gms | German Medical Science

Objective: Spreading Depolarization (SD) occurs frequently after malignant hemispheric stroke (MHS) and may promote lesion growth. In the experimental setting, several physiologic parameters were shown to influence SD and its features. In this study we analyzed the impact of temperature (T°), intracranial pressure (ICP), mean arterial blood pressure (MAP) and cerebral perfusion pressure (CPP) on the incidence and duration of SD in patients with MHS.

Methods: 60 patients with MHS requiring hemicraniectomy were included in the clinical study. Electrocorticography (ECoG) of the periinfarct zone was performed with a linear subdural electrode strip (6 Pt/Ir contacts spaced at 10mm). Body temperature, MAP and ICP were monitored continuously. Mean values of 30 minute-periods before and after every SD were compared to the level of physiologic variable at the moment of SD in a linear mixed model with random intercept. The duration of each SD was correlated with the measurements of physiologic variable at this SD.

Results: During 7480h of ECoG, 1692 SD occurred with a total depression time of 821h and a mean number of 7.1±6.7 SD per patient per day. All the parameters of interest showed specific patterns around the incidence of an SD. Mean T° was increased during SD and dropped afterwards (p=.0002). ICP levels started rising shortly before SD, was highest during SD and fell again after (p<.00001). On the other hand, MAP was lower during SD than before and after the event (p=.002); the CPP pattern was accordingly (p=.002). There was no correlation between the depression duration and the four parameters of interest T° (p=.29), MAP (p=.66), ICP (p=.068), CCP (p=.40).

Conclusion: Compared to patients with traumatic brain injury [1], differences in T°, MAP, ICP or CPP between time points with and without SD were smaller, but our data is a proof of principle of the experimental findings in humans. This finding might explain an important mechanism in the pathophysiology of SD and can be relevant for the prevention of secondary damage in the treatment of MHS patients.