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

The purpose of the present study was to design a standard battery of tests capable of quantitatively characterizing ataxia and concomitant neurological signs in the rat. In addition to a systematic analysis of the walking gait of animals, tests for activity, catalepsy, rigidity and various reflexive responses were included in the battery. The standardization of the test system was performed by determining and comparing neurobehavioral effects produced by 3-acetyl pyridine, acrylamide, pyrithiamine and thiamine deficiency, four experimental treatments reported to induce ataxia in animals. Results indicate that profiles of neurobehavioral disturbances accompanying ataxia in animals varied distinctively with each experimental treatment.
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PMID:Comparison of neurobehavioral effects induced by various experimental models of ataxia in the rat. 29 76

In the course of multiple episodes of thiamine deficiency in the rhesus monkey, the triad of anorexia, apathy, and hind limb weakness is the earliest clinical manifestation. In later episodes, nystagmus, abducens paresis, midline ataxia, dysmetria, and congestive heart failure are also seen. With the exception of dysmetria, the neurologic signs promptly respond to thiamine administration. Pair-fed controls showed no clinical signs. Neither peripheral neuropathy nor edema was observed. Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.
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PMID:Clinical manifestations of chronic thiamine deficiency in rhesus monkey. 40 80

The purpose of the present study was to design a standard battery of tests capable of quantitatively characterizing ataxia and concomitant neurological signs in the rat. In addition to a systematic analysis of the walking gait of animals, tests for activity, catalepsy, rigidity, and various reflexive responses were included in the battery. The standardization and validation of the test system was performed by determining and comparing profiles of neurobehavioral effects produced by 3-acetyl pyridine, acrylamide, pyrithiamine, and thiamine deficiency, four experimental treatments reported to induce ataxia in animals. Results indicate that profiles of neurobehavioral disturbances accompanying ataxia in animals varied distinctively with each experimental treatment.
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PMID:Measurement of ataxia and related neurological signs in the laboratory rat. 48 13

Wernicke-Korsakoff's syndrome (W.K.S.) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, ataxia and disorder of retentive memory. The disease results from deficiency of vitamin B1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. We report a seriously ill, nonalcoholic surgical patient, who developed W.K.S. in the postoperative period as a result of thiamine deficiency, during prolonged intravenous therapy. It is recommended that malnourished patients receive 100 mg parenteral thiamine especially when glucose infusions are administered.
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PMID:[Wernicke-Korsakoff syndrome caused by prolonged infusion therapy during the postoperative period]. 181 4

Wernicke encephalopathy and Korsakoff psychosis are two facets of the same disease with well-determined cerebral lesions caused by thiamine deficiency. The disease occurs mainly in alcoholics, but other conditions (malabsorption or severe malnutrition) also predispose to the risk of Wernicke-Korsakoff syndrome. The incidence in Denmark is unknown. In the period 1.1.1979-31.12.1988, 24 patients (18 men and six women) were discharged from Rigshospitalet with the diagnosis Wernicke encephalopathy or Korsakoff psychosis. This represents about 0.05% of all admissions in the period. Eighteen out of the 24 cases (75%) were admitted in the past three years (1986-88). The mean age was 55 years. Twenty patients admitted alcohol abuse. The presenting symptoms and the patients' complaints showed great variety and were often related to other alcoholic complications, which could mask the disease. The classic symptom combination: eye movement abnormalities- ataxia and disorders of consciousness were found in seven patients (29%). Sixteen patients had disorders of consciousness or orientation. All the patients were treated with thiamine. The eye-movement disorder has recovered in eight out of ten known cases (80%), nystagmus--in six out of seven cases (86%) while ataxia, disorders of orientation and confabulation recovered in about 50% of cases. The average duration of hospitalisation was 50 days. Altogether nine patients died during the observation period. The condition is most probably underdiagnosed and the traditional diagnostic criteria are considered too rigid. The diagnosis should be considered in alcoholics who present even only one of the classical symptoms and in patients with alcohol dementia. Thiamine should be given on wide indications.
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PMID:[Wernicke-Korsakoff syndrome at the Rikshospitalet in 1979-1988. A retrospective study]. 192 15

Wernicke's encephalopathy should be considered as a possible diagnosis in comatose and hypothermic patients. The classic triad of confusion, ophthalmoplegia (or nystagmus) and ataxia may be absent, and the history of alcohol abuse or other causes of thiamine deficiency may be unknown. Left untreated, acute Wernicke's encephalopathy has a 17 percent mortality rate. Since the morbidity from Wernicke's encephalopathy is potentially reversible with parenteral thiamine, and large doses of thiamine can be given without documented ill effects, it is recommended that all comatose or hypothermic patients, as well as those with more classic presentations of Wernicke's encephalopathy, be given parenteral thiamine before administration of glucose.
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PMID:Wernicke's encephalopathy. 218 37

Disorders of the vestibular system are common in veterinary practice and result in a clinical syndrome characterized by head tilt, asymmetric ataxia, and nystagmus. These signs may occur with lesions involving the peripheral or central vestibular structures. Careful neurologic evaluation of the animal and knowledge of surrounding neuroanatomic structures and their functions enable the clinician to differentiate between peripheral and central disorders. Conditions resulting in peripheral vestibular symptoms include idiopathic syndromes, otitis interna, trauma, neoplasia, drug-induced ototoxicity, and congenital disorders. Radiographs of the petrous temporal bone and tympanic bulla and examination of the tympanic membrane are useful in determining the specific etiology. Central vestibular dysfunction may result from inflammatory CNS diseases, neoplasia, trauma, thiamine deficiency, and storage diseases. Cerebrospinal fluid analysis, skull radiographs, and computed tomography are diagnostic tests useful in animals with central vestibular symptoms. Once the etiology is identified, specific therapy may be provided and a more accurate prognosis can be determined.
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PMID:Disorders of the vestibular system. 328 49

Exposure to 1,3-dinitrobenzene (1,3-DNB) in humans induces methaemoglobinaemia, nausea and nervous symptoms. When given to conventional rats, twice-daily oral doses of 10 mg kg-1 1,3-DNB produce methaemoglobinaemia and frequently ataxia after four or five doses. In germ free rats given only a single oral dose of 20 mg kg-1, similar symptoms occur but are of more rapid onset. Light and electron microscope examinations reveal an acute thiamine deficiency-like lesion in the brain stems of both ataxic and apparently normal rats. Bilaterally symmetrical vacuolated lesions involve cerebellar roof, vestibular and superior olivary nuclei and the inferior colliculi. Frequent petechial haemorrhages are associated with these lesions, the erythrocytes usually being limited to enlarged Virchow-Robin spaces but sometimes spreading more widely. The primary cellular targets appear to be astrocytes, oligodendrocytes and vascular elements with secondary neuronal involvement. It is suggested that 1,3-DNB interferes with intracellular redox mechanisms resulting in impaired glucose oxidation.
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PMID:1,3-Dinitrobenzene-induced encephalopathy in rats. 368 48

Electrophysiological aspects of thiamine depletion in the rat induced by dietary deficiency are described. Behavioral changes as well as qualitative and quantitative alterations in the sensitivity of cerebellar Purkinje cells to iontophoretically-applied 5-hydroxytryptamine (5-HT) were observed. Thiamine-deficient rats were characterized essentially by ataxia, piloerection, paresis, apparent weakness, and hypothermia after 4-6 weeks on a thiamine-free diet. Basal Purkinje cell firing frequency was unaffected by thiamine deficiency. The response of Purkinje cells to iontophoretically-applied 5-HT was solely inhibitory in deficient rats. In control rats, however, responses to 5-HT were excitatory, biphasic, or inhibitory. Neurons in the thiamine-deficient animals were more sensitive to the inhibitory effects of 5-HT, as demonstrated by a significant parallel shift to the left of the dose-response curve. Durations of 5-HT effects were similar in both groups. Dose-response relationships for GABA-induced inhibition of Purkinje cell firing from thiamine deficient and control rats did not differ from one another. These data demonstrate a relatively selective effect of thiamine depletion on cerebellar serotonergic neurotransmission assessed electrophysiologically. We believe there is up-regulation of 5-HT receptors on Purkinje cells caused by thiamine deficiency-induced impairment of indoleamine input to the cerebellum from raphe and related nuclei.
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PMID:Enhanced sensitivity of cerebellar Purkinje cells to iontophoretically-applied serotonin in thiamine deficiency. 398 3

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.
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PMID:Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans. 402 52


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