Abstract
Subarachnoid hemorrhage (SAH) is a devastating stroke subtype with a high rate of mortality and morbidity. The poor clinical outcome can be attributed to the biphasic course of the disease: even if the patient survives the initial bleeding emergency, delayed cerebral ischemia (DCI) frequently follows within 2 weeks time and levies additional serious brain injury. Current therapeutic interventions do not specifically target the microvascular dysfunction underlying the ischemic event and as a consequence, provide only modest improvement in clinical outcome. SAH perturbs an extensive number of microvascular processes, including the “automated” control of cerebral perfusion, termed “cerebral autoregulation.” Recent evidence suggests that disrupted cerebral autoregulation is an important aspect of SAH-induced brain injury. This review presents the key clinical aspects of cerebral autoregulation and its disruption in SAH: it provides a mechanistic overview of cerebral autoregulation, describes current clinical methods for measuring autoregulation in SAH patients and reviews current and emerging therapeutic options for SAH patients. Recent advancements should fuel optimism that microvascular dysfunction and cerebral autoregulation can be rectified in SAH patients.
Highlights
Cerebral aneurysms are common [1–5% prevalence [1, 2]] and pose a “silent risk” of severe brain injury
As examples: in 9 studies reporting the clinical response to hypertension in 187 subarachnoid hemorrhage (SAH) patients, improvement of neurological deficits ranged from 50 to 100%, with most studies reporting improvement in around 80% of patients [123, 173, 175, 176, 181,182,183,184,185]; in 5 studies reporting long-term functional outcome at 2 to 6 months (141 patients), a good functional outcome was seen in 38 to 54% of the patients [181, 186,187,188,189]
Autoregulatory status can be measured in a clinical setting: while these measures are generally predictive of outcome, future efforts need to establish a “gold standard” procedure with sufficient numbers in order provide appropriate diagnostic and prognostic guidance
Summary
Cerebral aneurysms are common [1–5% prevalence [1, 2]] and pose a “silent risk” of severe brain injury. It must be emphasized that pressure autoregulation is not the sole determinant of cerebral perfusion: in addition to automatically adjusting microvascular resistance to pressure, vascular smooth muscle cells sense and integrate a variety of metabolic signals, which superimpose on autoregulation to elicit regional perfusion changes in response to heightened local metabolic demand [49,50,51,52] Examples of these metabolic signals include, but are certainly not limited to, pH, O2 and CO2 tensions, lactate, adenosine, nitric oxide, potassium ions, and vasoactive neurotransmitters (e.g., dopamine and acetylcholine) [49,50,51,52].
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