Introduction Delayed cerebral ischemia (DCI) is a major determinant for poor neurological outcome after aneurysmal subarachnoid hemorrhage (aSAH). Detection and treatment of DCI is a key component in the neurocritical care of patients with aSAH after initial aneurysm repair. Methods Narrative review of the literature. Results Over the past 2 decades, there has been a paradigm shift away from macrovascular (angiographic) vasospasm as a main diagnostic and therapeutic target. Instead, the pathophysiology of DCI is hypothesized to derive from several proischemic pathomechanisms. Clinical examination remains the most reliable means for monitoring and treatment of DCI, but its value is limited in comatose patients. In such patients, monitoring of DCI is usually based on numerous neurophysiological and/or radiological diagnostic modalities. Catheter angiography remains the gold standard for the detection of macrovascular spasm. Computed tomography (CT) angiography is increasingly used instead of catheter angiography because it is less invasive and may be combined with CT perfusion imaging. CT perfusion permits semiquantitative cerebral blood flow measurements, including the evaluation of the microcirculation. It may be used for prediction, early detection, and diagnosis of DCI, with yet-to-prove benefit on clinical outcome when used as a screening modality. Transcranial Doppler may be considered as an additional noninvasive screening tool for flow velocities in the middle cerebral artery, with limited accuracy in other cerebral arteries. Continuous electroencephalography enables detection of early signs of ischemia at a reversible stage prior to clinical manifestation. However, its widespread use is still limited because of the required infrastructure and expertise in data interpretation. Near-infrared spectroscopy, a noninvasive and continuous modality for evaluation of cerebral blood flow dynamics, has shown conflicting results and needs further validation. Monitoring techniques beyond neurological examinations may help in the detection of DCI, especially in comatose patients. However, these techniques are limited because of their invasive nature and/or restriction of measurements to focal brain areas. Conclusion The current literature review underscores the need for incorporating existing modalities and developing new methods to evaluate brain perfusion, brain metabolism, and overall brain function more accurately and more globally.

Subarachnoid haemorrhage is a devastating disease and results in neurocognitive deficits and poor functional outcome in a considerable proportion of patients. In this study, we investigated the prognostic value of microtubule-associated tau protein measured in the cerebral microdialysate for long-term functional and neuropsychological outcome in poor-grade subarachnoid haemorrhage patients. We recruited 55 consecutive non-traumatic subarachnoid haemorrhage patients who underwent multimodal neuromonitoring including cerebral microdialysis. Mitochondrial dysfunction was defined as lactate-to-pyruvate-ratio > 30 together with pyruvate > 70 mmol/L, and metabolic distress as lactate-to-pyruvate-ratio > 40. Multidimensional 12-month outcome was assessed by means of the modified Rankin Scale (poor outcome: modified Rankin Scale ≥ 4) and a standardized neuropsychological test battery. We used multivariable generalized estimating equation models to assess associations between total microdialysate-tau levels of the first ten days after admission and hospital complications and outcomes. Patients were 56 ± 12 years old and presented with a median Hunt & Hess score of 5 (interquartile range, 3 - 5). Overall mean total microdialysate-tau concentrations were highest within the first 24 hours (5585 ± 6291 pg/ml), decreased to a minimum of 2347 ± 4175 pg/ml on day four (p < 0.001) and remained stable thereafter (p = 0.613). Higher total microdialysate-tau levels were associated with the occurrence of delayed cerebral ischaemia (p = 0.001), episodes of metabolic distress (p = 0.002) and mitochondrial dysfunction (p = 0.034). Patients with higher tau levels had higher odds for poor 12-month functional outcome (adjusted OR, 2.61; 95% CI 1.32–5.17; p = 0.006) and impaired results in the Trail Making Test-B (adj. OR, 3.35; 95% CI, 1.16–9.68; p = 0.026) indicative of cognitive flexibility. Total microdialysate-tau levels significantly decreased over the first ten days (p < 0.05) in patients without delayed cerebral ischaemia or good functional and remained high in those with delayed cerebral ischaemia and poor 12-month outcome, respectively. Dynamic changes of total tau in the cerebral microdialysate may be a useful biomarker for axonal damage associated with functional and neurocognitive recovery in poor-grade subarachnoid haemorrhage patients. In contrast, ongoing axonal damage beyond day three after bleeding indicates a higher risk for delayed cerebral ischaemia as well as poor functional outcome.