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Results for “CEREBELLAR DISEASES”

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At least 811 records · Page 45Linked to original sources
PubMed1986

Central nervous system cysticercosis simulating an acute cerebellar hemorrhage.

We report the case of a Mexican man who suddenly developed severe occipital headache, vomiting, vertigo, and ataxia. Neurologic examination showed nystagmus and cerebellar findings. Computed tomography of the brain demonstrated a large left cerebellar cystic lesion consistent with the diagnosis of cysticercosis. The patient was treated with dexamethasone and praziquantel and required surgical removal of the lesion to prevent herniation. He recovered without neurologic sequelae. The abrupt onset of cerebellar findings is an unusual presentation of this disease. Central nervous system cysticercosis is being recognized with increasing frequency in the United States, where it is found primarily in Hispanic and Asian immigrants. The literature of central nervous system cysticercosis is reviewed and the pathogenesis, clinical presentation, and therapy are discussed.

Acute Disease↗
PubMed2002

Imaging of bilateral striopallidodentate calcinosis.

Bilateral symmetric striopallidodentate calcinosis, also known as Fahr's disease, is characterized by bilateral calcifications of the basal ganglia, thalami, dentate nuclei of the cerebellum, and the white matter of the cerebral hemisphere. Intracranial calcifications are easily visible as high-density areas on computed tomographic images. On magnetic resonance images, the calcifications exhibit different signal intensities. The differences in signal intensity are thought to be related to the stage of the disease, differences in calcium metabolism, and the volume of the calcium deposit. The moderate reduction of cerebral blood flow in bilateral thalami was also identified using brain SPECT.

Aged↗
PubMed1982

Hypothalamic and medullary lesions caused by an aliphatic triamine unrelated to goldthioglucose.

A single subcutaneous injection of 3.3'-methyliminobis-(N-methylpropylamine) caused edema and necrosis in the hypothalamus and medulla oblongata of rats, mice, and gerbils. Most other aliphatic triamines were ineffective. The lesions were very similar in character and distribution to those caused by goldthioglucose or bipiperidyl mustard. When compared to closely-related analogs, the biological activity of each of these three compounds is determined by a highly specific chemical structure, yet they have no structural similarities to each other. These data cast doubt on the theory that goldthioglucose causes lesions and, eventually, obesity by binding to a hypothalamic glucoreceptor. Alternatively, the localization of brain damage in hypothalamus and medulla has been attributed to proximity to median eminence and area postrema, and to the lack of a blood-brain barrier in the latter structures. This theory is supported by our finding that artificial disruption of blood-brain barrier in the cerebral cortex induced the localization of necrosis from the triamine in that area. Furthermore, these experiments provide evidence for the role of ischemia in the development of necrotic triamine-induced lesions.

Animals↗
PubMed1985

Contribution of CT scan to the diagnosis of Fahr's syndrome.

Of 7040 patients who were examined with CT scan for various reasons, 72 (1.02%) showed symmetrical intracranial calcifications. On the basis of the extent of the calcifications, the patients were divided into 3 groups of which the first (10 cases), with extensive calcifications, showed clear findings of hypoparathyroidism; the second (4 cases), with less extensive calcifications, showed borderline laboratory findings and the third (58 cases), with calcifications only in the internal part of the globus pallidus, had no relation to any disturbance of the parathyroid function. The limited percentage (4.2%) of calcifications detected by ordinary cranial X-rays was discussed as compared to those diagnosed by CT scan; this is due to the weakening of the relationship which existed in the past between hypoparathyroidism and calcifications. Patients with extensive calcifications do not seem to have a significantly higher proportion of neurological impairment (35.8%) than patients who showed limited calcifications (34.5%). On the other hand, patients with extensive calcifications showed more frequent mental disorders (50%) compared to those who showed limited calcifications (34.5%). The proportion of mental disorders is still higher in patients with dilatation of the subarachnoid spaces (56.7%) compared to those who do not show dilatation (23.8%). Finally, of the 72 patients with calcifications, 15 (20.8%) showed extrapyramidal syndrome, possibly due to calcium salt deposits in the metasynaptic dopamine receptors while 13 (18%) were taking anticonvulsant drugs which, apart from influencing the metabolism of calcium, also influence the activity of alkaline phosphatase and are involved in the creation of calcifications.

Adult↗
PubMedDate not supplied

Diagnosis of retrocochlear and central vestibular disease by magnetic resonance imaging.

Magnetic resonance imaging has become the study of choice for the diagnosis of retrocochlear and central vestibular disease. Three groups of lesions, each characterized by a specific site of origin, have been recognized: 1) petrous apex lesions such as congenital cholesteatomas and cholesterol granulomas involving the eighth cranial nerve within the internal auditory canal; 2) cerebellopontine angle tumors, mainly acoustic neuromas and meningiomas; and 3) CNS disease involving the brain stem and the central auditory and vestibular pathways such as tumors, multiple sclerosis, infarcts, and hemorrhage.

Auditory Diseases, Central↗
PubMed1982

Joseph disease: a multisystem degenerative disorder of the nervous system.

We studied Joseph disease clinically and pathologically in two patients of Portuguese ancestry, but from different families. We found involvement of spinocerebellar tracts, Clarke's column, anterior horn cells, motor cranial nerve nuclei, and substantia nigra. One patient also had pallidosubthalamic and pontocerebellar degeneration with normal inferior olives. The second patient, a Joseph family member, had nerve cell loss in the subthalamic nucleus. The neostriatum appeared normal in both cases. The pigmented nuclei contained a few Lewy bodies. The almost identical pathology in two families support the hypothesis that Joseph disease is a genetic entity.

Adult↗
PubMed1994

The effect of uvulonodular lesions on horizontal optokinetic nystagmus and optokinetic after-nystagmus in cats.

The effect of uvulonodular lesions on horizontal optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) was investigated in alert cats. A lesion in each of 6 cats was made by suction-ablation under anesthesia. In the 3 cats with only a uvular lesion, both the initial slow phase velocity and the time constant of OKAN were unchanged. In the remaining 3 cats whose lesions included the nodulus as well as the uvula, the time constant of OKAN was markedly prolonged, but the initial slow phase velocity of OKAN was not affected. The postoperative average time constant of OKAN increased from the normal value of 9 s to about 40 s. In contrast, OKN parameters (the steady-state velocity and the rising time constant) were not affected by uvular or uvulonodular lesions. These results strongly suggest that the nodulus is involved in the velocity storage mechanism and might control the discharge characteristics of the velocity storage integrator.

Animals↗