Features of regional blood flow in chronic ischemic optic neuropathy and dyscirculatory encephalopathy

Purpose: to investigate the indicators of regional blood circulation according to ultrasound dopplerography of the neck vessels and rheoencephalography with “isolated” dyscirculatory encephalopathy (DE) and in combination with chronic ischemic neuroopticopathy to clarify the possible pathogenetic mechanisms of the comorbid state formation.
Materials and methods of research. 77 patients aged 58 to 72 years were examined, 15 patients were in the control group, 62 patients were diagnosed with stage 2 dyscirculatory encephalopathy. According to the presence/absence of chronic ischemic neuroopticopathy, the latter group was divided into two: the first – with “isolated” DE (n=30), the second – with DE in combination with chronic ischemic neuroopticopathy (n=32). All patients underwent Doppler Ultrasonography of brachiocephalic vessels (DU BCV) and rheoencephalography (REG).
Results. In patients with DE, against the background of atherosclerotic lesions of brachiocephalic arteries of varying severity, the tone of large cerebral arteries increases; a tendency to angiospasm of small arterial vessels is recorded; venous outflow from the cranial cavity is disturbed. The addition of chronic ischemic neuroopticopathy in dyscirculatory encephalopathy is accompanied by changes in the DU BCV and REG: pronounced atherosclerotic lesion of the neck vessels, an increase in the intima-media complex thickness; the formation of stenoses in the bifurcation area from 2 sides; a decrease in the speed of blood flow through the carotid arteries and its branches; a decrease in systolic blood flow in all brain basins; an increase in peripheral vascular resistance reflecting angiospasm of arterioles, more pronounced in VBB; an increase in hypertension of large, medium and small arteries; deterioration of venous outflow from the cranial cavity.
Conclusions. The revealed violations of regional blood circulation according to the DU BCV and REG data in patients with dyscirculatory encephalopathy may be pathogenetic mechanisms of the comorbid pathology formation and accompany the debut and progression of chronic ischemic neuroopticopathy in these patients.

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