Cases reported "Parkinson Disease"

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1/827. Transplant of cultured neuron-like differentiated chromaffin cells in a Parkinson's disease patient. A preliminary report.

    BACKGROUND: Treatment of Parkinson's Disease (PD) has been attempted by others by transplanting either the patient's own adrenal medullary tissue or fetal substantia nigra into caudate or putamen areas. However, the difficulties inherent in using the patient's own adrenal gland, or the difficulty in obtaining human fetal tissue, has generated the need to find alternative methods. methods: We report here of an alternative to both procedures by using as transplant material cultured human adrenal chromaffin cells differentiated into neuron-like cells by extremely low frequency magnetic fields (ELF MF). RESULTS: The results of this study show that human differentiated chromaffin cells can be grafted into the caudate nucleus of a PD patient, generating substantial clinical improvement, as measured by the Unified Rating Scale for PD, which correlated with glucose metabolism and D2 DA receptor increases as seen in a PET scan, while allowing a 70% decrease in L-Dopa medication. DISCUSSION: This is the first preliminary report showing that transplants of cultured differentiated neuron-like cells can be successfully used to treat a PD patient.
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2/827. Improvement of depression and parkinsonism during ECT: a case study.

    Improvement in signs of parkinsonism and symptoms of depression was observed in a patient with Parkinson's disease who underwent a course of ECT for depression. Empirically this patient was observed by a blind rater to show a pattern of improvement in parkinsonian signs similar to that observed in parkinsonian patients treated with L-dopa. The time course of improvement of this patient's depression was also seen to parallel improvement in his Parkinson's disease. These results are consistent with the hypothesis that ECT increases catecholamine synthesis and more specifically would be evidence that ECT improves depression by increasing norepinephrine synthesis.
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3/827. Postural hypotension in idiopathic Parkinson's disease. Etiopathology.

    Postural changes in blood pressure were recorded in all 391 patients suffering from Parkinson's syndrome over a period of six years. Intraarterial blood pressure studies were carried out in those with significant postural hypotension. Histological examination of the entire central nervous system and the sympathetic ganglia was performed in six patients suffering from idiopathic Parksinson's disease. Five of the six patients had lewy bodies in the sympathetic ganglia. Loss of nerve cells was noted in the sympathetic ganglia in those patients that demonstrated postural hypotension. The severity of the lesions in the ganglia correlated with the severity of postural hypotension in idiopathic Parkinson's disease, One case of shy-drager syndrome was similarly studied to demonstrate the differences in spinal cord and sympathetic ganglia lesions in the two conditions.
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4/827. Selected legal issues in movement disorders.

    This article explores the long-standing question of whether trauma causes Parkinson's disease, and discusses the impact of informed consent and confidentiality in issues of genetic testing for Huntington's disease. Neurologists are appropriately concerned about the legal aspects of genetic testing, and this article attempts to address that subject from a medical-legal perspective.
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5/827. Lymphoedema, lymphatic microangiopathy and increased lymphatic and interstitial pressure in a patient with Parkinson's disease.

    New microvascular findings in a woman with Parkinson's disease and lower leg oedema are presented. Microlymphography showed enhanced filling of the microlymphatic network with the fluorescent contrast medium comparable to the findings in lymphoedema. The microlymphatic and interstitial pressures of the skin were increased (27 mm Hg and 16 mm Hg respectively). The increased interstitial and microlymphatic pressures are the result of insufficient venous and lymphatic drainage due to impairment of calf muscle function during walking in Parkinson's disease. Manual lymph drainage and compression therapy, in combination with improvement of calf muscle function, resulted in regression of the oedema.
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6/827. Tau pathology in a family with dementia and a P301L mutation in tau.

    Familial forms of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) have recently been associated with coding region and intronic mutations in the tau gene. Here we report our findings on 2 affected siblings from a family with early-onset dementia, characterized by extensive tau pathology and a Pro to Leu mutation at codon 301 of tau. The proband, a 55-year-old woman, and her 63-year-old brother died after a progressive dementing illness clinically diagnosed as alzheimer disease. Their mother, 2 sisters, maternal aunt and uncle, and several cousins were also affected. autopsy in both cases revealed frontotemporal atrophy and degeneration of basal ganglia and substantia nigra. Sequencing of exon 10 of the tau gene revealed a C to T transition at codon 301, resulting in a Pro to Leu substitution. Widespread neuronal and glial inclusions, neuropil threads, and astrocytic plaques similar to those seen in corticobasal degeneration were labeled with a battery of antibodies to phosphorylation-dependent and phosphorylation-independent epitopes spanning the entire tau sequence. Isolated tau filaments had the morphology of narrow twisted ribbons. Sarkosyl-insoluble tau exhibited 2 major bands of 64 and 68 kDa and a minor 72 kDa band, similar to the pattern seen in a familial tauopathy associated with an intronic tau mutation. These pathological tau bands predominantly contained the subset of tau isoforms with 4 microtubule-binding repeats selectively affected by the P301L missense mutation. Our findings emphasize the phenotypic and genetic heterogeneity of tauopathies and highlight intriguing links between FTDP-17 and other neurodegenerative diseases.
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7/827. An interdisciplinary home healthcare program for patients with Parkinson's disease.

    The long-term treatment of Parkinson's disease presents a special challenge in the home healthcare setting. This article describes a successful interdisciplinary home healthcare program that addresses the special needs of patients with Parkinson's disease and associated disorders. The program, which combines skilled assessment, professional healthcare services, patient and family education, and case management to optimize patient outcomes, has become a national model for agencies hoping to start or expand Parkinson's disease programs.
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8/827. essential tremor in Papua, New Guinea.

    The clinical features of 175 cases of essential tremor are related. This disorder is prevalent among a population of the Eastern Highlands of papua new guinea. It affects predominantly women in middle and old age; only 27 per cent of the cases were males. The disorder is slowly progressive and significant disability appears in elderly women when the trunk muscles are involved. Epidemiological studies have shown that the presence of tremor can be correlated with linguistic distinctions between high and low prevalence populations. Although only 30 patients reported a first degree relative with tremor, the syndrome would seem to stem from a genetic predisposition. In a number of patients essential tremor appeared to be associated with Parkinson's disease.
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9/827. Immunohistochemical and subcellular localization of Parkin protein: absence of protein in autosomal recessive juvenile parkinsonism patients.

    Autosomal recessive juvenile parkinsonism (AR-JP) is a distinct clinical entity characterized by a selective degeneration of nigral neurons. Recently, the parkin gene responsible for AR-JP has been identified. Now, we report the subcellular localization of Parkin protein in patients with AR-JP or Parkinson's disease (PD) and in controls by immunoblotting and immunohistochemistry using antibodies raised against the Parkin molecule. Parkin protein was absent in all regions of the brains of patients with AR-JP. Parkin protein was not decreased in the brains of sporadic PD patients. Immunoreactivity was detected in a few lewy bodies. Parkin protein was located in both the Golgi complex and cytosol.
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10/827. Developmental stuttering and Parkinson's disease: the effects of levodopa treatment.

    The effects of dopamine on developmental stuttering was studied in a 44 year old man with developmental stuttering and Parkinson's disease during three levodopa "on" periods and three "off" periods. When compared with the "off" periods, during the "on"' periods he demonstrated an increase of speech dysfluencies. These findings lend support to the dopamine hypothesis of developmental stuttering.
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