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Elevated body temperature (T core ) is associated with poor outcome after subarachnoid hemorrhage (SAH). Brain temperature (T brain ) is usually higher than T core . However, the implication of this difference (T delta ) remains unclear. We aimed to study factors associated with higher T delta and its association with outcome. We included 46 SAH patients undergoing multimodal neuromonitoring, for a total of 7879 h of averaged data of T core , T brain , cerebral blood flow, cerebral perfusion pressure, intracranial pressure and cerebral metabolism (CMD). Three-months good functional outcome was defined as modified Rankin Scale ≤2. T brain was tightly correlated with T core (r = 0.948, p  < 0.01), and was higher in 73.7% of neuromonitoring time (T delta +0.18°C, IQR -0.01 - 0.37°C). A higher T delta was associated with better metabolic state, indicated by lower CMD-glutamate ( p  = 0.003) and CMD-lactate ( p  < 0.001), and lower risk of mitochondrial dysfunction (MD) (OR = 0.2, p  < 0.001). During MD, T delta was significantly lower (0°C, IQR -0.2 - 0.1; p  < 0.001). A higher T delta was associated with improved outcome (OR = 7.7, p  = 0.002). Our study suggests that T brain is associated with brain metabolic activity and exceeds T core when mitochondrial function is preserved. Further studies are needed to understand how T delta may serve as a surrogate marker for brain function and predict clinical course and outcome after SAH.

Spreading depolarizations (SDs) are highly active metabolic events, commonly occur in patients with intracerebral hemorrhage (ICH) and may be triggered by fever. We investigated the dynamics of brain-temperature (T brain ) and core-temperature (T core ) relative to the occurrence of SDs. Twenty consecutive comatose ICH patients with multimodal electrocorticograpy (ECoG) and T brain monitoring of the perihematomal area were prospectively enrolled. Clusters of SDs were defined as ≥2 SDs/h. Generalized estimating equations were used for statistical calculations. Data are presented as median and interquartile range. During 3097 h (173 h [81-223]/patient) of ECoG monitoring, 342 SDs were analyzed of which 51 (15%) occurred in clusters. Baseline T core and T brain was 37.3℃ (36.9-37.8) and 37.4℃ (36.7-37.9), respectively. T brain but not T core significantly increased 25 min preceding the onset of SDs by 0.2℃ (0.1-0.2; p < 0.001) and returned to baseline 35 min following SDs. During clusters, T brain increased to a higher level (+0.4℃ [0.1-0.4]; p = 0.006) when compared to single SDs. A higher probability (OR = 36.9; CI = 36.8-37.1; p < 0.001) of developing SDs was observed during episodes of T brain  ≥ 38.0℃ (23% probability), than during T brain  ≤ 36.6℃ (9% probability). Spreading depolarizations - and in particular clusters of SDs - may increase brain temperature following ICH.

Low brain tissue glucose levels after acute brain injury are associated with poor outcome. Whether enteral nutrition (EN) reliably increases cerebral glucose levels remains unclear. In this retrospective analysis of prospectively collected observational data, we investigate the effect of EN on brain metabolism in 17 poor-grade subarachnoid hemorrhage (SAH) patients undergoing cerebral microdialysis (CMD) monitoring. CMD-values were obtained hourly. A nutritional intervention was defined as the clinical routine administration of EN without supplemental parenteral nutrition. Sixty-three interventions were analyzed. The mean amount of EN per intervention was 472.4 ± 10.7 kcal. CMD-glucose levels significantly increased from 1.59 ± 0.13 mmol/l at baseline to a maximum of 2.03 ± 0.2 mmol/l after 5 h (p < 0.001), independently of insulin-treatment, baseline serum glucose, baseline brain metabolic distress (CMD-lactate-to-pyruvate-ratio (LPR) > 40) and the microdialysis probe location. The increase in CMD-glucose was directly dependent on the magnitude of increase of serum glucose levels (p = 0.007). No change in CMD-lactate, CMD-pyruvate, CMD-LPR, or CMD-glutamate (p > 0.4) was observed. Routine EN also increased CMD-glucose even if baseline concentrations were critically low ( < 0.7 mmol/l, neuroglucopenia; p < 0.001). These results may have treatment implications regarding glucose management of poor-grade aneurysmal SAH patients.

Pathophysiologic mechanisms of secondary brain injury after intracerebral hemorrhage and in particular mechanisms of perihematomal-edema progression remain incompletely understood. Recently, the role of spreading depolarizations in secondary brain injury was established in ischemic stroke, subarachnoid hemorrhage and traumatic brain injury patients. Its role in intracerebral hemorrhage patients and in particular the association with perihematomal-edema is not known. A total of 27 comatose intracerebral hemorrhage patients in whom hematoma evacuation and subdural electrocorticography was performed were studied prospectively. Hematoma evacuation and subdural strip electrode placement was performed within the first 24 h in 18 patients (67%). Electrocorticography recordings started 3 h after surgery (IQR, 3-5 h) and lasted 157 h (median) per patient and 4876 h in all 27 patients. In 18 patients (67%), a total of 650 spreading depolarizations were observed. Spreading depolarizations were more common in the initial days with a peak incidence on day 2. Median electrocorticography depression time was longer than previously reported (14.7 min, IQR, 9-22 min). Postoperative perihematomal-edema progression (85% of patients) was significantly associated with occurrence of isolated and clustered spreading depolarizations. Monitoring of spreading depolarizations may help to better understand pathophysiologic mechanisms of secondary insults after intracerebral hemorrhage. Whether they may serve as target in the treatment of intracerebral hemorrhage deserves further research.