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 37-year-old housewife, who had physical characteristics of cerebral gigantism, such as the tall stature, acromegaly, macrocephalia, high arched palate and antimongoloid slant, developed cerebellar ataxia and dysarthria. Her mother, uncle and grandmother were also reported to have slowly progressive gait disturbance. Her mother was also tall. Endocrinological studies failed to show any definite abnormality. CT and MRI revealed remarkable cerebellar atrophy. Though cerebral gigantism is often associated with clumsiness and incoordination, the etiology of the ataxia is poorly understood. This case indicates that the ataxia in cerebral gigantism may be, at least partly, caused by cerebellar atrophy.
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PMID:[A case of cerebral gigantism with cerebellar atrophy]. 240 Nov 12

In dwarf goats fasted for 2 h, i.v. administration of the benzodiazepine (BZ) agonists diazepam (60 micrograms/kg), brotizolam (2 and 4 micrograms/kg) and climazolam (100 micrograms/kg) induced hyperphagic effects, whereas i.v. injections of the BZ-antagonist flumazenil (R degrees 15-1788; 0.5 mg/kg), the anthelmintic ivermectin (0.1 mg/kg), the 5-HT2 antagonist ritanserine (0.1 mg/kg), ACTH (10 micrograms/kg) and prednisolone (1 mg/kg) were inactive in a 30-min feeding test. Both the BZ-antagonist R degrees 15-3505 (greater than or equal to 0.1 mg/kg) and the opiate receptor antagonist naloxone (0.1 mg/kg) had anorectic effects in dwarf goats given 30 min access to a palatable pelleted concentrate. The hyperphagic effects of climazolam and brotizolam were not antagonized by flumazenil, whereas similar doses of this drug completely reversed muscle incoordination and ataxia induced by much higher doses of these BZ-agonists. In the combination experiments with naloxone and BZ-agonists, naloxone antagonized the hyperphagic effects of both diazepam and brotizolam. Similarly, in the diazepam-R degrees 15-3505 study, there was a significant effect of diazepam and a significant inhibition of this effect by R degrees 15-3505 (50 micrograms/kg). In the diazepam-ivermectin combination experiment no evidence for drug potentiation was found. These results and the mode of action of the above mentioned drugs are discussed in relation to feeding behaviour.
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PMID:Appetite-modulating drugs in dwarf goats, with special emphasis on benzodiazepine-induced hyperphagia and its antagonism by flumazenil and RO 15-3505. 250 11

With the great progress in the imaging technique of cerebro-cerebellar perfusion and metabolism, it has been revealed that supratentorial cerebrovascular disorders often cause some reduction of contralateral cerebellar blood flow and metabolism. The phenomenon, termed crossed cerebellar diaschisis (CCD), is interpreted to be brought about by transneuronal deactivation of cerebellum via the corticopontocerebellar pathway and usually not to accompanied by limb-incoordination. We have experienced 2 cases presenting ataxia clinically and CCD in positron emission tomography (PET) which are thought to be caused by the interruption of two distinctive neural pathways, the corticopontocerebellar and cerebellorubrothalamic pathways. Case 1 was a 34-year-old housewife with cerebral infarction which magnetic resonance imaging disclosed in the left parietal cortex and subcortical white matter. She showed mild right-sided hemiataxia featured by dysarthria, hypermetria, dysrhythmia, decomposition, dysdiadochokinesis and rebound phenomenon. Cheirooral syndrome, a hand-pronation sign and defects of combined sensation were present on the right but not accompanied by any disturbances of deep sensation. PET with 15O-labeled CO2 and O2 demonstrated the left frontoparietooccipital and contralateral cerebellar hypoperfusion and hypometabolism. Case 2 was a 69-year-old female suffering from aftereffects of old thalamic hemorrhage. Neurological examination revealed moderate degree of right-sided hemiataxia suggesting a cerebellar type of dysfunction like in case 1. Muscle power and sensory system were well-preserved. Brain CT revealed a small and restricted low density area in the left posterolateral thalamus indicating destruction of the Vim nucleus. PET study confirmed reduced blood flow and oxygen metabolism in the left thalamus and contralateral cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical and etiological study of crossed cerebellar diaschisis. Report of two cases]. 261

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.
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PMID:Selenium toxicosis in three California sea lions (Zalophus californianus). 261 40

The lethality of Poa huecu, a plant toxic to cattle and sheep, was followed by injection of chromatographic fractions in mice. The lethal aqueous extract was administered i.p. to Rockland mice of either sex and produced motor incoordination, transient ataxia, rough hair coat, tremors and muscle contractions and, occasionally, blindness. Doses greater than 1.5 g/kg mouse were always lethal. Fractionation of this lethal extract included dialysis, column chromatography on Sephadex G-25 and fractional precipitation with ethanol. Precipitates obtained with 70% and 85% ethanol were further purified on a DEAE-cellulose column. Eight fractions were obtained, each was injected into mice. Only fractions 3-6 were toxic. Fraction 3 produced slight hepatosis and hyperemia in the liver and gliosis in the brain. None of the other tissues exhibited histological lesions. Fractions 4 and 5 caused death of all animals within 30 min to 4 hr after injection. Polyacrylamide gel electrophoresis and acid hydrolysis showed that fractions 4 and 5 contained a glycoprotein of nearly the same mol. wt (67,000-94,000). Microscopic pathology in the mice treated with the lethal glycoprotein of fraction 4 included hyperemia in the kidneys, megakaryocytes in the spleen, slight hepatosis and focal coagulative necrosis with nuclear pyknosis and karyonexis in the liver, gliosis, intracellular brain edema with axon degeneration and swollen astrocytes in the brain. These brain injuries may relate to the motor incoordination of cattle that causes a delayed righting reflex. The major monosaccharides of the lethal glycoprotein are glucose and mannose, while rhamnose, arabinose, xylose and galactose are present in low percentages. Proline and the acidic amino acids (glutamic and aspartic acids) are the most abundant in the peptidic residue.
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PMID:The lethal principle of Poa huecu (coiron blanco): a plant indigenous to Argentina. 262 69

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

Charles Foster male and female rats were exposed only once to 3.52 and 35.32 ppm doses of methyl isocyanate in separate experiments for 10 min each in an acute toxicity study, while in subacute toxicity experiments, they were exposed to 0.212, 0.265, and 0.349 ppm doses for 30 min daily, for 6 days, by inhalation. Clinical signs, mortality, body and organ weights, and changes in hematology and clinical pathology were routinely monitored to determine the principal organ sites damaged on exposure to the gas. During exposure, animals were observed to have congestion in eyes, lachrymation, nasal secretion and dyspnea, progressively increasing ataxia, and immobility. Uncoordinated movements were also observed, indicating effects on the nervous system. Upon microscopic examination of the viscera, pathological findings confined to bronchial tree, lung parenchyma, liver, and kidneys were observed.
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PMID:Acute and subacute toxicity study of inhaled methyl isocyanate in Charles Foster rats. 277 90

We examined the effects of chinoform (CF) on the spinal reflexes and the descending influences on the spinal reflexes from the locus coeruleus (LC) and the nucleus raphe magnus (NRM) in rats. The spinal reflex potential was recorded from the L5 ventral root following stimulation of the L5 dorsal root, and the effects of electrical stimulation of the LC and the NRM were tested in anesthetized rats. CF was suspended in Tween 80 and administered for two days (400 mg/kg, i. p./day) before the measurement of the spinal reflexes. In all rats treated with CF, death or motor incoordinations such as abnormal gait and hindlimb ataxia were observed. However, the control and CF-treated groups are not different in the amplitude and shape of the reflexes and in the influences of the LC and the NRM on the reflexes from the LC and the NRM. These results suggest that segmental spinal reflexes and descending influences from the LC and the NRM are not affected in rats suffered from motor incoordination by acute CF.
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PMID:Spinal reflexes in chinoform-administered rats. 294 92

B6C3F1 mice and Sprague-Dawley rats displayed the characteristic signs of pyrethroid intoxication following single oral doses ranging from 56 to 320 and 133 to 1000 mg/kg fenvalerate, respectively. The LD50s for mice and rats were 180 and 776 mg/kg, respectively, with corn oil as the vehicle. Signs of neurologic deficit such as splayed gait, tremors, ataxia, and hind limb incoordination were observed at doses of greater than or equal to 100 mg/kg (mice) and greater than or equal to 133 mg/kg (rats) within 1-8 hr after dosing. These signs had disappeared in most animals within 72 hr. Slight peripheral nerve fiber damage was detected in surviving mice and rats sacrificed 10 days after dosing. The incidence and severity were dose related at doses greater than or equal to 56 and greater than or equal to 180 mg/kg; however, even at lethal doses, evidence was lacking for the presence of nerve lesions in several animals. Thus two distinct neurologic effects were observed: a reversible ataxia/incoordination and a neuropathologic effect manifested as sparse axonal damage in peripheral nerve.
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PMID:Neuropharmacologic and neuropathologic effect of fenvalerate in mice and rats. 298 61

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute ethanol poisoning and the ethanol withdrawal syndrome. 304 Dec 44


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