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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old man began to suffer from progressive truncal ataxia and mental alterations typical of Wernicke-Korsakoff syndrome. He showed confusional state, hallucinations, delirium of jealousy and a serious impairment of recent memory. The symptomatology lasted 13 months, but only in the last weeks was it complicated by myoclonias. Triphasic pseudoperiodic sharp-waves characterized the EEG-recordings only in the final stage. Macroscopic examination of the brain showed marked atrophy of the mammillary bodies and superior vermis. However, the histological features were consistent with Creutzfeldt-Jakob disease (CJD) with focal accentuation of the changes in the latter structures. This case supports the hypothesis that CJD-changes begin focally in the CNS and, subsequently, spread along neuronal pathways, probably via central axons. Only in the final stage does the pathological process involve most parts of the gray matter. A focal accentuation of the CJD process in the cerebello-mammillo-thalamic system caused in this case a Wernicke-Korsakoff-like syndrome.
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PMID:Creutzfeldt-Jakob disease presenting as Wernicke-Korsakoff syndrome. 151 46

An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.
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PMID:[An autopsy case of ataxic form of Creutzfeldt-Jakob disease]. 156 39

A herd of 15 mature riding horses with a history of anorexia, weight loss, and lethargy was examined. The animals had been fed a 50/50 mixture of commercial sweet feed and corn screenings contaminated with a heavy growth of Fusarium moniliforme. Thirteen of the horses had one or more neurologic signs. The most characteristic signs were profound depression and mild ataxia. Over the 19-day course of the epizootic, the horses had increasing severe neurologic deficits, including unilateral blindness and delirium. Despite the clinical appearance of dehydration, 12 horses had low PCV (16 to 27%), hematocrit (21.2 to 31.0%; determined by automated cell counter), and RBC counts (3.76 to 5.5 x 10(6) RBC/microliters). White blood cell counts were variable (4,900 to 17,000 WBC/microliters). Necropsy findings included diffuse malacia of the white matter of the frontal cortex and severe multifocal perivascular hemorrhage in the white matter of the temporal cortex, basal ganglia, anterior medulla, and pons. One horse had a hepatic lesion consisting of a mixed inflammatory cell infiltrate and bile duct proliferation. The attack rate of this epizootic was 100%. The course of disease was unusually long in some animals. In an experiment, the fusarium-infected corn screenings were fed to horses and did not cause clinical signs or alterations in blood or serum biochemical values.
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PMID:Clinical and epidemiologic features of an epizootic of equine leukoencephalomalacia. 204 19

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

Development of severe ataxia and mild pyramidal signs without mental deterioration, tetraparesis or pseudobulbar palsy during recovery from withdrawal delirium and initial hyponatraemia are unusual clinical features consistent with central pontine myelinolysis. This diagnosis was confirmed by magnetic resonance imaging (MRI) in an alcoholic man. Clinical and electrodiagnostic improvement occurred, whereas the MRI findings remained unchanged in a follow-up study.
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PMID:Cerebellar ataxia with recovery related to central pontine myelinolysis. 317 22

We describe a 37-year-old man with a 30-month history of progressive dementia, myoclonus and prominent ataxia with the additional clinical features of dysautonomia and delirious psychomotor excitement and with relatively preserved verbal responses. The pathological changes include 1) severe neuronal loss and gliosis without spongiform change of the thalamus and inferior olives associated with gliosis of the midbrain tegmentum, and demyelination and gliosis of the central tegmental tract, olivo-cerebellar fibers and spino-olivary tract, and 2) mild spongiform encephalopathy of the cerebral cortex. Although the latter implies that the present case may be an example of the rare thalamic form of Creutzfeld-Jakob disease, the preferential and severe involvement of the thalamus and inferior olives without spongiform change as well as the clinical features are quite reminiscent of primary thalamic degeneration [Stern 1939]. This case draws further attention to the relationship between spongiform encephalopathy and degeneration without spongiform change of the thalamus and olivary system.
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PMID:Degeneration of the thalamus and inferior olives associated with spongiform encephalopathy of the cerebral cortex. 329 94

In a study of enteric fever, cerebellar ataxia was found to be the commonest neurological manifestation, second only to toxic delirium. Excluding toxic delirium (found in 25-30% of cases) neurologic deficit was noted in 5.0% of a series of 718 consecutive cases; 2.3% showed cerebellar ataxia, either as an isolated feature or in association with other lesions. The ataxia usually appeared in the second week, and lasted a mean of 9.4 days. In 90% of cases it had cleared completely within a month.
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PMID:Cerebellar ataxia in enteric fever. 403 14

From the clinical point of view, the nervous system effects of alcohol are the most important when work-related problems are considered. Alcohol is a primary, descending, central nervous system depressant that causes a familiar dose-dependent progression of acute intoxication from euphoria to ataxia, stupor, and ultimately coma. Chronic effects of alcohol on the nervous system are more difficult to diagnose. Particularly an insidiously developing alcoholic psychoorganic syndrome is a very difficult problem in occupational health. The interactions of low-level, chronic exposure to solvents and heavy drinking are interesting but, unfortunately, poorly understood. Withdrawal phenomena ranging from common hangover to tremulousness, cerebral convulsions, and delirium can also severely disturb normal worklife. The multitude of factors which regulate drinking behavior among the working population provides a challenge for investigators in the field of occupational health. More research should be focused on alcohol diseases and their effects on work, the effects of work on alcohol consumption, and the interactions of alcohol and compounds present in the work environment. The first step towards these problems is the development of valid methods for the early detection of heavy drinkers among the working population.
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PMID:Alcohol, work and the nervous system. 639 13

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.
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PMID:Magnesium deficiency. Etiology and clinical spectrum. 702 Mar 47

Typical clinical signs and symptoms of bismuth intoxication are illustrated in a cases of a 45-year-old woman. Initially psychasthenia appears followed by acute delirium with ataxia, myoclonic jerks and occasionally coma. If patients survive the acute phase they recover only gradually following discontinuation of bismuth medication. In cases of extreme intoxication, permanent memory deficits may occur. Etiology, pathogenesis, laboratory findings, differential diagnosis and therapy of this rare iatrogenic encephalopathy are discussed.
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PMID:[Acute delirium in bismuth poisoning]. 713 55


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