption of blood-brain barrier.…”

Evolution of diffusion tensor imaging parameters after acute subarachnoid haemorrhage: a prospective cohort study

“…Involvement of the cerebellum in ischemic lesions secondary to DCI has been described in a few studies [29][30][31], affecting up to 20% of patients [32]. However, DTI changes observed the cerebellum of patients with SAH do not appear to be related the location of the ruptured aneurysm and more probably reflect a global parenchymal insult.…”