Biomedical subjects

F Seitelberger

Publications and source records attributed to F Seitelberger.

At least 37 records · Page 2Linked to original sources

PubMed1986

[New aspects of senile and presenile dementia].

Problems of research in dementia are presented. It is a matter both of structural disturbances in the texture of conditions which impair the texture of conditions of possible functions, as well as of actual functional disturbances of the brain. The numerous etiological and diagnostic aspects resulting from this show distinctly that the dementia does not exist. In the numerous dementias which appear as diseases of higher age, the distinction between true old age diseases (Alzheimer, Pick, progressive glial dystrophy) and the cerebrovascular dementias (multi-infarct-dementia, Binswanger's disease) is of importance. The classification of dementias may be carried out both by descriptive neuropathological criteria and by functional neuropathological criteria. This is demonstrated by way of examples.

Aged↗

PubMed1985

Kainic acid-induced seizures: dose-relationship of behavioural, neurochemical and histopathological changes.

Behavioural, neurochemical and histopathological changes induced by systemic injection of kainic acid were investigated at various doses of the neurotoxin (3, 6 and 10 mg/kg s.c.). There was a positive correlation between the dose of kainic acid and the extent of both the acute neurochemical changes 3 h after the injection (increases of 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid levels and a decrease in noradrenaline levels in all brain regions investigated), the acute histopathological changes (shrinkage and condensation of nerve cells and brain oedema in the entire forebrain) and the extent of behavioural alterations (immobility, 'wet dog shakes' and limbic seizures). However, the slope of the dose-response curves was very steep. Late and irreversible alterations included losses of the enzyme markers glutamic acid decarboxylase and choline acetyltransferase and, histopathologically, incomplete parenchymal necrosis and haemorrhages. These changes, however, were restricted to a few brain regions, the most important being the hippocampus, amygdala, entorhinal and pyriform cortex, and olfactory bulb, and they were seen only in animals which had undergone severe convulsions. It is suggested that the irreversible brain lesions in this animal model of limbic (temporal lobe) epilepsy are not solely induced by a direct action of kainic acid, but may be caused--at least in part--by additional, secondary pathogenetic mechanisms.

Animals↗

PubMed1985

[Pathology and pathogenesis of multiple sclerosis from the viewpoint of neurologic disease research].

The pathology of multiple sclerosis (MS) is characterized by the trias: inflammation, primary demyelination and reactive gliosis. However, besides these obligatory alterations a high inter- and intraindividual variability of structural aspects is found in MS lesions. Recent experimental studies in a model disease for MS, in chronic relapsing experimental allergic encephalomyelitis, provide a better understanding of the dynamics of lesions development in MS brains.

Blood-Brain Barrier↗

PubMed1984

The role of brain edema in epileptic brain damage induced by systemic kainic acid injection.

Edema formation and blood-brain barrier permeability was studied in animals with epileptic seizures induced by subcutaneous injection of kainic acid. Brain edema was most pronounced between 3 and 24 h after kainic acid injection. It was reflected by massive swelling of perineuronal and perivascular astroglia. Three hours after kainic acid perivascular astroglia swelling resulted in disturbance of local microcirculation in the affected brain areas. In addition, compression of drainage veins by the edematous brain induced focal perivenous hemorrhages similar to herniation damage in human brain edema. Tracer studies with sodium fluorescein, Evans blue, albumin and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. This finding indicates the presence of cytotoxic brain edema in kainic acid-induced epileptic brain damage. Treatment of brain edema with dexamethasone did not influence the incidence and severity of kainic acid-induced epileptic brain damage. However, in 54% of animals injected with kainic acid, lesions were completely prevented by treatment of brain edema with mannitol. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic kainic acid intoxication. It is suggested that in this model of limbic epilepsy the brain edema is due to the massive ionic imbalance elicited in the affected brain regions by the kainic acid-induced persistent neuronal excitation.

Animals↗

PubMed1984

Structural manifestations of leukodystrophies.

Following the definition of the leukodystrophies as degenerative demyelinating processes caused by metabolic disorders a pathogenetical classification of the leukodystrophies is given. Metabolic processes in the narrower sense (enzymopathies) and dysgenetic processes are distinguished. In the special part according to this classification the neuropathological characters of the representative leukodystrophies are described. Different types of loss of myelin sheaths, structural features of stored products, localisation patterns etc. are demonstrated. Etiogenetic, nosological and diagnostic aspects are discussed. Probable conditions of the inflammatory demyelination syndrome of adrenoleukodystrophy are considered. The possible coincidence of dysmyelination and demyelination in early manifested leukodystrophies in the frame of the Pelizaeus-Merzbacher-syndrome is emphasized. The findings in a connatal case of Pelizaeus-Merzbacher-syndrome are described.

Atrophy↗

PubMed1984

[Neuropathology of polyneuropathies].

The concept of polyneuropathies is defined; some basic anatomical data about the peripheral nerve are reviewed. The structural substrates of the 3 main types of polyneuropathies are demonstrated: 1. demyelination, i.e. elective loss of myelin sheaths; 2. axonal degeneration which can appear in a) desintegrative form or in b) dystrophic form, especially as "dying back", 3. peripheral neuroaxonal dystrophy. The pathogenetic conditions and respective etiologies are discussed, clinical manifestations are described.

Axons↗

PubMed1983

Kainic acid induced seizures: neurochemical and histopathological changes.

Behavioural, histopathological and neurochemical changes induced by systemic injection of kainic acid (10 mg/kg, s.c.) were investigated in rats. The most pronounced behavioural changes were strong immobility ("catatonia"), increased incidence of "wet dog shakes", and long-lasting generalized tonic-clonic convulsions. The behavioural symptoms were fast in their onset and lasted for several hours. Two distinct phases of histopathological and neurochemical changes were observed. (1) Early partially reversible changes were seen up to 3 h after kainic acid injection. They consisted of shrinkage and pyknosis of neuronal perikarya together with swelling of dendrites and axon terminals. These changes were accompanied by generalized signs of edema throughout the whole brain. Neurochemically, there was a marked decrease in noradrenaline levels (up to 70%) and an increase in levels of 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid and homovanillic acid (up to 200%) in all analysed brain regions, suggesting a strongly increased firing rate of aminergic neurones during the period of generalized seizures. These histological and neurochemical changes were found in all the brain regions examined; they were greatly reduced or only sporadically seen after 1-3 days, when the animals had recovered from the seizures. (2) Late irreversible changes developed 24 h and later following kainic acid injection. They consisted of incomplete tissue necrosis with loss of nerve cells and oligodendrocytes, demyelination, astroglial scar formation, small perivenous hemorrhages and extensive vascular sprouting. The changes were restricted to the pyriform cortex, amygdala, hippocampus (most pronounced in the CA1 sector), gyrus olfactorius lateralis, bulbus olfactorius and tuberculum olfactorium. Neurochemically, a selective decrease was seen in choline acetyltransferase activity (40%) of the amygdala/pyriform cortex area, and of glutamate decarboxylase activity in the dorsal hippocampus (45%) and amygdala/pyriform cortex (55%). No such changes were found in the frontal cortex and the striatum/pallidum. Since at these later time periods the widespread early changes in monoamine metabolism were mostly normalized, loss of acetylcholine and gamma-aminobutyric acid neurons in the affected brain regions represented a selective neurochemical change typical for this stage of kainic acid action. The observed neurochemical and histopathological changes may be directly related to the excitotoxic and convulsive properties of kainic acid. However, brain edema resulting in herniation damage of the basal portions of the brain in addition to disturbances of microcirculation and +

Amygdala↗

PubMed1982

[Pick's disease. A special type of pathological aging of the brain].

Pick's disease (circumscribed lobar atrophy of the brain) in its typical form, is a so-called presenile type of dementia, i.e. a cerebral disease which begins in the sixth decade of life, and leads to a progressive loss of intellectual capacity traits. Neuropathologically, Pick's disease is characterised by severe focal atrophy of the cerebral cortex, mainly of basal parts of the temporal and frontal lobe. In the long run, all the nerve cells of the affected areas and their processes are destroyed. This also involves the subcortical white matter (loss of nerve fibres and cicatrisation). Concomitant atrophies of other parts of the brain are frequent. The article reports on the results of the clinico-neuropathological examination of 30 cases of Pick's disease basing on the author's own observations. Special emphasis is placed on "neuronal atrophising dystrophy" of cortical systems as a characteristic change caused by Pick's disease; this phenomenon is interpreted as an endogenous disturbance of the neuronal structural metabolism. This process is, as a matter of principle, identical with the physiological "atrophising dystrophy" which represents part of cerebral aging. There are also pathogenetical parallels to orthological neuronal reactions to damaging of the axis cylinder processes. Pick's disease is characterised by the pathological extent and type of manifestation of "neuronal atrophising dystrophy". This pathological distortion of physiological processes is probably due to a specifically genetic and sometimes hereditary constellation. Finally, the article discusses the functional neuropathology or neuropsychology of Pick's disease. The importance of the basal temporofrontal cortex for the quality and preservation of human personality is emphasised; the changes of the high-class performances of the human brain, as caused by Pick's disease, are interpreted. Referring to the peculiarities of Pick's disease compared with normal cerebral aging, particular attention is drawn to the concept of "disease" and the definition of senile cerebral aging.

Aged↗

PubMed1982