Cases reported "Atrophy"

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1/12. Memory disorder in Korsakoff's psychosis: a neuropathological and neuropsychological investigation of two cases.

    Neuropathological findings in the brains of two alcoholic patients with Korsakoff's psychosis are reported. Their memory defects had been studied in detail quantitatively over a period of nine years in one case and three years in the other, relevant details of which are presented. Both patients had had a relatively pure long-term memory impairment in the absence of other cognitive deficits and in the absence of a short-term memory impairment. Their retrograde amnesia for public events and famous faces had been measured and found to have extended backwards over at least twenty-five years. There was severe impairment in anterograde recognition memory for both verbal and non-verbal material. On a newly prepared memory quotient battery both patients had scored well below the bottom of the normal scale (less than 60, where 100 is the mean with a standard deviation of /- 15). Both patients had also shown the characteristic differential improvement in retention when tested by cued recall and also the characteristic 'prior learning effect', i.e. normal retention of one list of words when tested by cued recall but impaired retention of a second list sharing the same cues as the first list. There had been a slight but significant deterioration in intelligence in one of the patients in the two years prior to his death, although his IQ still fell within the normal range. The other patient remained undeteriorated until his death, and his IQ also was close to an estimated measure of his premorbid IQ. In the brains of both patients there was marked gliosis, shrinkage and discolouration bilaterally in the medial nuclei of the mammillary bodies. In addition there was a thin band of gliosis bilaterally between the wall of the third ventricle and the medial dorsal nucleus, the rostral limit lying anterior to the medial dorsal nucleus. In the patient with no intellectual deterioration these were the only pathological changes that were seen. In neither patient was there evident local loss of nerve cells, gliosis or any other qualitative evidence of abnormality in the hippocampi, the white matter of the temporal lobes or the greater part of the medial dorsal nuclei, although it is difficult to be certain whether there was any overlap between the band of gliosis and the most medial region of the medial dorsal nueleus and other adjacent thalamic nuclei. In the other patient there was also a small zone of softening in the cerebellum and an increase in astrocytes in other regions of the cerebral hemispheres, including the basal ganglia, amygdala, and brain-stem, but without noticeable loss of cells. The question of the minimal lesion for the alcoholic Korsakoff amnesic state, and some aspects of the related anatomy, is discussed in the context of other reports in the literature which are, however, difficult to assess in the absence of details of the specificity, severity and character of the memory disorders.
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2/12. frontotemporal dementia with co-occurrence of astrocytic plaques and tufted astrocytes, and severe degeneration of the cerebral white matter: a variant of corticobasal degeneration?

    We report two patients who exhibited frontotemporal dementia (FTD) with unusual neuropathological features. The ages of the patients at death were 65 and 67 years, the disease durations were 6 and 5 years, and the clinical diagnoses were Pick's disease and corticobasal degeneration (CBD), respectively. At autopsy, both cases exhibited neuropathological findings compatible with those of CBD, including atrophy of the frontal and parietal lobes, neuronal loss and gliosis in the cortical and subcortical regions, and presence of cortical ballooned neurons and astrocytic plaques (APs). In both cases, immunoblotting of insoluble tau exhibited the pattern of selective accumulation of four-repeat tau, a finding that is also compatible with CBD. However, severe degeneration was evident in the frontal and parietal white matter in both cases. Moreover, a striking finding was the widespread presence in the affected cortex of tufted astrocytes (TAs), which are characteristic of progressive supranuclear palsy (PSP). Neither co-occurrence of APs and TAs nor severe degeneration of the cerebral white matter is a feature of either CBD or PSP. No mutations were found in the tau gene in either case. In conclusion, the possibility that these two cases represent a new neuropathological phenotype of non-familial FTD rather than simply a variant of CBD cannot be completely excluded.
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3/12. Progressive dysphasic dementia with localized cerebral atrophy: report of an autopsy.

    A 64-year-old Japanese woman showed an initially aphasic disturbance followed by complete mutism, progressive dementia, parkinsonism and muscular atrophy. autopsy revealed localized cortical atrophy confined to the pars triangularis, pars opercularis of the inferior frontal gyrus, supramarginal and angular gyri of the inferior parietal lobe, precuneus and posterior half of the middle and inferior temporal gyrus predominantly on the left hemisphere. The right cerebellar hemisphere showed crossed cerebellar atrophy with shrinkage of the right middle cerebellar peduncle. In the atrophied cerebral areas there were diffuse outfall of neuronal cells in all cortical layers and remaining neurons generally showed simple atrophy, and there were a few swollen neurons. gliosis of the subcortical white matter was confined to the affected gyri and GFAP positive astrocytes were observed in the 1st, 2nd, 5th and 6th layers of the cortex. In addition, the degenerative changes of the substantia nigra, gliosis of the amygdaloid complex and inferior olivary nucleus were bilaterally observed. The distribution and characteristics of the cortical and white matter degeneration are different from those of Pick's disease, and it is likely that this case belongs to a group of so-called degenerative dysphasic dementias.
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4/12. A quantitative analysis of human astrocytosis.

    The number of astrocytes in an atrophic human brain was counted with the aid of immunohistochemistry for glial fibrillary acidic protein. Microscopically, astrocytosis was remarkable in the cerebral neocortex and white matter. Taking the cortical atrophy into consideration, however, the total number of astrocytes in the cortical layers II-VI was not increased. The number of astrocytes in the white matter was not increased either. It is indicated that astrocytosis does not always mean hyperplasia (net increase of total number) of astrocytes.
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5/12. cockayne syndrome: unusual neuropathological findings and review of the literature.

    Two siblings with cockayne syndrome (CS) are described and the literature on the subject is briefly reviewed. Of particular interest were the unusual neuropathological findings in 1 of the patients. These included microcephaly, white matter atrophy with patchy loss of myelinated fibers, calcifications of the basal ganglia, occasional ferrugination of cerebral and cerebellar neurons, and severe cerebellar degeneration. Findings not previously reported in CS were proliferation of extremely bizarre astrocytes, neurofibrillary tnagles, and pigmentation of the globus pallidus. We conclude that brain involvement in CS is a result of primary degeneration in the central nervous system rather than being secondary to angiopathy or normal pressure hydrocephalus, as previously suggested.
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6/12. An autopsy case of multiple leucoencephalitis showing hemiatrophy of the brain.

    A 39-year-old female died 25 years after the onset of epileptic seizure. In the clinical course, she suffered epileptic seizures, left hemiparesis and muscular atrophy of the left upper extremity, psychological character change, dementia, forced laughter and hallucinatory and delusional states. Pathologically, severe changes were found in the right hemisphere consisting of lesions of white matter with myelin loss, especially in the frontal, temporal and occipital lobes. gliosis was diffusely observed in the white matter excepting areas with severe changes. In some parts of the cortex, the cytoarchitecture was destroyed and in this area, blood vessels numerously increased. In the left occipital white matter, perivascular infiltration mainly consisting of lymphocytes was observed with numerous fat granule cells and gemystocytic astrocytes around them. The present case may belong to the category of multiple leucoencephalitis, however, it had many characteristic features, such as a long clinical course (25 years) and pathologically revealed hemiatrophy of the brain.
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7/12. Immunohistochemical and ultrastructural studies on the exenterated orbital tissues of a patient with Graves' disease.

    The exenterated orbital contents obtained post mortem from a 47-year-old man who had an eight-month history of treated hyperthyroidism and a two-month history of visual complaints were examined histopathologically, immunohistochemically, and by electron microscopy. All of the extraocular muscles were massively enlarged, due to early diffuse endomysial fibrosis, mucopolysaccharide deposition, and a predominantly perivascular lymphocytic and plasmacytic infiltration. Histochemical stains revealed that the intramuscular mucopolysaccharides were weakly sulfated and polycarboxylated, establishing that they were products of fibroblastic activation rather than derived from mast cells. Subsarcolemmal deposits in the myofibers were shown by electron microscopy to be collections of glycogen rosettes with intermixed lipid deposits. These inclusions were interpreted as secondary phenomena due to abnormal muscle energetics from restrictions in contractility, and not as evidence of a primary degeneration of the extraocular muscle fibers themselves. The sarcomeric organization of the striated muscle cells was undisturbed, and therefore the pathologic changes occurred int he interstitial space of the endomysium. A monoclonal antibody specific for neurofilaments (antibody 4.3 F9) revealed, in comparison with normal controls, a preferential loss of large-type axons of the proximal segment of the orbital portion of the optic nerve as well as in the intracanalicular portion. The axonal loss was associated with a mildly increased number of astrocytes as demonstrated by an antibody against glial fibrillary acidic protein. The meninges of the optic nerve, the orbital fat, and the tendons of the extraocular muscles were uninflamed. The foregoing findings are compatible with a compressive optic neuropathy mediated by the massively swollen extraocular muscles impinging upon the optic nerve at the orbital apex.
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8/12. A distinct form of adult polyglucosan body disease with massive involvement of central and peripheral neuronal processes and astrocytes: a report of four cases and a review of the occurrence of polyglucosan bodies in other conditions such as Lafora's disease and normal ageing.

    We have described 4 patients with progressive lower and upper motor neuron deficits, marked sensory loss in the legs, 'neurogenic bladder', and, in 2 of the 4, dementia. autopsy of two revealed a profusion of microscopic bodies resembling corpora amylacea or Lafora bodies, but restricted to processes of neurons and astrocytes. Similar (but especially large) bodies were seen within axons of sural nerves taken at biopsy from the other two patients. A general term--'polyglucosan body'--is introduced to refer to these structures in all the circumstances in which they may occur, such as in Lafora's disease, in a syndrome of longstanding double athetosis, in some cases of amyotrophic lateral sclerosis, in type IV glycogenosis, in diabetic rats, and in the normal course of ageing. Except in type IV glycogenosis, the causes for accumulation of polyglucosan bodies are unknown. They may damage tissue by more than one mechanism--probably by impeding axonal flow and impairing perivascular diffusion of metabolites.
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9/12. Intrauterine multisystem atrophy in siblings: a new genetic syndrome?

    A condition is described in two siblings, dying in early infancy, characterized by an extreme degree of cerebellar hypoplasia, hypoplasia or atrophy of the brain stem with partial preservation of cranial and spinal nerve nuclei, total degeneration of basal ganglia and thalamus, laminar atrophy of the cerebral cortex, and accumulation of sudanophil lipid in astrocytes and macrophages of the hemispheric white matter. It is suggested that this condition, possibly inherited as an autosomal recessive, may represent a progressive multisystem atrophy occurring in utero, affecting various parts of the neuraxis in different stages in their development.
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10/12. An autopsy case of atypical senile dementia with atrophy of the temporal lobes--a clinical and histopathological report.

    A man aged 70, descendant of an apparently healthy family, showed disorientation, delusional ideas and rages at 66. Later there was slowly advancing deterioration with muteness, disorientation and dysphagia. He died of cardiac failure. There was the diffuse atrophy of the cerebrum, which was remarkably accentuated on both temporal lobes (poles, T2 and T3), where the loss of nerve cells and proliferation of astrocytes were found in the cortex and pallor and conspicuous fibrillary gliosis were noted in the white matter. These findings fundamentally suggest Pick's disease. On the one hand, numerous senile plaques and Alzheimer's neurofibrillary changes, suggestive of Alzheimer's disease (senile dementia), were observed throughout the cerebral cortex. On the other hand, a few inflated cells were also seen in the cingulate, superior frontal gyri and temporal lobes. basilar artery was moderately atherosclerotic and cerebrovascular disorders were distributed throughout the cerebral cortex and basal ganglia, especially in the field of supply of middle cerebral artery. This case is similar to rare cases reported by berlin (1949), Neumann (1949) and Oyanagi et al. (1975). The nosological situation as a disease entity remains to be determined.
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