Observational study reveals disrupted neurovascular coupling in severe subarachnoid hemorrhage, indicating that impaired blood flow matching may drive delayed cerebral ischemia.
Subarachnoid hemorrhage (SAH) is a devastating form of stroke. Approximately one in four patients develop progressive neurological deterioration and silent infarction referred to as delayed cerebral ischemia (DCI). DCI is a complex, multifactorial secondary brain injury pattern and its pathogenesis is not fully understood. We aimed to study the relationship between cerebral blood flow (CBF) and neuronal activity at both the cortex and in scalp using electroencephalography (EEG) in poor-grade SAH patients undergoing multimodality intracranial neuromonitoring. Twenty patients were included, of whom half had DCI median 4.7 days (interquartile range (IQR): 4.0-5.6) from SAH bleed. The rate of decline in regional cerebral blood flow (rCBF) was significant in both those with and without DCI and occurred between days 4 and 7 post-SAH. The scalp EEG alpha-delta ratio declined early in those with DCI. In the group without DCI, CBF and cortical EEG alpha-delta ratio were correlated (r = 0.53; p < 0.01) and in the group without DCI, inverse neurovascular coupling was observed at CPP < 80 mmHg. We found preliminary evidence that as patients enter the period of highest risk for the development of DCI, the absence of neurovascular coupling may act as a possible pathomechanism in the development of ischemia following SAH.
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Foreman et al. (2017) studied this question.
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