No abstract

This novel association between clusters of CSDs, brain metabolic distress, and increased MMP-9 levels expands our knowledge about secondary brain injury after ICH. The role of ketamine after this devastating disorder needs further studies.

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) and core-temperature (T) relative to the occurrence of SDs. Twenty consecutive comatose ICH patients with multimodal electrocorticograpy (ECoG) and T 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 and T was 37.3℃ (36.9-37.8) and 37.4℃ (36.7-37.9), respectively. T but not T 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 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 ≥ 38.0℃ (23% probability), than during T ≤ 36.6℃ (9% probability). Spreading depolarizations - and in particular clusters of SDs - may increase brain temperature following ICH.

Neuroinflammation after aSAH is associated with intraparenchymal bleeding, deranged cerebral metabolism and TAU-protein release. The impact of potential anti-inflammatory treatment strategies on secondary brain injury after aSAH has to be investigated in future studies.