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Updated: Mar 21, 2026
A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
Pathophysiologic differences in cerebral autoregulation after subarachnoid hemorrhage
Gabriela A Santos1, Nils Petersen1, Amir A Zamani1
1From the Department of Neurology, Stroke Division (G.A.S., S.L., A.M., F.A.S.), Department of Radiology (A.A.Z.), and Department of Neurosurgery (R.D.), Harvard Medical School, Brigham and Women's Hospital; Cerebrovascular Research Laboratory and Department of Physical Medicine and Rehabilitation (C.O.T.), Harvard Medical School, Spaulding Rehabilitation Hospital, Boston, MA; and Division of Neurocritical Care and Emergency Neurology (N.P.), Yale School of Medicine and Yale-New Haven Hospital, New Haven, CT.
Objective:
To understand the physiologic basis of impaired cerebral autoregulation in subarachnoid hemorrhage (SAH) and its relationship to neurologic outcomes.
Methods:
The cohort included 121 patients with nontraumatic SAH admitted to a neurointensive critical care unit from March 2010 to May 2015. Vasospasm was ascertained from digital subtraction angiography and delayed cerebral ischemia (DCI) was defined as new cerebral infarction on high-resolution CT. Cerebral blood flow and beat-by-beat pressure were recorded daily on days 2-4 after admission. Autoregulatory capacity was quantified from pressure flow relation via projection pursuit regression. The main outcome was early alterations in autoregulatory mechanisms as they relate to vasospasm and DCI.
Results:
Forty-three patients developed only vasospasm, 9 only DCI, and 14 both. Autoregulatory capacity correctly predicted DCI in 86% of training cohort patients, generalizing to 80% of the patients who were not included in the original model. Patients who developed DCI had a distinct autoregulatory profile compared to patients who did not develop secondary complications or those who developed only vasospasm. The rate of decrease in flow was significantly steeper in response to transient reductions in pressure. The rate of increase in flow was markedly lower, suggesting a diminished ability to increase flow despite transient increases in pressure.
Conclusions:
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.
