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Results for “CEREBELLAR DISEASES”

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PubMed1981

Cerebellar degeneration with Hodgkin's disease: computed tomographic correlation and literature review.

A 62-year-old man with progressive cerebellar degeneration, corticospinal tract dysfunction, and mild dementia was found to have Hodgkin's disease. Serial computed tomographic studies revealed progressive cerebellar atrophy. The clinical features and neuroradiologic studies in nine previous cases are reviewed. A thorough search for lymphadenopathy should be made in patients with unexplained cerebellar degeneration.

Atrophy↗
PubMed1988

Ubiquitin is a common factor in intermediate filament inclusion bodies of diverse type in man, including those of Parkinson's disease, Pick's disease, and Alzheimer's disease, as well as Rosenthal fibres in cerebellar astrocytomas, cytoplasmic bodies in muscle, and mallory bodies in alcoholic liver disease.

Polyclonal antibodies were raised which have a high affinity for conjugated ubiquitin. Immunocytochemistry was performed on paraffin sections of tissues showing well-characterized inclusion bodies. Ubiquitin was found as a component of the intermediate filament inclusion bodies characteristic of several major diseases including Lewy bodies of Parkinson's disease, Pick bodies of Pick's disease, Mallory bodies of alcoholic liver disease, cytoplasmic bodies of a specific myopathy, and Rosenthal fibres within astrocytes. Ubiquitin was also present in the three histological lesions characteristic of Alzheimer's disease. These observations suggest a fundamental role for ubiquitin in the formation of intermediate filament inclusion bodies in man, and have implications regarding the pathogenesis of these important diseases.

Alzheimer Disease↗
PubMed1996

Neuroanatomical and functional alterations resulting from early postnatal cerebellar insults in rodents.

This review examines neuroanatomical and functional alterations in rodents resulting from postnatal insults during cerebellar development. Treatments such as irradiation and methylazoxymethanol (MAM) administration produced near birth (< postnatal day 8 for irradiation treatment and < postnatal day 4 for MAM administration) result in more severe cerebellar damage than do similar treatments administered several days after birth. Prominent among the more severe alterations are foliation abnormalities, misalignment of Purkinje cells and continued multiple innervation of climbing fibers; few or none of these occur as a result of later treatments (> postnatal day 8 for irradiation treatment and > postnatal day 4 for MAM treatment). The functional alterations also differ: insults produced near birth result in hypoactivity, ataxia, tremor and accompanying learning deficits, whereas those produced later result in hyperactivity and few learning deficits. This hyperactivity may have relevance to human disorders. Brief discussions of cerebellar and functional alterations (e.g., hyperactivity) resulting from neonatal infection with the Borna disease virus and induction of hypo- and hyperthyroidism during the preweaning period are also presented.

Animals↗
PubMed1976

Hereditary cerebellar cortical and extrapyramidal nuclear abiotrophy in Kerry Blue Terriers.

Ten Kerry Blue terriers from a kennel in New York and 3 from a kennel in California developed clinical signs of a progressive cerebellar disorder, with its onset between 9 and 16 weeks of age. In 9 sequential necropsies, progressive cerebellar cortical degeneration, with loss of Purkinje's cells, was demonstrated. As the disease progressed, there was bilateral symmetric degeneration of the olivary nuclei followed by degeneration of the substantia nigra and caudate nucleus, bilaterally. The California and New York dogs were related, and an autosomal recessive inheritance was proposed for the disease.

Animals↗
PubMed2000

[Continuous nursing of incurable patients at home--the case of a patient with Parkinson's disease].

At the Department of Neurology and Internal Medicine at our hospital, there are 22 outpatients who are nursed at home. Their diseases are Parkinson's disease, spinal cerebellar degeneration, dementia and other diseases. The problem is how we should care for and support these patients in the future, now that the official Care Insurance System has started. We discuss how we could support such patients, through the case of a patient suffering from Parkinson's disease. The patient was a 69-year-old female. In 1991, she developed Parkinson's disease, accompanied with trembling in her right upper limb. Her condition was controlled at our hospital. Is April 1999, she lost strength in her right thigh without any previous notice, so she was hospitalized for treatment. For a period, she became aggressive from hallucinations and delusions and she had to be taken care of all day. Her only daughter lived apart and her 72-year-old husband was also suffering from Parkinson's disease. In spite of such conditions, she hoped to receive home care and her husband accepted that. We asked what they would want us to do. We had meetings together with the staff of the local administration, doctors, nurses, and pharmacists. The report from our hospital staff says, "It may be difficult for only her family to support her. She needs other supporting systems." She came to our hospital twice a month. We made an effort to understand her condition with the help of the report of a visiting nurse. However, her illusions and delusions made it difficult even to utilize the short-stay. Her husband sometimes uses violence and says. "I can't stand this any more--her unrest, micturition at night and refusal to eat." Nevertheless, she continues to say "I want to stay at home." They have had considerable trouble. The following are necessary for home care of some patients. 1. Understanding what a patient and her family want to do. Cooperating with the staff of the administration, in consideration of the Care Insurance System. 2. Studying with incurable neurology patients using pamphlets or other materials and supporting them, 3. Discussing how to act in concert with patients at home and outpatients at the hospital involving a risk without MSW.

Aged↗
PubMed1976

Quantitative morphological studies of developing human cerebellar cortex in various disease states.

A quantitative morphological assessment was carried out of the cellularity and staining properties of the cells of the layers of the human cerebellar cortex, both in the normal child and in 41 children suffering from a series of disorders including mental retardation. A computerized image analyser and highly standardized procedures were used. All of the cases of mental retardation and some cases with congenital cardiac anomalies showed abnormal cell concentrations and staining properties. 3 cases of 'cot death' also showed abnormal results. These findings are presented as a new measurable aspect of brain disease, and as a indication for further study.

Cerebellar Cortex↗