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A Murine Model of Subarachnoid Hemorrhage

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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.

|May 11, 2016

Summary

Impaired cerebral autoregulation in subarachnoid hemorrhage (SAH) predicts neurological complications like delayed cerebral ischemia (DCI). Understanding these autoregulatory changes can guide targeted treatments to reduce patient morbidity.

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Area of Science:

Neuroscience
Critical Care Medicine
Cerebrovascular Physiology

Background:

Subarachnoid hemorrhage (SAH) frequently leads to secondary brain injury.
Cerebral autoregulation, the brain's ability to maintain stable blood flow despite pressure changes, is often impaired after SAH.
Impaired autoregulation is linked to poor neurological outcomes, including vasospasm and delayed cerebral ischemia (DCI).

Purpose of the Study:

To investigate the physiological basis of impaired cerebral autoregulation in SAH patients.
To determine the relationship between autoregulatory capacity and the development of vasospasm and DCI.
To assess the predictive value of autoregulatory function for neurological complications.

Main Methods:

A cohort of 121 non-traumatic SAH patients in a neurointensive care unit were studied.
Cerebral blood flow and beat-by-beat pressure were recorded daily for the first 2-4 days post-admission.
Autoregulatory capacity was quantified using pressure-flow relations, and vasospasm/DCI were identified via angiography and CT scans.

Main Results:

86% of patients with DCI were correctly predicted by autoregulatory capacity in the training cohort, generalizing to 80% in the test cohort.
Patients who developed DCI exhibited a distinct autoregulatory profile, with steeper flow decreases and blunted flow increases in response to pressure changes.
Impaired autoregulation was more pronounced in patients who developed DCI compared to those with only vasospasm or no secondary complications.

Conclusions:

The degree and pattern of autoregulatory impairment accurately predict individual neurological complications post-SAH.
These findings suggest potentially distinct physiological mechanisms underlying autoregulatory dysfunction.
A deeper understanding of these mechanisms may enable targeted interventions to mitigate neurological morbidity in SAH patients.