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Biomedical subjects

V A Morgunov

Publications and source records attributed to V A Morgunov.

At least 19 recordsLinked to original sources
PubMed2006

[Diagnosis of sarcoidosis of the brain].

Based on 15 years' their own experience and clinical observations of 65 patients with sarcoidosis of the brain, the authors have formulated diagnostic algorithms and a battery of studies that can suspect this disease. Since the clinical manifestations of sarcoidosis of the brain are non-specific, particularly at the early stages of its development, the condition of its recognition is the application of all required high-informative diagnostic neuroimaging techniques that are available to a neurological clinic. Nevertheless, sarcoidosis cannot be timely and correctly recognized in all cases. Diagnostic errors in its recognition are caused by the fact that X-ray computed tomography and/or magnetic resonance imaging is untimely made, tomographic changes are erroneously interpreted, and the studies are conducted improperly.

Brain Diseases↗
PubMed2004

Brain vessels in the rats exposed to primary and repeated tail-suspension. Minimization of structural changes after repeated exposure.

The aim of study was histological examination of brain vessels in the rats exposed to repeated tail-suspension (TS). The rats were subjected to 30-day TS, then readapted to horizontal position for 30 days and again exposed to 14-day TS simultaneously with the rats which were underwent to 14-day TS for the first time. 30-day TS induced in brain vessels the adaptive changes hindering the excessive blood inflow to brain--spasm and hypertrophy of muscle-elastic valves in extra- and intracerebral arteries and also the destructive changes--loss of vascular tone in extra- and intracerebral arteries, plethora in extra- and intracerebral veins, intracerebral venules and capillaries, conglutination of erythrocytes in capillaries, plasmatization of veins and capillaries and edema of brain tissue pointing out in total the increase in blood inflow to the brain and difficulty of blood outflow. After 30-day readaptation of TS-rats to horizontal position only adaptive changes in extracerebral arteries and intracerebral capillaries (cell proliferation) and edema of brain tissue were revealed. After repeated, 14-day TS in spite of new redistribution of blood to the head, in contrast to the vessel alterations after primary 14-day TS, the adaptive and destructive changes in brain vessels were lack, excluding only moderate plethora of intracerebral veins, cell proliferation in capillaries and weak signs of edema.

Adaptation, Physiological↗
PubMed1991

[Angiodysgenetic necrotizing myelopathy (the Foix-Alajouanine syndrome)].

One observation of a rare disease--angiodysgenetic necrotizing myelopathy--in a 50-year-old patient is described. The diagnosis was established at necropsy and did not confirm suspected spinal cord tumor and myelitis. The disease is angiodysplasia with resulting necrotizing myelopathy. Large dysplastic intra- and extramedullary vessels with a disturbed wall permeability, vascular malformations and necrotic foci in the spinal cord are characteristic for this condition.

Humans↗
PubMed1987

[Pathogenesis and etiology of amyotrophic lateral sclerosis (clinico-morphological research)].

The authors describe a 22-year-long course of lateral amyotrophic sclerosis; 14 of these years the patient was maintained by artificial ventilation of the lungs. Total paralysis was associated with intact consciousness and the function of the eye-moving muscles. According to morphological findings the death of motoneurons of the spinal cord and brain stem, as well as of corticospinal tracts was combined with signs of slowly progressive inflammatory process. Virus-like inclusions detected in the cytoplasm of neurons and astrocytes point to a possible infectious nature of the disease.

Adult↗
PubMed1986

[Hypertensive angiopathy of the brain].

Cerebral vessels were studied by light microscopy in 20 autopsies after hemorrhagic stroke from arterial hypertension. Primary (acute), secondary (reparative) changes, as well as changes reflecting compensatory-adaptive processes, were found in the intracerebral and superficial arteries of the brain. The whole complex of these vascular changes was defined as hypertonic angiopathy. The usage of such terms as "angiopathy" and "combined angiopathy" were discussed. Criteria of morphologic diagnosis of angiopathies were proposed.

Adaptation, Physiological↗
PubMed1983

[Lacunar infarct--special form of focal vascular pathology of the brain in arterial hypertension].

Lacunar infarctions were studied morphologically in 22 subjects who died of a cerebral hemorrhage associated with arterial hypertension. It has been established that lacunar infarctions developed in the intracerebral arteries 100-500 microns in diameter. Narrowing or obliteration of these arteries are brought about by the changes associated with arterial hypertension. An analysis of clinical and computer-tomographic data obtained from 32 patients with lacunar infarction showed that characteristic of these patients were the following features: 1) elevated arterial pressure, often without any cephalgia; 2) gradually developing (over a period of several hours or days) focal neurologic symptomatology; 3) the absence of either higher cortical dysfunctions or psychopathologic symptomatology with infarctions localized in the left or the right cerebral hemisphere respectively; and 4) considerable recovery of impaired functions.

Adult↗
PubMed1980

[Lacunar condition and hemorrhage into the brain].

Morphological lesions in the brain in 11 cases of combined lacunar condition and cerebral hemorrhages in arterial hypertension were studied. Lacunes were found to be cavities arising as a result of small infarctions developing in the basin of intracerebral arteries with narrowed or obliterated lumen. Lesions in the arterial walls are due to arterial hypertension. Examination of hemorrhage foci revealed structural elements of lacunes located on the edge and around hemorrhage. The lacunes and cerebral lesions accompanying them (criblurs, perivascular encephalolysis foci, incomplete necrosis foci) in some cases favour the development of cerebral hemorrhages and blood spread from the hemorrhage focus.

Brain↗
PubMed1978

[Combined infarct of the brain in the basin of the middle and anterior cerebral arteries].

The report contains a description of the morphology, pathogenesis and clinical picture of combined brain infarctions in 16 cases developing in the basin of the middle and anterior arteries. The mechanisms of their development are discussed: thrombosis, thrombembolia of the middle and anterior brain arteries and their branches, pressure of the cortical branches in the anterior brain artery by the lower edge of the large crescentic process of the dura mater.

Adult↗
PubMed1977

[Clinico-anatomic and virologic findings in a case of subacute sclerosing panencephalitis].

The report contains a description of I case of a subacute sclerosing panencephalitis in a 12 year old girl. The diagnosis was determined clinical and confirmed by serological studies which detected very high titres of antimeasle antibodies. The autopsy demonstrated pathomorphological changes typical for subacute slcerosing panencephalitis. An infectious agent was eliminated from the brain which according to its antigenic properties was identical to a measle virus.

Antibodies, Viral↗
PubMed1975

[Epileptic status in hemorrhage into the brain in hypertension].

The authors present a clinico-anatomical correlation of 3 cases with an epileptical status developing in the acute period of a hemorrhage stroke of hypertensive disease. The morphological examination, beside new hemorrhages in the hemisphere, revealed preceding focal and diffuse changes in the brain matter, due to a severe development of the hypertensive disease, brain traumas and disorders of brain circulation. It was established that the epileptical status appearing for the first time during the acute period of brain hemorrhages, has a complex mechanism. One of the conditions of its development is preceding focal and diffuse brain changes. Hemorrhages with oedema is a precipitating factor for a convulsive readiness of the brain.

Acute Disease↗