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Results for “CEREBELLAR DISEASES”

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At least 91 records · Page 5Linked to original sources
PubMed1994

Conditional associative learning is impaired in cerebellar disease in humans.

Eight patients with lesions restricted to the cerebellum were compared with a total of 25 age-matched controls on a reaction time (RT) task allowing the recording of simple and choice RTs as well as RTs to abstract visual patterns signifying the particular movement to be performed. In all conditions the actual movements required (either a left or a right button press) remained the same, but the cognitive requirements of the task varied. In the abstract patterns condition, the significance of the various patterns with regard to the required movement had to be learned by the subjects. The patients with cerebellar lesions were particularly impaired in this condition. It is concluded that the cerebellum is involved not just in the timing of movements but also in the decision process as to which movement should be performed under particular circumstances.

Adult↗
PubMed2004

Cerebellar disease and disease characterized by dysmetria or tremors.

Diseases of the cerebellum and diseases that cause signs of dysmetria or tremors occur infrequently in ruminants. A thorough neurologic examination should be performed to attempt to localize the lesion. A list of differential diagnoses can be organized in rank order based on the location of the lesion and the signalment, history,and results of physical examination. A definitive diagnosis is based on the results of diagnostic testing, response to treatment,or postmortem examination.

Animals↗
PubMed1977

Prevention of virus-induced cerebellar diseases by defective-interfering lymphocytic choriomeningitis virus.

Defective-interfering (DI) lymphocytic choriomeningitis virus (LCMV) prevented disease in the central nervous system produced by standard LCMV. Standard LCMV injected into Lewis rats two days after birth produced a disorder distinguishable clinically by weight loss and ataxia and histologically by infiltration of mononuclear cells and necrosis of the cerebellum. Concurrent injection of DI LCMV with standard LCMV prevented the disease and markedly reduced the synthesis of standard LCMV and of viral antigens in the brain. Because inhibition of viral synthesis occurred early (day 3) after infection and because no interferon activity could be demonstrated, it was concluded that the interference effect was likely due to DI virus-mediated homologous interference. Other experiments showed that DI LCMV blocked viral antigen synthesis in culture. The curtailed production of viral antigens and cytolytic standard virus by DI virus may play a role in control of acute and persistent viral infections.

Animals↗
PubMed1990

[Clinical and diagnostic considerations on degenerative spino-cerebellar diseases. A clinical and instrumental description of 2 cases].

Two cases of spino-cerebellar heredoataxia are reported. The first patient, aged 18, presented the clinical peculiarities of Friedreich's disease; subjected to encephalic CT and encephalomedullary NMR the proved normal; EMG study and visual, acoustic and somatosensorial evoked potentials were not normal but there was nothing specifically wrong. The second patient, aged 30, followed up for more than 10 years, presented the clinical aspects of Pierre Marie disease; stress is laid on encephalic CT examinations carried out at the age of 20 and 30. These were pathological due to the marked dilatation of the IVth ventricle and the basal cisternae; evoked potential changes were aspecific. The nosography is discussed, especially as regards clinical diagnosis, in the absence of typical neuroradiological or other instrumental aspects and, obviously, in the absence of anatomopathological signs.

Adult↗
PubMed1981

Stumbler, a new mutant mouse with cerebellar disease.

A new mutant mouse named Stumbler (stu) displays clinical features suggesting a cerebellar lesion. The main light microscopic findings, based on a Golgi technique and on sections of plastic embedded material, are that Purkinje cells in the mutant cerebellum have small dendritic arborizations and exhibit immature spines on their somata. Purkinje cells also contain an increased number of mitochondrial profiles both in cell bodies and in swellings on dendrites.

Animals↗
PubMed1997

Machado-Joseph disease: cerebellar ataxia and autonomic dysfunction in a patient with the shortest known expanded allele (56 CAG repeat units) of the MJD1 gene.

We describe an unusual case of a patient with Machado-Joseph disease (MJD) who showed autonomic dysfunctions in addition to cerebellar ataxia. The number of CAG repeat units in the expanded allele of the MJD1 gene of the patient is smaller (56 CAG repeat units) than all previously reported numbers of CAG repeat units in expanded alleles. Thus, the findings in this patient indicate that the clinical features of MJD cover a wider spectrum than previously thought.

Alleles↗
PubMed1999

Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy.

Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy. In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy had a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalopathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.

Adult↗
PubMed1991

Single photon emission computed tomography (SPECT) in cerebellar disease: cerebello-cerebral diaschisis.

Single photon emission computed tomography assessments were conducted in normal controls (n = 25), patients with unilateral cerebellar infarctions (n = 4), patients with olivopontocerebellar atrophy (OPCA; n = 15) and patients with Friedreich's ataxia (FA; n = 6). In subjects with unilateral cerebellar infarctions, crossed cerebellar-cortical diaschisis was observed: reduced cerebellar hexamethylpropyleneamine oxime (HMPAO) uptake was invariably accompanied by a diminution of HMPAO in the contralateral basal ganglia and frontoparietal cortex. OPCA and FA patients had various degrees of decreased HMPAO uptake in both the cerebellum and cerebral hemispheres.

Adult↗
PubMed1978

[Oculomotor signs in cerebellar disease shown in ataxia telangiectasia (Louis Bar) (author's transl)].

Disturbances of the eye movements are described in 2 brothers with ataxia telangiectasia (Louis Bar): pathological smooth pursuit and command movements of the eyes (hypometry) with a preseved doll's phenomenon, increased reaction times of voluntary saccades, failure of gaze holding, gaze nystagmus, altered optokinetic nystagmus, and distinct convergence defect. These oculomotor defects are the result of cerebellar lesions. The E.N.G.-findings in pathologically changed pursuit movements are in accordance with those disturbances of eye movements shown by Westheimer and Blair in cerebellectomized monkeys.

Animals↗
PubMedDate not supplied

Task-based profiles of the dysarthrias.

The dysarthrias are associated with a variety of motor disturbances distributed over several motor systems of speech production. The features of a given dysarthria often vary with the speaking task, and this task-dependency affords insights into the responsible neural lesion and its effects on the motor regulation of speech. Each task also is amenable to quantitative analyses with acoustic or physiologic methods, and these analyses may redefine the value of these speaking tasks. This article considers task-based analyses for the dysarthrias associated with Parkinson's disease, cerebellar disease, and stroke.

Brain Infarction↗
PubMed1990

Microglia in cerebellar plaques in Alzheimer's disease.

Cerebellar amyloid deposits in Alzheimer's disease were studied by immunocytochemistry and with a series of antibodies that recognize human microglia, including anti-HLA-DR, LN-1, Leu-M5 and leukocyte common antigen. Microglia formed a dense reticular array throughout the cerebellum in areas with and without amyloid deposits. In areas with compact and reticular amyloid deposits, microglia had morphological features consistent with activation, such as cytoplasmic swelling and shortening and thickening of cell processes. In areas with diffuse amyloid deposits, microglia had delicate and highly ramified processes. Nevertheless, microglial cells or their processes were detected in association with amyloid deposits of all morphological types. These results raise the possibility that microglia may play a fundamental role in the pathogenesis of amyloid deposition in the cerebellum in Alzheimer's disease.

Aged↗