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Biomedical subjects

V F Shefer

Publications and source records attributed to V F Shefer.

At least 19 recordsLinked to original sources
PubMed1987

[Hypo- and hyperdiagnosis of senile dementia and Alzheimer's disease in psychiatric practice].

A total of 714 brains from patients of predominantly advanced age who died in mental (n = 546) and somatic (n = 168) institutions have been examined macro- and microscopically. It has been found on the basis of accurate postmortem verification of Alzheimer's disease (AD) and senile dementia (SD) that in 20% of cases psychiatrists erroneously diagnose feeblemindedness in old age and in about the same proportion of cases they fail to diagnose the actual disease (most often AD and SD). The author has revealed a marked hyperdiagnosis of hypophrenias of vascular genesis at the expense of AD and SD whose rates are obviously underreported and which play a greater role in gerontopsychiatric practice than is generally accepted.

Aged↗
PubMed1985

[Ultrastructure of epileptic foci in temporal epilepsy].

An electron microscopy study was conducted on the material of biopsies from the removed epileptic foci localized in the hippocamp and fields 21 and 38 of the temporal cortex of 11 patients with temporal epilepsy. There was the constant presence of so-called dark and altered light neurocytes whose cytoplasm had experienced considerable changes and was saturated with various inclusions. The axons and dendrites of the cells underwent peculiar degeneration. The authors revealed multiple agglutination of synaptic vesicles in the preterminals and synaptic buds, and also dark degeneration of the axonal endings in the absence of Waller's degeneration of axons. Marked changes in the walls of the capillaries were also found.

Adolescent↗
PubMed1985

[Muli-infarct dementia].

Two hundred and fifty-five cases of dementia of advanced age were studied. In 142 of them (56%) the clinical diagnosis was vascular dementia. In 55 the anatomical diagnosis was senile dementia or Alzheimer's disease and in only 40 cases with established multiple infarcts (in 38 cases they were localized in the area of the subcortical ganglia) the diagnosis was multiinfarction dementia. In 11 of these 40 cases, multiinfarction dementia was combined with senile dementia and Alzheimer's disease. In relation to all 255 studied dementias of advanced age multiinfarction dementia constituted 11% in its pure form and 18% in its mixed form.

Alzheimer Disease↗
PubMed1984

[Relation between the degree of severity of the dementia and the extent of the manifestation of the pathomorphological changes in the cerebral cortex in senile dementia and Alzheimer's disease].

A study of 169 patients with senile dementia and Alzheimer's disease included history collection and the examination of the temporal pole. In the preparations impregnated according to Bilshovsky (in strictly the same volume of the cortex), senile plaques, neurofibrillar nodes and neurofibrillar skeletons were counted. Subsequently, the degree of the pathomorphological changes in each case was scored. The collation of the anamnestic and pathomorphological findings demonstrated a marked correlation (r = 0.99 +/- 0.0015) between the severity of dementia and the degree of pathomorphological changes in the cortex of the temporal pole.

Alzheimer Disease↗
PubMed1984

[Special forms of ultrastructural changes in dendrites and axons in the human and cat brain].

The investigation has been performed in the human brain of persons at the age of 75-87 years, in the auditory cortex of old cats and in bioplates obtained from epileptic foci of the hippocamp and the temporal cortex of 11 patients suffering from temporal epilepsy (at the age of 12-29 years). Distal parts of the dendrites contain a large amount of myelin-like membranous and electron opaque inclusions. In most cases these dendrites have no axodendritic contacts. In large trunks of the dendrites there are noted a comparatively large number of neurotubules with definitely seen contours against the background of small conglomerates of loose fine fibrillar material. Myelin axons contain a large amount of sharply contoured neurotubules which fill axoplasm. Similar dendrites and axons are revealed in the cerebral cortex both at age changes and in tissue of the epilepsy foci. These changes are supposed to result from the effect of the same factor.

Adolescent↗
PubMed1983

[Age-related changes in interneuronal synapses in human cerebral cortex].

In 5 persons that did not suffer from any psychical or neurological illnesses, at the age of 75-83 years, ultrastructure of dendrites, axons and axonal terminals was studied in the 40th field of the cerebral cortex, layer after layer. Various forms of changes in the dendrites were revealed demonstrating certain degenerative alterations in them and their loss of synaptic contacts with the axonal terminals. Two types of the axonal changes were followed. One of them, the most spread, has features of functional alterations (a tight arrangement of a great number of coarse neurotubules, while the axoplasm is remained). The state of such fibers is considered by the authors as a reversible one. Changes of the other type of axons (they are deprived of normal organells of axoplasm) are considered by the authors as irreversible. Degeneration of the axonal terminals, noted in all cortical layers, is realized mainly according to the "dark" type and seldom--according to the "light" one. In most cases these contacts are performed by unchanged dendrites. A gradual degeneration and death of neurocytes should be considered as a main course of the disturbances in the interneuronal connections of the cortex.

Aged↗
PubMed1983

[Hereditary demyelination in mutant quaking mice (breeding and light microscopy)].

Data on breeding of mutant Quaking mice (MQM) and the results of light microscopy and morphometric examination of the central and peripheral nervous systems in them and in control mice varying in ages from 12 days to 4 months are presented. MQM were shown to have a decreased total volume of the white matter due to underdevelopment of myelin because of disturbed function of myelin-forming cells (oligodendrocytes). At the same time oligodendrocytes retain their capacity for proliferation and are normally located interfascicularly in the white matter having the same density of occurrence and the same average volume of the nucleus as in controls, but morphologically they are similar to oligodendroblasts. Another morphological feature of MQM consists of intensive vacuolation of their gray and white matter. However, light microscopy could not determine whether the vacuoles 1 to 9 microns in diameter were located intra- or extracellularly. No pathological changes in neurocytes, astrocytes or capillaries were observed.

Animals↗
PubMed1983

[Hereditary demyelination in mutant quaking mice (electron microscopy study)].

Light and electron microscopic examinations of the nervous system in autosomal recessive mutant Quaking mice varying in ages from 12 days to 4 months revealed significant dysmyelination in which one of the most important morphological manifestations consisted of formation of "watery" astrocytes. The primary edema of astrocytes extended to other cerebral structures and produced their vacuolation, as a result of which significant disorders in the normal process of myelogenesis were observed, such as a decrease in the total volume of the white matter because of underdevelopment of myelin, disorders of the function of myelin-forming cells, oligodendrocytes. Pathological changes were also observed in some neurons and synapses. In contrast to the current opinion, the authors believe dysmyelination to be due not to primary involvement of oligodendrocytes but to edema of astrocytes. This does not rule out the genetic nature of this disease.

Animals↗
PubMed1982

[Pathologo-anatomic morphometric diagnosis of senile dementia and Alzheimer's disease].

The numbers of senile plaques, neurofibrillar bundles, and neurofibrillar "skeletons" in a certain constant volume of the left temporal pole cortex were calculated in 131 psychically healthy subjects who died at an age of 41 to 101 years, and in 111 subjects who suffered at lifetime from debilitating diseases of the type of senile dementia (dotage) and Alzheimer's disease. Each senile plaque was estimated at 0.1 point, and each neurofibrillar bundle and neurofibrillar "skeleton" at 1.0 point. In each case the points were summed up. In 86% of the cases of senile dementia and Alzheimer's disease the total of the points exceeded the maxima found in the psychically healthy subjects. This gives one grounds to recommend this method for making reliable pathoanatomic diagnoses of debilitating diseases of the type of senile dementia or Alzheimer's disease.

Adult↗
PubMed1982

[Morphological bases for age changes in memory].

The electrone microscopy of cerebral cortex (the 40th Brodmann's area) in 78, 79 and 83-year-old humans with no nervous or psychic disturbances and deceased during surgical intervention revealed significant changes of neuronal cytoplasm, dendrites, spines, axons and axonal synaptic terminals. Ultrastructural investigation of different acoustic areas of old cats cortex revealed the same changes and served as the control of harmlessness of the studies in humans. According to modern hypothesis on the memory mechanisms and their morphological substrate, the changes discovered in human cerebral cortex may serve as a possible cause of the age-induced memory changes.

Aged↗
PubMed1981

[Pathogenesis and pathomorphology of human leukodystrophies].

A review of foreign literature on the pathogenesis and pathomorphology of hereditary diseases of the human nervous system with the myelin involvement is presented. Five forms of leukodystrophies are mainly dealt with: (1) metachromatic, with the defect of their deposition in the form of a metachromatic substance; (2) globoid, with deficiency of galactoceramide beta-galactase enzyme catabolizing cerebrozides and with accumulation of the latter, particularly in the forming "globoid" cells; (3) sudanophilic, with sudanophilic degeneration of the myelin and obscure defect of the enzyme; (4) Pelizaeus-Merzbacher disease with insularly intact myelin; and (5) adrenoleukodystrophy with sudanophilic degeneration of the myelin and involvement of the adrenals. All the forms of leukodystrophies by the time of the onset of the disease are divided into prenatal, late infantile, juvenile, and adult.

Adolescent↗
PubMed1981

[Changes in the cerebral cortex in temporal lobe epilepsy].

Biopsy specimens of the temporal cortex were taken from three patients suffering from temporal epilepsy of different origin. As a result of examining the specimens under optic and electron microscopes and subsequent morphometric processing of the data a picture of layer-by-layer changes in the cortex (field 21/38) was obtained. These changes consisted in appearance of the so-called dark cells, degenerating synaptic buds and myelin fibres, and increase of the percentage of astrocytes and proliferation of their processes. The data obtained suggest that in this disease there occurs a gradual destruction of neurocytes which leads to disturbances of the interneuronal relations.

Adolescent↗
PubMed1981

[Age-related changes in the dendrites in the cat cerebral cortex (an electron microscopic study)].

Various zones of the acoustic cortex (A1, A3, A4, Ep after Voolsey) have been serially studied in two cats 12-14 years of age at electron microscopic level. Various forms of age changes have been revealed in their dendrites. The most often occurring form of the changes is the dendrites with lipofuscin granules in them. The dendrites with neuroplasm filled with numerous, sometimes aggregating electron opaque formations of various size and contour make the second form. Appearance of separate electron opaque round myelin-like bodies scattered in the dendritic neuroplasm precede the appearance of the third form. There is a various degree of disturbances in the interneuronal contacts. They depend on age alterations in the dendrites which are the most widespread postsynaptic components in the cerebral cortex. The importance to perform age selection of animals for an experimental morphological interneuronal connection investigations is stressed.

Aging↗
PubMed1980

[Neurocellular index].

If in an experimental or a clinico-morphological investigation a possible destruction of neural cells is suggested, it is recommended to apply the neurocellular index which is calculated as an average ratio of neural cells with a visible nucleus and nucleolus to neural cells with an indistinguishable nucleus or nucleolus or both in the same histological section. The index can serve as an objective proof on the process of cellular destruction and given an idea of its degree, expressed in numbers, suitable for comparative statistical-probable estimation. Applying this method, it is possible to objectively prove the fact of a gradual diffuse destruction of a certain amount of neural cells in the brain of old persons.

Adult↗
PubMed1977

[Development of senile plaques in the human brain].

In 100 persons, the development of senile plaques in 8 different parts of the brain was studied by means of Bielschowsky, Miagawa-Alexandrovskaja, phase contrast and morphometric methods. Appearance, within an unchanged brain tissue of a fine fibrillar structure, of a ball-shaped body (average diameter of 8.9 mcm) with a marked peripheral radiancy is believed by the author to be the first morphological stage of the senile plaque formation. Around this central focus, brain tissue necrosis separated from the normal brain tissue by a demarcation zone further develops. At final stages, desintegration and resolving of the central focus, and then of the whole senile plaque is observed.

Aged↗
PubMed1976

[Hippocampal pathology as one of the possible factors in the pathogenesis of several dementias of old age].

In the light of comtemporary concepts concerning the functional significance of the limbic system, the author reports of some results in the subiculum in young and old individuals (39 cases) with different forms of dementia of old age (senile and vascular dementia, Pick's and Alzheimer's disease). The authors assessed the thickness of the subicular cortical stratum, the relative and absolute amount of nervous and glial cells and capillaries. In old age the thickness of the subicular cortical stratum is decreased by 28%, while the absolute amount of neurons by 29%. In old age dementia the thickness of the subicular cortical stratum decreased by 47--71% and the absolute amount of neurons becomes 2--3 times less. In old age in general and in dementia of old age in particular there was no "substitutional" gliosis because the absolute amount of glial cells in the cortical stratum is reduced in this group of individuals by 20--50%.

Aged↗