• Rajat Dhar and Michael N Diringer.
• Department of Neurology (Neurocritical Care Section), Washington University in St. Louis School of Medicine, 8111, 660S Euclid Avenue, St. Louis, MO, 63110, USA, dharr@neuro.wustl.edu.
• Acta Neurochir. Suppl. 2015 Jan 1;120:161-5.

AbstractDelayed cerebral ischemia (DCI) and cerebral infarction are major contributors to poor functional recovery after subarachnoid hemorrhage (SAH). Cerebral vasospasm, the narrowing of proximal intracranial arteries after SAH, has long been assumed to be the primary cause of DCI, and has therefore been the primary therapeutic target in attempts to diminish disability after SAH. However, emerging evidence has questioned the strength and causality of the relationship between vasospasm and DCI. To address this fundamental question, we performed two parallel studies assessing the relationship between the presence of vasospasm in a vascular territory and both regional reductions in cerebral blood flow (CBF) and development of cerebral infarction.In a cohort of SAH patients at high-risk for DCI, we identified regions of hypoperfusion using positron emission tomography (PET) and compared their distribution with territories exhibiting vasospasm on concurrent angiography. We found that regional hypoperfusion was common in the absence of proximal vasospasm and that some patients without any significant vasospasm still could have hypoperfused brain regions. Similarly, our parallel study demonstrated that both patients and brain territories without vasospasm could develop delayed cerebral infarction, and that such vasospasm-independent infarcts account for more than a quarter of the infarct burden from DCI. These findings suggest that other processes, perhaps at a microvascular level, contribute at least part of the burden of DCI and future interventions should also address these other pathophysiologic processes.

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