Cases reported "Atrophy"

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1/16. glucocorticoids and hippocampal atrophy after heart transplantation.

    The glucocorticoid cascade hypothesis proposes that hippocampal atrophy may result from excessive steroid exposure. Although demonstrated in animal models and some human hypercortisolemic states, hippocampal damage as a possible consequence of posttransplant steroid immunosuppression has not been investigated in human heart transplant recipients. We report a case of a 37-year-old female heart transplant recipient who had the clinical, neuropsychiatric, and neuroimaging findings consistent with hippocampal atrophy after 5 years of steroid exposure.
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2/16. knowledge of the human body: a distinct semantic domain.

    BACKGROUND: patients with selective deficits in the naming and comprehension of animals, plants, and artifacts have been reported. These descriptions of specific semantic category deficits have contributed substantially to the understanding of the architecture of semantic representations. OBJECTIVE: This study sought to further understanding of the organization of the semantic system by demonstrating that another semantic category, knowledge of the human body, may be selectively preserved. methods: The performance of a patient with semantic dementia was compared with the performance of healthy controls on a variety of tasks assessing distinct types of body representations, including the body schema, body image, and body structural description. RESULTS: Despite substantial deficits on tasks involving language and knowledge of the world generally, the patient performed normally on all tests of body knowledge except body part naming; even in this naming task, however, her performance with body parts was significantly better than on artifacts. CONCLUSIONS: The demonstration that body knowledge may be preserved despite substantial semantic deficits involving other types of semantic information argues that body knowledge is a distinct and dissociable semantic category. These data are interpreted as support for a model of semantics that proposes that knowledge is distributed across different cortical regions reflecting the manner in which the information was acquired.
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3/16. ketamine for refractory status epilepticus: a case of possible ketamine-induced neurotoxicity.

    A 44-year-old man with treated neurosyphilis presented with subclinical status epilepticus (SE) refractory to intravenous high-dose lorazepam, phenytoin, and valproic acid over 4 days. ketamine infusion was instituted after low-dose propofol sedation with gradual control of electrographic seizures over 72h. Reevaluation 3 months later revealed diffuse cerebellar and worsened cerebral atrophy, consistent with animal models of N-methyl-D-aspartate antagonist-mediated neurotoxicity. Animal studies of prolonged ketamine therapy are required before widespread human use in SE.
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4/16. Dissociating person-specific from general semantic knowledge: roles of the left and right temporal lobes.

    The cognitive architecture and neural underpinnings of different semantic domains remains highly controversial. We report two patients with focal temporal lobe atrophy who presented with contrasting and theoretically informative dissociations of person-specific versus general semantic knowledge. Subject J.P. showed severely impaired person-specific semantics, with relative preservation of knowledge about objects and animals, while subject M.A. exhibited the opposite pattern of performance (good knowledge of people in the context of impoverished general semantics). Voxel-based morphometric analysis of MR images in the two cases established predominantly right temporal atrophy associated with J.P.'s deficit for person knowledge and predominantly left temporal atrophy in M.A. who was impaired in general conceptual knowledge.
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5/16. Semantic dementia. Progressive fluent aphasia with temporal lobe atrophy.

    We report five patients with a stereotyped clinical syndrome characterized by fluent dysphasia with severe anomia, reduced vocabulary and prominent impairment of single-word comprehension, progressing to a stage of virtually complete dissolution of the semantic components of language. A marked reduction in the ability to generate exemplars from restricted semantic categories (e.g. animals, vehicles, etc.) was a consistent and early feature. Tests of semantic memory demonstrated a radically impoverished knowledge about a range of living and man-made items. In contrast, phonology and grammar of spoken language were largely preserved, as was comprehension of complex syntactic commands. reading showed a pattern of surface dyslexia. Autobiographical and day-to-day (episodic) memory were relatively retained. Non-verbal memory, perceptual and visuospatial abilities were also strikingly preserved. In some cases, behavioural and personality changes may supervene; one patient developed features of the kluver-bucy syndrome. Radiological investigations have shown marked focal temporal atrophy in all five patients, and functional imaging by single positron emission tomography and positron emission tomography (one case) have implicated the dominant temporal lobe in all five. In the older literature, such cases would have been subsumed under the rubric of Pick's disease. Others have been included in series with progressive aphasia. We propose the term semantic dementia, first coined by Snowden et al. (1989), to designate this clinical syndrome.
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6/16. Neuropathological, biochemical and molecular findings in a glutaric acidemia type 1 cohort.

    Glutaric acidemia type 1 (GA-1) is an autosomal recessive disorder characterized by a deficiency of glutaryl-coa dehydrogenase (GCDH) activity. GA-1 is often associated with an acute encephalopathy between 6 and 18 months of age that causes striatal damage resulting in a severe dystonic movement disorder. Ten autopsy cases have been previously described. Our goal is to understand the disorder better so that treatments can be designed. Therefore, we present the neuropathological features of six additional cases (8 months-40 years), all North American aboriginals with the identical homozygous mutation. This cohort displays similar pathological characteristics to those previously described. Four had macroencephaly. All had striatal atrophy with severe loss of medium-sized neurons. We present several novel findings. This natural time course study allows us to conclude that neuron loss occurs shortly after the encephalopathical crisis and does not progress. In addition, we demonstrate mild loss of large striatal neurons, spongiform changes restricted to brainstem white matter and a mild lymphocytic infiltrate in the early stages. Reverse transcriptase-PCR to detect the GCDH mRNA revealed normal and truncated transcripts similar to those in fibroblasts. All brain regions demonstrated markedly elevated concentrations of GA (3770-21 200 nmol/g protein) and 3-OH-GA (280-740 nmol/g protein), with no evidence of striatal specificity or age dependency. The role of organic acids as toxic agents and as osmolytes is discussed. The pathogenesis of selective neuronal loss cannot be explained on the basis of regional genetic and/or metabolic differences. A suitable animal model for GA-1 is needed.
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7/16. How Berlusconi keeps his face: a neuropsychological study in a case of semantic dementia.

    A patient (V.Z.) is described as being affected by progressive bilateral atrophy of the mesial temporal lobes resulting in semantic dementia. Vis-a-vis virtually nil recognition of even the most familiar faces (including those of her closest relatives) as well as of objects and animals, V.Z. could nevertheless consistently recognize and name the face of Silvio Berlusconi, the mass media tycoon and current Italian Prime Minister. The experimental investigation led to the conclusion that Mr Berlusconi's face was seen as an icon rather than as a face. This telling effect of Mr Berlusconi's pervasive propaganda constitutes an unprecedented case in the neuropsychological literature.
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8/16. Transient brain shrinkage in infantile spasms after ACTH treatment. Report of two cases.

    This is the report of two cases of infantile spasms, manifesting transient brain shrinkage in computerized tomography (CT) after ACTH treatment. ACTH was given for 8 weeks to a 8-months-old Japanese girl with infantile spasms. First CT performed at 2 weeks after the final ACTH injection, displayed moderate brain shrinkage. Second CT at 4 months showed marked diminution of the shrinkage. ACTH was also given for 8 weeks to a 14 months old Japanese boy with infantile spasms. First CT, just before ACTH treatment, showed mild cortical atrophy, the second at 7 days after the final ACTH injection revealed marked brain shrinkage and moderate ventricular dilatation, and the third at 2 months, disclosed mild improvement of the shrinkage. ACTH or corticoateroid has widespread effects on the developing nervous system. In animal experiments, ACTH or steroids interfere with brain growth of young rats. CT findings of transient brain shrinkage in a child with infantile spasms might suggest that intensive treatment with ACTH or steroids in infancy interferes with brain growth as seen in the results of animal experiments.
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9/16. Conventional and human insulin: complications of insulin therapy in children.

    The management of complications of insulin therapy, such as lipoatrophy, allergic reactions, insulin resistance, and insulin edema, is outlined. Human and animal insulin preparations currently available in the united states are discussed, highlighting the comparative costs and indications for use.
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10/16. GM1 gangliosidosis, type 2: ocular clinicopathologic correlation.

    The clinical and pathological manifestations of a case of juvenile GM1 gangliosidosis are presented and the pathological findings compared with those previously reported for GM1 gangliosidosis in man and in animal models. The most striking finding in the present case was the marked degeneration of the retinal ganglion cell and nerve fiber layers. Although such extensive ganglion cell loss was not observed in any of the other cases reviewed, the presence of multimembranous inclusion bodies in retinal ganglion cells strongly suggests that the pathological process was similar in all cases. Much remains to be learned about the function of gangliosides in the healthy retina and about the pathophysiological consequences of deranged ganglioside metabolism. The many parallels, including those observed in pathological studies, between the human and animal forms of GM1 gangliosidosis allow an optimistic appraisal of the value of further research using the animal models.
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