Assessment of Chronic Subdural Hematoma Perifocal Zone Microvasculature According to Perfusion Computerized Tomography Data
The aim of the investigation was to explore possibilities of assessment of cerebral microcirculation and blood flow autoregulation in chronic subdural hematoma (CSH) perifocal zone using present-day algorithms of perfusion computerized tomography.
Materials and Methods. The concentric retrospective non-randomized study comprised 20 patients with unilateral CSH developed in result of craniocerebral injury sustained at term from 15 days to several months to admission date. Mean age of the casualties was 54.7±15.6 years (from 17 to 87 years old). 11 patients had the CSH settled on the right, while 9 patients had the CSH settled on the left. Average hematoma volume amounted to 84.2±12.4 cm3 (from 56 to 117 cm3), condition severity according to Markwalder scale was 1.8±0.5 points (from 0 to 3 points).
Colored perfusion parameter charts were plotted to describe cerebral perfusion in the cortex area adjacent to CSH and in the symmetrical area of the opposite hemisphere without the use and with the use of the mode (algorithm) for perfusion computation exclusive of flows in Remote Vessels great vessels.
Results. Perfusion indices of microvasculature in the CSH perifocal zone have no statistically significant variations from the norm and indices in the symmetrical area of the opposite hemisphere. This statement holds for assessment of perfusion status both without the use and with the use of perfusion calculation algorithm exclusive of flows in great vessels.
Conclusion. Constancy of microvasculature perfusion in the CSH perifocal zone is indicative of cerebral blood flow autoregulation retention in patients with chronic subdural hematomas.
Use of present-day cerebral perfusion assessment algorithms allows for CSH forecast in casualties with craniocerebral injury. Development of cerebral hyperperfusion local nidi, which do not affect the pial flow in patients who had a cerebral damage may serve as an early marker of CSH capsule formation with cerebral compression development.
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