[Diphtheritic polyneuropathy: clinico-morphologic study]. / Difteriinaia polineiropatiia: kliniko-morfologicheskoe issledovanie.

18 patients with grave DP treated with a long-term artificial pulmonary ventilation and feeding through a naso-gastric probe were studied. Biopsies of n. suralis taken at different periods after the appearance of the first signs of DP (from the 19th to the 69th day) were studied at light and electronic microscopy. The basis of DP is toxic myelopathy with paranodal demyelination mainly in the large myelinated neural fibers and a segmentary one in the smaller neural fibers. Axonal degeneration was observed in the gravest cases of DP and was secondary being the result of axon squeezing by a folded myelin and voluminous Schwann cell cytoplasm invaginated into the axon. In no case of DP inflammatory changes and(or) involvement of the immunocompetent cells were found. There was pronounced proliferation and activation of Schwann cells due to intensive utilization of the degradation products of myelin and remyelinization. Morphological signs of remyelinization were observed on the 35th day of DP in the presence of enhancing neurological symptoms. But remyelinization was not complete even on the 69th day of DP.

[The Guillain-Barré syndrome]. / Sindrom Giiena--Barre.

A clinicomorphological study was conducted in 11 patients with severe forms of Guillain-Barré syndrome (GBS) at different periods of the disease. Five postmortem cases of GBS were investigated. In all the cases there was a multifocal loss of myelin in the peripheral nervous system with axon degeneration of various degree. Macrophages always took part in demyelination sometimes followed by lymphocytic infiltration. Ultrastructural investigation of nerve biopsies from 6 patients with GBS showed macrophage-associated demyelination with little or no lymphocytic infiltration. It is likely that axonal damage revealed in the biopsies and at the autopsies occurs as secondary consequence of demyelination.

[Hypertensive angio-encephalopathy and vascular dementia]. / Gipertonicheskaia angioéntsefalopatiia i sosudistaia dementsiia.

A clinicomorphological analysis of 60 postmortem cases with brain circulation disturbances against the background of arterial hypertension (AH) is performed. Lacunar infarcts, areas of incomplete necrosis and perivascular encephalolysis, small hemorrhages, criblures, persistent oedema and widespread spongiosis are found in the white matter (WM) of the brain in cases of AH of long duration with dementia. An important role in the WM lesions belongs to its ischemia due to hypertension angiopathy and disturbances of hemodynamics and liquor circulation. Complex of these lesions is called "hypertension leucoencephalopathy".

[Pathologic aspects of disorders of cerebral circulation in arterial hypertension and atherosclerosis]. / Patologoanatomicheskie aspekty narushenii mozgovogo krovoobrashcheniia pri arterial'noi gipertonii i ateroskleroze.

1500 lethal cases of apoplexy have been analyzed. The site, morphology and pathogenesis of small disturbances of brain circulation characteristic for each type of vascular encephalopathies are studied. Anatomo-pathologic classification of brain circulation disturbances are enlarged by meningeal hemorrhages and vascular encephalopathies. Pathologic and adaptive alterations are investigated starting from the major head arteries up to microcirculatory bed of the brain.

[The astrocyte reaction to an experimental herpes infection]. / Reaktsiia astrotsitov na gerpeticheskuiu infektsiiu v ékperimente.

The experimental research carried out on rabbits was aimed at determination of astrocytes reaction during brain inflammation caused by Herpes simplex virus. The study was made with the help of glia marker. Immunocytochemical findings showed that the earliest structural brain responses to the infection were changes in astrocyte glia. This was evident from the swelling and hypertrophy of vessel crus and from increased number of astrocytes around the vessels. Glia complexes (astrocyte agglomeration) were formed in the affected sites. During the exudative reaction the hyperplastic alterations of astrocytes were not observed. Later the injured spots of brain tissue were replaced by proliferating astrocytes. The conducted investigation has shown the astrocyte glia to be different during different stages of the infectious process. One may suppose that different subtypes of astrocytes response has place during each stage which should be further confirmed. One may also suppose that a similar alterations of astrocytes coincide with interferon and interleukin secretion by these cells. This is suggested to be a structural base of immune response of the brain.

[Arterial hypertension and pathology of cerebral white matter]. / Arterial'naia gipertoniia i patologiia belogo veshchestva golovnogo mozga.

White matter of the brain in 25 autopsy cases with the stroke and chronic cerebro-vascular pathology produced by arterial hypertension (AH) was studied morphologically. Focal and diffuse changes of the white matter were found against the background of the hypertonic angiopathy. These changes were represented by lacunar infarcts, foci of incomplete necrosis, perivascular encephalolysis, more seldom by small haemorrhages in combination with edema, cribriform lesions and widespread spongiosis of the white matter. Alterations of the cortex-medullary arteries, microcirculatory bed, disturbances of the dynamics of liquor and permeability of blood-brain barrier play the most important role in the white matter damage. The authors distinguish 3 forms of this damage. The complex of these alterations is regarded as a morphological substrate of a vascular dementia associated with AH.

[Morphologic changes in the skin and superficial temporal arteries in Sneddon's syndrome]. / Morfologicheskie izmeneniia v kozhe i poverkhnostnykh visochnykh arteriiakh pri sindrome Sneddona.

Skin biopsies from livedo's areas of 25 patients and fragments of superficial temporal arteries of 10 patients with Sneddon's syndrome were examined. Pathological changes in the dermis arteries of small and medium calibers were found in the form of the intima hyperplasia, proliferation of vascular wall cell elements (80%), arterial thrombosis (with diameter of 60-200 microns). These changes were found in 68% of observations when clinical and morphological signs of vasculitis were lacking. "Arteriopathy" is the most appropriate term for such lesions. Focal and diffuse fibro-muscular elastic hyperplasia of the intima and muscular layer fibrosis in the wall of superficial temporal arteries may be considered as age-associated lesions. Ultrastructurally, a selective damage of the non-adrenergic part of the nervous apparatus of the dermal arteries and superficial temporal arteries were observed; this suggests the participation of the damaged vascular neurogenic regulation in the formation of organic vascular changes.

[Hyperbaric oxygenation in acute compression-dislocation syndrome (experimental-morphological study)]. / Giperbaricheskaia oksiganatsiia pri ostrom kompressionno- dislokatsionnom sindrome (éksperimental'no-morfologicheskoe issledovanie).

Acute compression dislocation syndrome was reproduced in rabbits by means of epidural brain compression with a balloon. After elimination of brain compression the main group were treated by HBO whereas the control group did not receive HBO. The use of HBO resulted in a decrease of the lethality in hyperextension manifestations. Using the total water measurement in the brain the main group was discovered to have a decrease of brain edema at different times, associated with compression and eliminated compression thereof. Microscopy revealed a reduction of pericellular, perivascular and subependymal edema as well as of edema of vascular plexus and venous brain plethora under the influence of HBO.

[Morphology and pathogenesis of changes in the substantia alba of the cerebral hemispheres in arterial hypertension]. / K morfologii i patogenezu izmenenii belogo veshchestva polusharii golovnogo mozga pri arterial'noi gipertonii.

Morphological examination of the brain in 17 autopsies of patients with arterial hypertension and cerebral stroke has revealed damage of the white matter of the large cerebral hemispheres of a focal and diffuse nature. The main role in stroke development is ascribed to changes in the intracerebral cortico-medullar arteries manifested in hypertension and persistent brain edema. The following 3 forms of white matter damage associated with arterial hypertension have been described: (1) multi-infarctional; (2) periventricular (periventricular spongiosis); (3) combined (diffuse).

[Hypertensive angiopathy of the brain]. / Gipertonicheskaia angiopatiia golovnogo mozga.

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.

[Features of changes in vessels of the cortex and white matter of the cerebral hemispheres in arterial hypertension]. / Osobennosti izmenenii sosudov kory i belogo veshchestva polusharii golovnogo mozga pri arterial'noi gipertonii.

The authors examined morphologically the arteries of the surface and intracerebral arteries of the cortex and white substance of different areas of the cerebral hemispheres in 11 necropsies of patients with arterial hypertension who died from hemorrhagic strokes. It was established that arteries of the cerebral surface 200-500 micron in diameter were characterized by compensatory-adaptive processes reflecting structural adaptation of the vessels to a prolonged elevation of blood pressure. The intracerebral arteries were considerably more frequently characterized by changes induced by hypertonic crises expressed in the form of plasmorrhagias and isolated necrosis of the tunica media. The cortico-medullary arteries 100-150 micron in diameter were predominantly affected which accounts for a more severe damage to the cerebral white substance in arterial hypertension.

[Hypertonic angioencephalopathy in its pathomorphological aspect]. / Gipertonicheskaia angioéntsefalopatiia v patomorfologicheskom aspekte.

This is a report on 20 autopsies of patients with arterial hypertension and atherosclerosis who died of a hemorrhagic stroke. Morphological changes characteristic of hypertonic angioencephalopathy were detected in the intracerebral vessels and cerebral substance. They included plasmorrhagia with arterial stenosis and necrosis, miliary aneurysms, isolated necrosis of the pia mater attended with vascular deformation, complete and incomplete necrosis of the cerebral substance, gliomesodermal cicatrices, perivascular hemorrhages, lacunar infarctions at various stages of their progression, etc. The pathomorphological classification of cerebral circulation impairments has thus incorporated an additional notion "hypertonic angioencephalopathy".

[Morphology of "resuscitation-induced encephalopathy"]. / K morfologii "reanimatsionno-obuslovlennoi éntsefalopatii"

Two groups of changes in the cerebral substance were revealed by histological examinations of the central nervous system in a case of clinical death followed by respiratory resuscitation for 12 days. Changes of the 1st group consisted in foci of incomplete necrosis in the stage of organization in the cortex and dentate nuclei of the cerebellum, lower olives of the medulla, Zommer sector of the Ammon horn, and caudate nuclei. Their development is due to ischemia and circulatory hypoxia in the early resuscitation period. Changes of the 2nd group included acute disorders of microcirculation and extensive protein and carbohydrate dystrophy of nerve cells of the cortex and subcortical ganglia in the form of hyperchromatosis hydropic degeneration. "alzheimerization", accumulation of glycogen in the cytoplasm of neurons and astrocytes. The degenerative changes were combined with signs of gradual death of neurons and pseudolaminar losses in the cerebral cortex. Changes of the 2nd group may be classified as the so-called secondary nor delayed cerebral hypoxia in the development of which microcirculatory disorders are of importance. The observed morphological changes in the brain after clinical death and prolonged respiratory resuscitation represent morphological expression of "resuscitation-conditioned encephalopathy".

[Morphology and pathogenesis of "brain death" in stroke]. / Morfologiia i patogenez "smerti golovnogo mozga" pri insul'te.

The results of morphological examinations of the central nervous system and hypophysis in 15 cases of insult and "brain death" developing in patients under conditions of application of artificial lung ventilation (ALV). Isolated death of the brain was observed to be due to discontinuation of intracerebral circulation owing to a sharp increase of intracranial pressure. Morphologically, cerebral edema, necrosis of all parts of the brain without reactive changes in neuroglia and vessels, necrosis of the 1st and 2nd cervical segments of the spinal cord, necroses in adenohypophysis, zones of demarkation in the hypophysis capsule and at the level of the 3rd and 4th cervical segments of the spinal cord, and arrest of the blood stream in the brain vessels were observed. The intensity of the morphological changes was found to depend on the duration of ALV.

[Combined infarct of the brain in the basin of the middle and anterior cerebral arteries]. / Sochetannye infarkty mozga v basseine srednei i perednei mozgovykh arterii.

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.