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)

The behavioral effects of 450191-S and its metabolites were investigated in mice, rats, cats and rhesus monkeys, and they were compared with those of related benzodiazepines (BDZ) such as diazepam and nitrazepam. Oral administration of 450191-S consistently caused sedation without excitability in mice and rats, and it was only 1/2 to 1/266 as potent as the BDZ in producing motor incoordination as assessed by traction, rotarod performance and inclined screen tests in mice, induced much less ataxia in cats and monkeys, and inhibited respiration in anesthetized cats. The locomotor activities of mice and rats measured by Animex and the open field test were not affected by 450191-S, but rearing and preening decreased with 450191-S as with the BDZ. 450191-S was equipotent with nitrazepam and 2 to 6 times more potent than diazepam and estazolam in potentiating chlorprothixene-induced hypnosis and thiopental-Na-induced anesthesia. These effects were not different with successive 14-day administration of 450191-S. Anti-pentylenetetrazol, picrotoxin and bicuculline convulsions of 450191-S had the same potency as nitrazepam, but caused much less anti-electroshock convulsion than the BDZ. 450191-S had potent antianxiety activity as observed by anti-aggressive and anti-conflict activities and had almost the same effect as diazepam on operant behavior. The metabolites M-1, M-2, M-A and M-3 showed approximately the same potency as 450191-S in inducing anesthetic potentiation and antianxiety activity, but they were much more potent in causing disturbance of the somatic functions. These results indicate that 450191-S possesses inhibitory effects on the central nervous system, including a potent sleep-inducing effect, and is characterized by markedly weak muscle relaxant activity and motor incoordination.
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PMID:[Pharmacological studies of a new sleep-inducer, 1H-1,2,4-triazolyl benzophenone derivatives (450191-S) (I). Behavioral analysis]. 614 74

The benzodiazepines are typified by a profile of side effects which includes drowsiness, ataxia and incoordination. Ro 15-1788, an imidazodiazepine derivative, exhibits marked antagonism of the behavioural and biochemical effects of the benzodiazepines in animals and man. It is devoid of any behavioural activity in animals, except at very high doses. In the present study the effects of single rising oral doses of Ro 15-1788 on cognitive, psychomotor and subjective function in man have been assessed using a battery of psychometric tests designed to identify the sedative action of the benzodiazepines. At all doses up to 600 mg, Ro 15-1788 demonstrated none of the classical behavioural effects of the benzodiazepines.
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PMID:Absence of central effects in man of the benzodiazepine antagonist Ro 15-1788. 641 Apr 50

Main Drain virus, which is thought to be transmitted normally among rabbits and various rodents by its natural vector, Culicoides variipennis, was isolated repeatedly from brain tissue of a sick horse from Sacramento County, California, and was implicated as the causative agent. Signs of illness were incoordination and ataxia, stiff neck, head pressing, inability to swallow, fever, and tachycardia.
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PMID:Main Drain virus as a cause of equine encephalomyelitis. 641 68

A progressive spinocerebellar degenerative disorder was characterized in nine patients, aged 11 to 37 years, from four unrelated Ashkenazi Jewish families; affected individuals had markedly deficient beta-hexosaminidase A activity. Symptoms included early onset of cerebellar signs (tremor, incoordination, and dysarthia) and, with maturity, the development of upper and lower motor neuron disorders, marked dysarthia, and ataxia. Three older patients, aged 26, 32, and 37 years, had dementia or recurrent psychotic episodes. Membrane-bound lamellar cytoplasmic inclusions, consistent with lysosomal ganglioside accumulation, were observed in rectal ganglia. The activity of beta-hexosaminidase A was markedly deficient in all sources analyzed. Parents had activities consistent with heterozygosity, confirming autosomal-recessive transmission of the beta-hexosaminidase A-deficient gene and the adult variant disorder. Residual beta-hexosaminidase A activity, partially purified by anion-exchange chromatography from cultured skin fibroblasts of the affected individuals, was heat-labile and co-electrophoresed with normal beta-hexosaminidase A. These findings suggest that these patients were allelic for a new beta-hexosaminidase A mutation and may represent a genetic compound of this allele and the allele causing Tay-Sachs disease.
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PMID:Chronic GM2 gangliosidosis masquerading as atypical Friedreich ataxia: clinical, morphologic, and biochemical studies of nine cases. 645 83

This study was designed to assess the sex differences in phencyclidine(PCP)-induced ambulatory activity in an open-field, stereotyped behaviors, motor incoordination, tremor, salivation, the regional and subcellular distributions of PCP in the brain and the half-life of PCP in the brain and plasma. Female rats appeared to be more sensitive to PCP as evidenced by hyperactivity, stereotyped behaviors, motor incoordination, tremor, salivation and ataxia. The concentrations of PCP in female rat brain were higher than in the male rats in some discrete brain areas and subcellular fractions. The half-life of PCP in the brain and plasma was longer in female rats than in male rats. The inverse relationship of pharmacological responses to PCP and biotransformation of PCP in both sexes of rats suggests that sex differences in pharmacological actions of PCP depend largely on differences in ability to biotransform the drug.
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PMID:Sex-dependent differences in the pharmacological actions and pharmacokinetics of phencyclidine in rats. 653 6

From their early twenties, a 56 year-old french woman and her 33 year-old son suffered from paroxysmal attacks of gait ataxia, incoordination of both hands, dysarthria and nystagmus. These attacks lasted from one to three hours and occurred at the rate of one to seven per week. On examination between attacks, there was only a bilateral horizontal and upward-beating gaze nystagmus. This was documented by E.O.G. Biological investigations were normal with the exception of a mild elevation of glucose blood level. Treatment with acetazolamide 250 mg daily, completely abolished the attacks in both patients. These cases meet the criteria of familial paroxysmal ataxia, a disorder only described in the United States up to the present. Although rare, this disease should be recognized because of its dramatic response to acetazolamide.
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PMID:[Familial paroxysmal ataxia responsive to acetazolamide]. 661 40

The mammalian neuromuscular toxicity of N'-(2,4-xylyl)-N-methyl formamidine hydrochloride (U-40481A) was evaluated by programmed screening. The LD50 for mice, determined 48 h after single, subcutaneous (s.c.) injections, was 107 mg/kg body wt. Acute toxicity signs included abnormal gait, hindlimb hyperextension, transient hyperactivity followed by a protracted phase of hypoactivity, ataxia, progressive respiratory difficulty, cyanosis, loss of righting reflex, and death. Relatively low doses of U-40481A (1, 5, 10, and 20 mg/kg, s.c.) markedly impaired the ability of trained mice to ride a rotating rod (rotarod). U-40481 (the base, 1-8 X 10(-4) M) reduced isometric contractions of the isolated rat hemidiaphragm obtained by supramaximal electrical stimulation of either the phrenic nerve or the diaphragm itself in a dose-dependent manner. The neurological deficit and motor incoordination signs observed during acute toxicity testing and in the rotarod study are, at least partly, due to the ability of U-40481A to (i) interfere with neuromuscular transmission, and (ii) decrease skeletal muscle contractility by a direct action on the muscle itself. These 2 effects may also be involved in U-40481A-induced mortality in mice.
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PMID:Potential neuromuscular toxicity of N'-(2,4-xylyl)-N-methyl formamidine HCl in rodents. 667 38

Five Rottweiler dogs were examined because of progressive ataxia of thoracic and pelvic limbs of several months' to 4 years' duration. Hypermetria, especially of the thoracic limbs, and head incoordination and tremors were obvious features in the 3 older dogs. None of the dogs had evidence of weakness or loss of conscious proprioception. An electroencephalogram in 1 severely affected dog was normal. Electromyograms in 2 severely affected dogs were normal except for some positive sharp waves and fibrillation potentials in the interosseus muscles of all 4 feet. Cerebrospinal fluid evaluations of 2 severely affected dogs were normal. A reduced number of sensory nerve endings, compared with age-matched controls, was seen on histologic examination of a conjunctival biopsy specimen in 1 severely affected dog. An antemortem diagnosis of neuroaxonal dystrophy was suspected from the signalment, history, and neurologic examination findings. The diagnosis was confirmed on the basis of microscopic findings in 3 dogs necropsied.
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PMID:Neuroaxonal dystrophy of Rottweiler dogs. 669 79

Recurrent encephalopathy affecting cerebellar and extrapyramidal structures was observed in five members of two families. The syndrome is characterized by sudden onset of truncal ataxia, occasionally accompanied by lethargy and impairment of speech. Choreic and athetoid movements were present, and there was loss of deep tendon reflexes with presence of pathological reflexes. Onset of the disease was early in childhood. Attacks lasted for days to weeks; residual symptoms comprising speech impairment and incoordination were seen in some patients. Both sexes were affected. The pedigrees suggest autosomal dominant inheritance. Pathogenesis remains unexplained by the laboratory studies done; metabolic or immunological processes predisposed by genetic factors are suggested. Similar reports from the literature are discussed; no identical family could be found.
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PMID:Autosomal dominant recurrent encephalopathy of childhood. 685 11

An unusual combination of disconnective syndromes is reported: transcortical motor aphasia, left arm apraxia and optic ataxia. Neuropathological examination showed a left parieto-occipital and a subcortical frontal infarct and a lesion of the dorsal part of the posterior two-fifths of the callosum. The frontal lesion caused the transcortical motor aphasia and produced the left arm apraxia. Visuomotor incoordination in the right hemispace was due to the left parieto-occipital infarct, while the crossed optic ataxia in the left hemispace was attributed to the callosal lesion. It is proposed that the pathway that serves crossed visual reaching passes through the dorsal part of the posterior callosum. This case reinforces the growing evidence that fibres in the corpus callosum are arranged in ventro-dorsal functional lamination.
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PMID:Crossed optic ataxia: possible role of the dorsal splenium. 687 86


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