gms | German Medical Science

Objective: Dysfunction of neuronal signal processing and transmission occurs after subarachnoid hemorrhage (SAH) and can be attributed to increased ICP, decreased CBF, disruption of the blood-brain barrier, brain edema but also direct influence of subarachnoid blood metabolites on neuronal signaling must be considered. The murine single injection SAH model bears several advantages, one being the distinction between effects of raised ICP and subarachnoid blood metabolites. Aim of the investigation was to use this model in order to identify pathologic electrocorticographic (ECoG) phenomena and to comprehend which are caused by raised ICP and which by subarachnoid blood.

Method: Using implantable radio telemetric transmitters, electrocorticographic recordings sampled at 1000 Hz were collected from 34 15–20 week old C57Bl6 mice, which underwent either intra-cisternal injection of blood or saline or a sham operation. Fast Fourier Transform based spectral analysis was performed using a Hamming window.

Results: ECoGs of sham operated and saline injected animals did not differ significantly however blood injected animals (SAH group) displayed both acute and delayed pathologic effects. Blood injection but not saline injection acutely reduced total power by 65%. The SAH group displayed significant ECoG slowing (increase of delta power / decrease in alpha/delta ratio) 12 hours and 24 hours after injection, which normalized after 3 days. Furthermore, recurrent episodes of low frequency depression possibly representing spreading depression were measured twice in the SAH group but not in the other groups.

Conclusions: Here we show, that subarachnoid blood has effects on electrocorticographic parameters in mice that are similar to those reported from ECoG or EEG recordings from humans suffering from subarachnoid hemorrhage. Interestingly, these effects are found only in the SAH group and not in the saline group, implying that the pathologic ECoG phenomena identified in this study are caused by subarachnoid blood and not by raised ICP or decreased CBF. Furthermore, as ECoG slowing is delayed reaching significance 12 and 24 hours after blood injection, one may consider the contribution of blood breakdown products to this phenomenon.