Imaging of early vasogenic edema in hyperperfusion zones of venous ischemic stroke

Abstract

Aim. The aim of the study was to investigate the features of cerebral edema in cases of venous ischemic stroke with cerebral venous sinus thrombosis.Material and Methods. The study included 33 patients with venous stroke as a result of cerebral venous sinus thrombosis. Comparison group comprised 33 patients with arterial ischemic stroke. The control group included 33 individuals. Neuroimaging included native computed tomography (CT) of the brain at admission and at days 5–7, perfusion CT (MSCT 64) within the first 40 minutes of admission to the hospital, and magnetic resonance imaging (MRI) of the brain (1.5T) within the first 24–48 hours of the disease.Results and Discussion. The relationships were found between the early intercellular edema development according to diffusion MRI and a signal inversion on diffusion-weighted imaging (DWI) (a decrease in the perifocal zone against the background of a high signal of cytotoxic edema), an increase in the signal with the average upper limit of apparent diffusion coefficient (ADC) range (0.82 ± 0.05) * 10-3 mm2 /s differing only from the central zone, and moderate plethora of perifocal zones (with an increase in rCBV and rCBF by 27–28%) according to perfusion CT. These phenomena could be unfavorable factors for the development of edema and probable hemorrhage (in 27% of cases in venous stroke versus 9% in arterial stroke), but were accompanied by a more favorable clinical outcome of venous stroke (improvement in 66% of cases with a complete regression of neurological deficit in 25% versus 57% without complete regression of symptoms in arterial) with a lower incidence of necrosis/infarction (in 50% of cases versus ¾ of cases of ischemic stroke). The presence of a significant correlation between the parameters of lesion area and the relative values of CT-based perfusion and MRI-based diffusion (r = 0.44; p < 0.05) suggested that the early vasogenic edema and hyperemia were the elements of a pathophysiological mechanism for the development of cerebral venous ischemia, which, unlike arterial ischemia, is secondary in nature, associated with mechanical arterial vasoconstriction due to intercellular edema.Conclusion. Probably, vasogenic edema in most cases of venous stroke, developing almost simultaneously with cytotoxic edema, does not reach the peak of pathological changes and stop in development at the stage of ionic edema with a functional impairment of permeability of the anatomically intact blood-brain barrier when it can reverse. The progressive development of vasogenic edema is a factor for the deepening of ischemia to necrosis/infarction and secondary hemorrhagic transformation.