Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method for testing a rat's physical-dependence liability to sedaditive-hypnotic agents and for evaluating that dependence was studied by using the method. Rats received phenobarbital- or barbital-admixed food on a graded-increase dosage schedule over 30-40 days. Manifestations of CNS-suppressing action of either drug (e.g., systemic muscle relaxation, motor incoordination, staggering gait, and ptosis) persisted day and night during the drug medication. Twenty-four to 48 h after withdrawal of either drug, abstinence symptoms (e.g., muscle fasciculation, nuchal twitching, vocalization, increased irritability, ataxia, hyperthermia, and clonic-tonic and grand mal-type convulsions) were evidenced in all animals (N = 6), some of which died after convulsions. These withdrawal signs in rats were classified and found to be closely correlated with the magnitude of weight loss during the withdrawal. The calssification provides a basis for quantitatively assessing physical-dependence liability. The data obtained in the present study suggest that rats, like dogs and monkeys, are suitable experimental animals for tests in early stages of dependence liability, and that the administration of drug-admixed food is a useful method of developing dependence on both barbiturate and morphine-type drugs.
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PMID:Experimental barbiturate dependence. I. Barbiturate dependence development in rats by drug-admixed food (DAF) method. 41 46

A stroke with a somewhat unusual neurologic formula was correlated with a small linear high-intensity T2 focus in the lateral tegmentum of the lower third of the pons. The clinical features included dysarthria, staggering gait, incoordination of handwriting, right facial weakness, nystagmus, ocular overshoot, right appendicular ataxia, and left-sided dissociated sensory loss for pain and temperature. Lacunar lesions of the tegmentum in the region of the pontomedullary junction, while not uncommon, have not been studied pathologically and have not been reported in the magnetic resonance imaging literature, to my knowledge.
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PMID:Lacunar infarct of the tegmentum of the lower lateral pons. 271 52

A spontaneous neurological disease in domestic cats is described. The clinical signs included staggering gait, hind limb ataxia, and paresis. Histologically, a nonsuppurative meningoencephalomyelitis with a characteristic distribution pattern was found, indicating a viral etiology. In serum samples from diseased cats, antibodies to Borna disease virus were demonstrated.
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PMID:Description of feline nonsuppurative meningoencephalomyelitis ("staggering disease") and studies of its etiology. 765 Feb 12

The role of the N-methyl-D-aspartate (NMDA) receptors in hyperlocomotion induced by (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801), a potent and selective noncompetitive NMDA receptor antagonist, was examined in male ddY mice. A low dose of MK-801 [0.2 mg/kg, intraperitoneally (IP)] produced a marked increase in locomotor activity without obvious staggering gait. In contrast, a high dose (1 mg/kg, IP) induced a typical motor syndrome characterized by increased locomotor activity, stereotyped behavior, and severe ataxia. NMDA (60-120 mg/kg, IP), an NMDA receptor agonist, dose dependently antagonized hyperlocomotion induced by a low dose of MK-801 (0.2 mg/kg). However, even a high convulsive dose of NMDA (240 mg/kg, IP) could not completely antagonize the hyperactivity induced by MK-801. On the other hand, neither a high dose of N-methyl-L-aspartate (400 mg/kg, IP), a stereoisomer of NMDA, nor a critical subconvulsive dose of kainate (10 mg/kg, IP), a non-NMDA receptor agonist, reversed MK-801-induced hyperlocomotion. The activity induced by MK-801 was potently suppressed by low doses of haloperidol (0.05-0.1 mg/kg, IP), a dopamine (DA) receptor antagonist, in a dose-dependent manner. These data for MK-801 were similar to those for phencyclidine and ketamine, other noncompetitive NMDA receptor antagonists. These results suggest that noncompetitive NMDA receptor antagonist-induced hyperlocomotion is mediated, at least in part, by NMDA receptor antagonism, although this hyperactivity may also involve dopaminergic mechanisms through indirect (perhaps by reducing NMDA receptor-mediated neurotransmission) and/or direct (by inhibiting DA uptake) effects on DA neurons.
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PMID:Involvement of N-methyl-D-aspartate (NMDA) receptors in noncompetitive NMDA receptor antagonist-induced hyperlocomotion in mice. 766 42

A 24-year-old pregnant woman started to have hyperemesis gravidarum 6 weeks before admission. Four weeks later she had vertigo, diplopia, staggering gait, mild dyspnea, dysphagia, and incontinence of urine. On admission she presented with ophthalmoplegia, ptosis, ataxia, decreased tendon reflex, and memory disturbance. Brain magnetic resonance imaging revealed abnormal intensities in medial thalamic-hypothalamic regions and the periaqueductal area, and she was diagnosed with Wernicke's encephalopathy. Urodynamic studies revealed decreased bladder volume and detrusor hyperreflexia. Six weeks after the administration of 100 mg/day of thiamine, urge incontinence gradually recovered, together with neurological signs. Lesions of the medial thalamic-hypothalamic area and the periaqueductal gray matter seemed to be mainly responsible for micturitional disturbance in our patient with Wernicke's encephalopathy.
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PMID:Micturitional disturbance in Wernicke's encephalopathy. 904 73

Gadobenate dimeglumine formulation (E7155) was evaluated for its general toxicity potential following a single intravenous and intracisternal administration to rats. Dosage levels tested were 3.3, 4.5, 6.0 and 8.0 mmol/kg at the injection rate of 6 ml/min and 7.50, 8.89, 10.54 and 12.50 mmol/kg at 1 ml/min for the intravenous administration route, and 0.15, 0.21, 0.29 and 0.40 mmol/kg for the intracisternal administration route. Parameters measured during the 14-day observation period were mortality, clinical signs and macroscopic examination. After intravenous administration at the injection rate of 6 ml/min, twitches, respiratory blocking and prostration were observed at 6.0 mmol/kg, and dyspnoea and sedation at 3.3 and 4.5 mmol/kg. Deaths occurred within 1 min after administration at 6.0 mmol/kg and above. LD50 values were 7.97 mmol/kg in males and 6.22 mmol/kg in females. After intravenous administration at the injection rate of 1 ml/min, shallow breathing, twitches and sedation were observed at 7.50 mmol/kg and above and respiratory arrest at 8.89 mmol/kg. Deaths occurred within 1 min after administration at 8.89 mmol/kg and above. LD50 values were 9.0 mmol/kg in males and 9.7 mmol/kg in females. After intracisternal administration, symptoms consisted of sedation, staggering gait, dyspnoea, twitches and ataxia at 0.15 mmol/kg and above, prostration, paralysis of forelimbs, and/or hind limbs and chromodacryorrhea at 0.21 mmol/kg, and convulsions at 0.29 mmol/kg and above. Deaths occurred within 7 days after administration at 0.21 mmol/kg and within 5 min at 0.29 mmol/kg and above. LD50 values were 0.42 mmol/kg in males and 0.25 mmol/kg in females.
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PMID:[General toxicity study of gadobenate dimeglumine formulation (E7155) (1)--single dose intravenous and intracisternal toxicity study in rats]. 1063 76

The present authors studied a 55-year-old-patient homozygous for the SCA6 gene who experienced frequent attacks of positional vertigo at 37 years of age with subsequent staggering gait and night blindness. Retinitis pigmentosa (RP), as well as cerebellar ataxia and vertical antidirectional nystagmus, were detected. The subject's parents were first cousins, and two of his three male cousins, whose parents were also first cousins, had RP without ataxia or nystagmus. The numbers of CAG repeats in the expanded alleles of the SCA6 gene found by molecular analysis were 21 and 21. The genetic results were negative for SCA1, SCA2, SCA3, SCA7 and dentatorubral pallidoluysian atrophy. The retinal degeneration in this patient is most likely to be secondary to a genetic disorder of autosomal or X-linked recessive inheritance rather than SCA6. Other reported cases of patients homozygous for the SCA6 gene are also reviewed.
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PMID:A patient homozygous for the SCA6 gene with retinitis pigmentosa. 1208 23

An apparently novel neurological disease clinically characterized by shaking, tremors, seizures, staggering gait, and ataxia was first observed in farmed mink kits in Denmark in 2000 and subsequently in Sweden, Denmark, and Finland in 2001, and again in Denmark in 2002. Lymphoplasmacytic encephalomyelitis was found in the affected kits. The lesions were most severe in the brainstem and cerebellum and consisted of neuronal degeneration and necrosis, neuronophagia, focal and diffuse gliosis, perivascular cuffs formed by lymphocytes, plasma cells and macrophages, and segmental loss of Purkinje cells. Testing was conducted to determine the cause of the disease, including general virological investigations (virus culture, negative-staining electron microscopy, immunoelectron microscopy, polymerase chain reaction for herpesviruses, adenoviruses, pestiviruses, and coronaviruses), tests for specific viral diseases (canine distemper, Borna disease, Louping ill, West Nile virus infection, tick-borne encephalitis, Aleutian disease), tests for protozoa (Toxoplasma gondii, Neospora caninum, Encephalitozoon cuniculi), bacteria (general culture, listeria, Clamydophila psittaci), and intracerebral inoculation of neonatal mice. The results of all these investigations were negative. One group of 3 mink kits inoculated intracerebrally with brain homogenate of affected mink developed clinical signs and histological lesions similar to those observed in naturally infected mink. Based on the histopathological features, it is postulated that the disease is caused by a yet unidentified virus.
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PMID:Investigations into shaking mink syndrome: an encephalomyelitis of unknown cause in farmed mink (Mustela vison) kits in Scandinavia. 1530 41

The cerebellum has almost never been considered responsible for conjugate deviation of the eyes (CDE). A few cases of CDE caused by cerebellar lesions without the involvement of the brainstem have been reported, but the lesions were too large to evaluate their localization in the cerebellum. In this report, we describe 2 cases of isolated CDE caused by small cerebellar vascular lesions and a case of CDE and staggering gait that occurred following cerebellar infarction. We further describe cases of head rotation without CDE and those of vertigo without CDE or head rotation due to a similar small lesion. Case 1: A 73-year-old woman with rheumatism was brought to our department because of sudden-onset of difficulty in looking to the right. She was admitted 3 hours after onset; at admission she was alert and well-oriented and denied both vertigo and nausea. Neurologic examination revealed CDE to the left; however, no limb ataxia was detected. Diffusion-weighted MRI showed a small infarction in the white matter of the right PICA area near the vermis. Her CDE disappeared spontaneously within 2 days. Case 2: A 79-year-old man with hypertension exhibited CDE to the right without vertigo or ataxia following a small hemorrhage in the cerebellan area mentioned in Case 1. Case 3: A 65-year-old man with hypertension presented with CDE to the right and staggering gait after a small infarction in an area lateral to that mentioned above. The first 2 cases suggest that a small cerebellar vascular lesion can produce isolated CDE to the side contralateral to the lesion. The region responsible for CDE in these cases was located in the white matter of the PICA area near the vermis, although similar lesions in Cases 4 and 5 produced no CDE.
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PMID:[Small cerebellar vascular lesion can produce isolated conjugate deviation of the eyes]. 1856 61

In 2000, farmed mink kits in Denmark were affected by a neurological disorder. The characteristic clinical signs included shaking, staggering gait, and ataxia. The disease, given the name shaking mink syndrome, was reproduced by the inoculation of brain homogenate from affected mink kits into healthy ones. However, the etiology remained unknown despite intensive efforts. In this study, random amplification and large-scale sequencing were used, and an astrovirus was detected in the brain tissue of three experimentally infected mink kits. This virus also was found in the brain of three mink kits naturally displaying the disease but not in the six healthy animals investigated. The complete coding region of the detected astrovirus was sequenced and compared to those of both a mink astrovirus associated with preweaning diarrhea and to a recently discovered human astrovirus associated with a case of encephalitis in a boy with x-linked agammaglobulinemia. The identities were 80.4 and 52.3%, respectively, showing that the virus described in this study was more similar to the preweaning diarrhea mink astrovirus. For the nonstructural coding regions the sequence identity was around 90% compared to that of the astrovirus, which is associated with preweaning diarrhea in mink. The region coding for the structural protein was more diverse, showing only 67% sequence identity. This finding is of interest not only because the detected virus may be the etiological agent of the shaking mink syndrome but also because this is one of the first descriptions of an astrovirus found in the central nervous system of animals.
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PMID:Detection of a novel astrovirus in brain tissue of mink suffering from shaking mink syndrome by use of viral metagenomics. 2092 5


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