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Results for “CEREBELLAR DISEASES”

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At least 847 records · Page 47Linked to original sources
PubMed1980

Dependence of reaction times on movement patterns in patients with Parkinson's disease and those with cerebellar degeneration.

Premotor times (PMTs) of both biceps muscles in flexion and supination of the forearms were examined in 13 patients with Parkinson's disease (PD), 10 with cerebellar degeneration (CD) and 14 control subjects. Compared with the control, PMT of CD increased definitely but that of PD was within normal range. The difference of PMTs between flexion and supination was lost in PD, but not in CD. It is assumed that the basal ganglia and the right cerebral cortex are functioning for the selection of movement patterns at the initiation of movements.

Adult↗
PubMed1980

Levels of gamma-aminobutyric acid in cerebrospinal fluid in various neurologic disorders.

Levels of gamma-aminobutyric acid (GABA) in CSF were measured by the ion exchange-fluorometric method in 136 patients who underwent evaluation for neurologic disorders. In 19 patients with no organic neurologic or mental disorders who acted as normal controls, the mean (+/-SD) GABA level in CSF was 239 +/- 76 picomoles/mL. Patients with acute hypoxic encephalopathy showed a mean GABA level in CSF higher than that of the controls, a difference that was statistically significant. In all the other disorders studied, the mean GABA level in CSF was either equal to or lower than that found in the controls. Statistically significant reductions of the GABA level in CSF were seen in patients with Huntington's disease, dementias, cerebellar cortical atrophy, multiple sclerosis, epilepsy, and Parkinson's disease.

Brain Chemistry↗
PubMed1989

Paraneoplastic subacute cerebellar degeneration in Hodgkin's disease. Report of three cases and review of the literature.

12 cases of paraneoplastic cerebellar degeneration with Hodgkin's disease have so far been reported. Three additional patients (Stage II-IA/IIA/IIIB) are presented. Although CT and MR-imaging (MRI) revealed a marked cortical atrophy of the cerebellum, there was no evidence of direct brain involvement. After irradiation and chemotherapy all patients showed a complete remission. There was no evidence of primary disease after an observation period of 3/2/5 years. Cerebellar symptoms also showed a partial remission. As compared to the literature, our treatment appears to be more favorable, probably due to the fact, that therapy was more aggressive than usual.

Adult↗
PubMed1978

Aspirin, hyperventilation, and cerebellar infarction in sickle cell disease.

Aspirin ingestion was followed by hyperventilation, cerebellar signs, and fatal brain stem dysfunction in a patient with sickle cell disease. Autopsy showed a swollen, recently infarcted cerebellum with tonsillar herniation compressing the medulla. We propose that hypocapnea from aspirin-induced hyperventilation caused carotid artery constriction and focal cerebral hypoxia, resulting in cerebellar sickling nad infarction. Hypocapnea should be treated promptly to prevent brain damage in patients with sickle cell disease.

Adult↗
PubMed1985

Autoimmune response of patients with paraneoplastic cerebellar degeneration to a Purkinje cell cytoplasmic protein antigen.

Sera from 6 of 12 patients with paraneoplastic cerebellar degeneration (PCD) contained anti-Purkinje cell antibodies, as determined by indirect immunofluorescence on frozen sections of normal human cerebellum. Samples of cerebrospinal fluid from 2 of the patients with serum antibodies were tested, and both specimens contained anti-Purkinje cell antibody. The anti-Purkinje cell antibodies were polyclonal, fixed complement, and were present in all patients at serum dilutions of 1:1,000 or greater. Antibody activity could not be suppressed by preabsorption of sera with human or animal brain and tissue powders or with fresh crude human cerebellar extracts. No anti-Purkinje cell antibodies were detected in control sera from 167 neurologically normal cancer patients, 32 normal volunteers, 10 patients with other causes of cerebellar degeneration, or 8 patients with other paraneoplastic neurological diseases. Preliminary evidence suggests that the Purkinje antigen is a protein that is often concentrated in the periphery of the cytoplasm in disc-shaped structures. Patients with antibodies often developed signs of PCD near the time of detection of the tumor and had relentless progression of neurological disease. Patients without antibodies frequently had cancer for months to years before PCD developed, and often had spontaneous stabilization of neurological disease with time. Four patients without and 3 patients with antibodies underwent plasmapheresis without response.

Aged↗
PubMed1985

Giant invasive cholesteatoma. Report of a case with cerebellar invasion.

We present a case of epidermoid cholesteatoma that killed the patient by relentless invasion, despite radical surgery. An autopsy disclosed a focus of dural and cerebellar invasion, which dramatized the aggressive nature of this disease. In fact, the epithelial cells of this disease are not thought to possess the ability to invade. Instead, inflammation is believed to both stimulate the squamous epithelial cells to proliferate and destroy adjacent tissues, thereby providing a pathway for epithelial cell migration. Epidermoid cholesteatoma, then, is a disease in which the processes of inflammation and hyperplasia combine to mimic a neoplasm.

Bone Diseases↗
PubMed2003

The natural history of cerebellar hemangioblastomas in von Hippel-Lindau disease.

BACKGROUND AND PURPOSE: Cerebellar hemangioblastomas (HBs) are traditionally classified into different morphologic types: cystic and solid. We have observed the progression from solid to cystic and have reviewed the cases seen at the regional von Hippel-Lindau (VHL) clinic to document the frequency of this progression. METHODS: A retrospective review of the notes and images of all patients with VHL disease seen at a regional referral clinic since its inception in 1991. Sporadic HBs were not included in this study. RESULTS: In eight patients, a total of 28 tumors were detected. Fourteen of these had or developed cysts. Of the 14 cystic tumors, eight increased in size over the follow-up period. Of the 14 solid tumors, only one increased in size without cystic change. In four patients, the tumor progressed from a cerebellar nodule to an enlarging cyst with a nodule, with the subsequent development of symptoms requiring surgical excision. CONCLUSION: We have demonstrated that, in VHL, cerebellar HBs begin as nodules, and some subsequently develop enlarging cysts that cause pressure symptoms. In our patient population, tumors that remained solid were asymptomatic and well tolerated in the cerebellum.

Adult↗
PubMed2002

Presymptomatic testing in Huntington's disease and autosomal dominant cerebellar ataxias.

OBJECTIVE: To report a 7-year experience of presymptomatic testing in persons at risk for Huntington disease (HD) and to compare their characteristics and outcomes with those of persons at risk for a less disabling condition, autosomal dominant cerebellar ataxias (ADCA). METHODS: The authors collected data on presymptomatic testing for HD (n = 712) and ADCA (n = 46) in 10 French centers. RESULTS: The characteristics of applicants were similar in HD and ADCA, revealing a predominance of women, a low rate of completing the presymptomatic testing program, and a high rate of follow-up. The frequency of serious events was low (2% for HD, 5% for ADCA), but such events were also found after favorable results. Family planning was a more frequent reason for seeking presymptomatic testing in ADCA than in HD. Prenatal diagnosis was performed in only half of the pregnancies in HD carriers (n = 35) but in all of those in ADCA carriers (n = 4). CONCLUSION: Counseling in multistep and multidisciplinary teams is important not only for presymptomatic testing in HD but also for less disabling diseases.

Adolescent↗
PubMed1993

Cerebrospinal fluid 28-kDa calbindin-D as a possible marker for Purkinje cell damage.

To examine the clinical value of 28-kDa calbindin-D (CaBP) in cerebrospinal fluid (CSF) as a marker for the damage to Purkinje cells, we measured CSF CaBP levels using an enzyme immunoassay method in 107 patients with cerebellar and other neurological diseases, and 26 controls. The mean CaBP level was markedly elevated in patients with cerebellar diseases, and the elevation of CaBP level was more frequent in the diseases involving Purkinje cells, such as multiple system atrophy (MSA) and subacute cerebellar degeneration in association with lung cancer. Further, in MSA patients, the CaBP levels decreased with duration of illness. The mean levels of CaBP were also elevated in some of the other diseases. We conclude that the elevations of CaBP levels are not specific for cerebellar diseases, but CSF CaBP may be a useful marker for examining the Purkinje cell involvement in cerebellar diseases.

Adolescent↗