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Biomedical subjects

F Koukolík

Publications and source records attributed to F Koukolík.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Neuropathology of the amnesia syndrome in old age].

In the 8-10th decade of life, people can be found who are not demented in the sense of WHO definition, but who are amnestic ("a memory problem only"). This defect is probably a result of the lesion of recent declarative memory. Immediate and remote memory are almost intact. Neuropathology of 17 such brains found numerous plaques and tangles in amygdalas and especially tangles in the IIth and IIIth strata of the entorhinal cortex and in subicula of hippocampi in 11 out of them. The number of plaques and tangles in frontal, parietal and temporal neocortex in these cases was not significant. In two other cases no significant ó "alzheimer-like" changes were found, but there was numerical atrophy of neurons of CA 1 sector of hippocampi in their caudal half perhaps due to chronic ischaemic lesion in one of them. In the other one there was an infarction of the left isthmus collateralis and retrosplenic cortex. In four cases no unequivocal structural basis for the amnesia was found--except slight numerical atrophy of large neurons of the nucleus basalis Meynerti. No significant diencephalic pathology was found. Severe "binswanger-like" changes were found in two cases of amnesia and in one case of control group, all of them were hypertonics. There exists a possibility that a part of "isolated" and relatively "benign" amnestic defects in old people is not a result of the aging of the brain but a sign of evolution of Alzheimer's disease and/or ischaemic vascular lesion of the brain destroying or disconnecting some of its information bottlenecks.

Aged↗
PubMed1989

[Thin-needle aspiration biopsy under ultrasonic control. The examination technic].

Based on experience with 298 aspiration biopsies (156 from the liver, 100 from the pancreas, 42 from other organs) made under ultrasonic control, the authors present a detailed description of the examination technique. At the same time they publish their own results with a mean sensitivity of 88%, specificity of 100% and diagnostic yield of 92%.

Biopsy, Needle↗
PubMed1989

[Structural changes in normal aging of the brain].

During normal ageing of the brain its weight and volume decrease significantly and the ventricles of the brain enlarge. The number of neurons of the brain stem in some areas does not decline, in the neocortex the number of neurons declines during the period between the age of 24 and 100 years by a maximum of 10-15%. As to neurotransmitting systems, the numeric atrophy during ageing affects mainly the noradrenergic locus coeruleus and the dopaminergic substantia nigra; the cholinergic n. basalis is probably not affected. The main change which takes place in neurons during ageing is their diminution. Dendritic systems of neurons undergo during ageing regressive as well as progressive changes; in some areas progressive changes predominate, in others regressive ones, in some areas both types of changes are in equilibrium. During ageing in neurons the nucleoli diminish at a varying rate. From this it is concluded that protein synthesis is altered and there is an increase of lipofuscin; both these changes take place in different ways in different neuronal populations, similarly as the diminution of Nissl's substance. The relationship of Alzheimer's disease and ageing of the brain is obscure from the pathogenetic aspect; there exist statistically significant but only quantitative differences. No evidence was provided that ageing of the brain per se is the cause of dementia.

Adult↗
PubMed1989

[Multi-infarct dementia--a disputed disease].

Isolated multiinfarction dementia is rare among general hospital demented patients who died and were subjected to necropsy (7.8%, i. e. 9 observations from 115 clinically and pathologically diagnosed syndromes of dementia during a period of more than four years). It is more frequently combined with Alzheimer' disease (18.3% of the same group). The development of multiinfarction dementia is suggested by cerebrovascular or cardiovascular disease in the case-history, similarly as hypertension, a varying course, focal neurological symptoms incl. impaired speech, gait and swallowing, a positive Hachinski score. Multiinfarction dementia and Binswanger's disease may be variants of the same process.

Aged↗
PubMed1989

[Binswanger's disease--a common disease of the brain and a frequent cause and component of dementia].

The author demonstrates on three selected observations clinical, radiological and neuropathological symptoms of Binswanger's disease. Its cause are changes of the long medullary arterioles which supply the white matter of the brain, most frequently in conjunction with hypertension. The basis of changes is ischaemic periventricular leucoencephalopathy. The disease is, contrary to recent ideas, very frequent and is formed by a spectrum of subclinical changes to deep dementia associated with neurological symptoms. Binswanger's disease is found isolated and combined with Alzheimer's disease or with multiinfarc dementia and is together with this unit the most frequent cause of vascular dementia in adult and old age.

Aged↗
PubMed1989

[Diagnosis of the most frequent causes of dementia].

Contemporary diagnosis of the most frequent causes of dementia is far from optimum. It may be influenced by problems in collecting clinical data, investigation, and clinico-pathological correlation at departments of pathology. The study suggests a course of this action. Clinicoanatomical diagnosis of dementia needs to estimate the patient was really demented and evaluate the quantitative morphological finding.

Alzheimer Disease↗
PubMed1988

Gerstmann-Straüssler-Scheinker disease.

In three out of six investigated cases of familially occurring dementia in adult age, the neuropathological examination disclosed Gerstmann-Sträussler-Scheinker disease, morphologically characterized by the presence of amyloid plaques and spongy condition of the brain grey matter. The spongy condition makes this disease related to Creutzfeldt-Jacob disease. The presence of the amyloid plaques signalizes an extreme production of the protein material which accumulates in them and which will be different from the amyloid in the senile plaques in Alzheimer's disease, and probably corresponds with infectious protein substances--prions or protein-like particles (PLP).

Adult↗
PubMed1986

[Gerstmann-Sträussler-Scheinker disease].

In three of six observations of familial dementia in adult age neuropathological examination revealed Gerstmann-Sträussler-Scheinker's disease characterized from the morphological aspect by amyloid plaques and a spongious state of the gray matter of the brain. As to the latter characterization the disease is close to Jacob-Creutzfeld's disease. The presence of amyloid plaques signalizes extreme production of protein material which cumulates. It is obviously different from amyloid of senile plaques in Alzheimer's disease and corresponds probably to infectious protein material-prions.

Adult↗