Altered orbito-frontal cortex in schizophrenic psychosis.
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Biomedical subjects
Publications and source records attributed to D Senitz.
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Bergmann glial (Golgi epithelial) cells were Golgi-impregnated in the cerebella of species with great differences in the thickness of the molecular layer, in small African native mouse, rat, rhesus monkey, and man. The thickness of the molecular layer determines the length of the radial Bergmann cell processes. Whereas the overall morphology of the cells was found to be strikingly similar in all species studied, there were great quantitative differences in length and diameter of the stem processes. Species with thick molecular layers (man, monkey) have thicker stem processes than species with short distances between Bergmann glial cell soma and pial surface (rat, mouse). This could mean that larger animals with longer gestation periods allow for prolonged growth of cell volumes. On the other hand, an increase in the diameter of long processes should reduce the cytoplasmic resistance against ionic currents; this would be important when Bergmann glial cells--like retinal Müller cells--would act as "cables" for spatial buffering of potassium ions released by electrically active neurons. By contrast, the fractal dimension--i.e., a quantitative measure of the complexity of the cell's border--of the cell processes was lower in species with long processes. In an age series of rat cells, the fractal dimension is shown to increase slightly up to a very old age.
Changes were described in the neuronal structure of neurones, impregnated after the method of Golgi-Bubenaite in schizophrenic patients. Investigations were done in area 11 (Brodmann 1909) of patients with paranoid-hallucinatory schizophrenia. Control cases were patients without any clinical or morphological brain diseases and patients with catatonic schizophrenia. 1.1 We investigated numerous typical triangle cells in lamina VI of patients with paranoid-hallucinatory schizophrenia. Only few were seen in the controls. 1.2 In the paranoid-hallucinatory schizophrenia brains there are lamina VI pyramidal cells with ramified apical dendrites reaching lamina II. 2. In lamina V there are many pyramidal cells with two to five apical dendrites, such cells were never seen in controls, these pyramids have only one main apical dendrite. 3. A small group of L III pyramids have atypical long spines. A lot of these spines have splitted spine heads. The spine number is significantly increased. 4. There is an atypical simplified angioarchitecture in paranoid hallucinatory schizophrenia-patients and no normal arborization of the brain vessels in three planes, like in controls. We think that the abnormal findings in paranoid-hallucinatory schizophrenia are not the consequence of specific therapeutics. We interpret our findings as possible variabilities of a normal brain structure.
Morin staining is a specific method by which to detect aluminium in the brain. In cases of Alzheimer disease, aluminium was found to occur in neurons and glial cells, dense cores of senile plaques, primitive plaques, and intracortical congophilic vessels. Findings obtained are likely to suggest concomitant presence of aluminium and amyloid. Aluminium is assumed to have high affinity for amyloid. Aluminium is thus capable of overcoming the blood-brain barrier.
In comparison with the silver impregnation methods and with the thioflavine-S fluorescence method astra blue staining is an adequate technique for the demonstration of senile plaque and changes in Alzheimer's fibrils. Astra blue staining proved to be a useful tool in routine tests.
An account is given of hypertensive encephalopathy on the basis of neurohistological studies into 54 brains, with additional reference being made to autopsies. Vasculopathy of peripheral arteries and arterioles along with thickening of vascular walls, change of media, and lumen stenosis were primarily recorded by means of optical light and electron microscopy. A difference of more than seven per cent was found to exist between wall thicknesses of arterioles in hypertensive brains, on the one hand, and those in normotensive brains, on the other. Vessels with thickened walls were not rigid but were rather capable of dilation just as under normotensive conditions. Their inner diameters, however, were below normal. Vascular wall fibrosis, to which little attention had been given in the past, was repeatedly recordable from the venous and capillary systems. Impairment of the endothelial barrier function was quite often recorded, with lipid deposits being incorporated in peripheral arterioles and capillaries. No relevance to pathogenesis can be reliably attributed at present to detection of IgG in the arterial system. Microinfarction, micro-haemorrhage as well as disseminated damage to nerve cells are recordable from roughly one third of all hypertensive brains and are primarily located in brain stem ganglia. Demyelinisation and cerebral oedema are quite infrequent. High-protein cerebral oedema was found in some rare cases. Hypertensive encephalopathy should be considered as a nosological entity in which morphological and clinical phenomena are not always correlated to each other.
Ultrasonics was used to produce a heavy post-traumatic brain oedema. The oedema that developed rapidly within 6 to 8 hours after the injury expanded intracellularly only without destroying any neurogen structures. Examinations with an electron microscope showed massive swelling of the astroglia, mainly in the area of the astrocytal processus in both of the hemispheres, that means even in the contralateral hemisphere away from the trauma. The intracranial pressure increased rapidly.
A report is given on the design of an equipment combination developed in co-operation with the Central Institute for Welding Technology of the GDR, by means of which cerebral tumour tissue can be emulsified and sucked off. The suitability of the equipment was tested experimentally and confirmed in clinical application.
A case report is given of a pleomorphic lipoma in a 41 year old man. This article reviews the histopathologic and clinical features of this rare neoplasm. Characteristics distinguishing it from liposarcoma are presented.
In the neocortex (in area 11) of the non-demented aged humans (average age: 72.6 years) preferably the pyramidal cells of layer III are subjected to a conspicuous aged-related alteration in that they develop spindle-shaped enlargements of their proximal axon segment. We found different degrees of these enlargements. A slender process arises distally from the dilatation showing the morphological characteristics of the axon. In Golgi impregnations, such layer III pyramidal cells with an axon alteration do not display obvious changes in the ramification or spine density of their dendrites.
Neurons of the Wistar-rats' occipital cortex were morphologically investigated after chronical application of amphetamine. The nerve cells impregnated according to the Golgi-Kopsch technique showed in part changes on both the dendrites and in the axonal region. Besides a partial reduction of spines and of peripheral dendritic arborizations round varicosities of different density could be observed on the dendrites and on the axon, either, which were discussed to be due to a neurotoxic effect of amphetamine.
By employing Golgi's method it is possible to demonstrate the whole neuron with all structural details in the brain of adults. In the orbitofrontal cortex of deceased persons with schizophrenic psychoses the following morphological findings can be obtained which are not demonstrable by other methods: 1. Mainly pyramidal cells with thick and partly sinuous main dendrites which suggest the presence of an increase in spines. 2. Irregularly arranged triangular cells in the lamina VI with thickened dendrites and increased density of spines. 3. Splitting of the myelin lamellae and deposits of various origins and structures. These findings can be interpreted as a possible expression of a changed function.
In four cases of oligophrenia we found significant alterations in dendritic spines of cortical pyramidal neurons (in area 10 and 11). Mostly, these changes consist in a decrease or absence of thick, short spines and in a priminence of abnormal long thin spines. We found also apical dendrites with areas of cystic degeneration. The number of spines in these pyramidal cells is extremely reduced. These neurons are also characterized by changes of basal dendrites. It is inferred that such microstructural alterations may sufficiently influence the functional competency of axospinodendritic synapses to disturb the integrative operation of cortical dendrite systems.
The light microscopical morphology of perinatal neuroglia caused by hypoxia was examined in 60 cases, in 5 of them corresponding structures were investigated electron microscopically. The astroglia was studied additional by using the silver impregnation technique Bubenaite in 20 cases of the group. The glial lipid accumulation is a perinatal pathological process and is not related to myelination. It was found in 71,5% of the cases in astroblasts and astrocytes but seldom in oligodendrocytes. At the ultrastructural level, the lipid-loaded neuroglial cells cannot be confused with macrophages. One third of the cases showed a proliferation of the macroglial. In 20% of the cases, a focal leukodystrophy was found. A hypoxical degeneration was revealed of astrocytes by the Golgi modification of Bubenaite. The study demonstrates pathological changes of myelin formation in connection with degeneration and immature myelination. These perinatal neuroglial reactions seem to be connected with diffuse leukodystrophies. The examination gives the impression that the oligodendroglial differentiation might be disturbed. In contrast to myelin degeneration, the glial cells lesions and myelination defects play a decisive role in postnatal CNS formation.
The authors report a case of a six week-old infant, who has died from postnatal brian hypoxia. The ultrastructural investigation of the neuroglia shows lipid accumulations in most of astroglia cells, but only in a few oligodendrocytes. There is no correlation between glial metamorphosis and myelinization. Furthermore, there were found an immature neuropil, disturbed myelinization, and myelin and neuropil resorption processes. The study demonstrates the important role of hypoxic glial lesions n the evolution of the brain.
The changes of orbitofrontal studied astroglia in 10 cases of senile dementia have been studied. The modification of Golgi-method by Bubenaite was used. The results reveal 4 different types of changed astroglia. A relation between changes of makroglia and the aging process of CNS is suggested. The changes of glia are not a result of nervous cell alterations, but an independent neuroglial process under the conditions of aging.
We observed primitive cells in human brains of aged individuals. The processes of the cells are connected with capillaries. It may be that this connection is a sign of the aging process.
Perinatal central-nervous-system lesions may be found in as many as one third of all subjects who died before, during, or after the time of birth. Today, hypoxia is considered to be an essential cause of such lesions; in contrast to views held previously, birth trauma, i.e., physical injury to an infant during its delivery, is of minor pathogenetic importance. Neurohistological studies showed that it is especially prolonged hypoxia - in addition to cerebral hemorrhage, damage to the cerebral parenchyma and medullary substance - which can cause lesion of the brain stem. A relatively frequent occurrence are isolated ischemic cerebrospinal nerve cell lesions. Their prognostic dignity in regard to the possible formation of synapses and the problem of damage to the neuroglia are as yet imperfectly understood.