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)

Ketamine, a highly lipophilic drug, was rapidly distributed into highly vascular organs and subsequently redistributed to less well perfused tissues, with concurrent hepatic metabolism and urinary and biliary excretion, after both i. m. and i. v. administration in the rat. Halothane, a potent cardiovascular depressant, was found to prolong the plasma and brain half-life of ketamine (50 mg/kg i.m.) and also increased the duration of ketamine-induced ataxia when the two drugs were administered concomitantly. Halothane anesthesia (0.8% halothane in oxygen) produced a decrease in the rate of uptake and delayed distribution and redistribution of ketamine (50 mg/kg i. m.), while the rate of urinary excretion of ketamine was not significantly altered. Similarly, redistribution of intravenously administered ketamine (30 mg/kg i. v.) was slowed in the presence of halothane. In vitro hepatic microsomal metabolism of ketamine and its principle N-demethylated metabolite, metabolite I, was inhibited noncompetitively by halothane with inhibitor constants (Ki) for halothane estimated to be 1.56 and 1. 64 mM,respectively. The gas anesthetic also decreased the overall rate of in vivo metabolism of ketamine (30 mg/kg i. v.) in a concentration-dependent manner. Thus halothane anesthesia by decreasing uptake, distribution, redistribution and metabolism of intramuscularly administered ketamine produced significant prolongation of its pharmacologic action on the central nervous system. Our results imply that concomitant use of inhalational anesthetics may prolong pharmacologic actions of other agents via effects on distribution/redistribution processes as well as on metabolism.
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PMID:Effects of halothane anesthesia on the biodisposition of ketamine in rats. 126 10

A combination of 0.5 mg/kg of methotrimeprazine, 0.1 mg/kg of midazolam and 100 mg/kg of a 10 per cent guaiphenesin solution was investigated for the induction of recumbency in 15 horses; the addition of 1.6 mg/kg of ketamine was also evaluated in 15 horses and anaesthesia was maintained with halothane in oxygen. The horses became recumbent quickly and smoothly and they recovered quietly, with little ataxia. Tachycardia occurred after induction, but no other changes from pre-operative values were observed until halothane in oxygen had been given, when hypothermia, hypotension, bradypnoea, hyperoxaemia, respiratory acidosis and decreased respiratory minute volume developed. Horses given ketamine in addition to methotrimeprazine, midazolam and guaiphenesin were easier to intubate and recovered more quickly than horses receiving only methotrimeprazine, midazolam and guaiphenesin.
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PMID:A combination of methotrimeprazine, midazolam and guaiphenesin, with and without ketamine, in an anaesthetic procedure for horses. 150 60

To study crossed cerebellar diaschisis (CCD), cerebellar blood flow and oxygen metabolism were measured with positron emission tomography (PET) in 12 patients who showed a minimal degree of hemiparesis due to single unilateral supratentorial lesion. Six patients presenting with mild to moderate cerebellar type hemiataxia showed CCD, that is, decreased blood flow and oxygen metabolism in the cerebellar hemisphere contralateral to the side of supratentorial lesion. Hemiataxia and reduced cerebellar blood flow and metabolism occurred in the ipsilateral side. Lesions were located in the thalamus in four patients and the parietal lobe and internal capsule in one each. The other six patients did not exhibit ataxia, and oxygen metabolism was not reduced in the contralateral cerebellar hemisphere. In two of these cases, however, reduced cerebellar perfusion was observed in the contralateral cerebellar hemisphere. These findings indicate that CCD occurs with hemiataxia and suggest that it results not only from disruption of the corticopontocerebellar pathway but also of the dentatorubrothalamic pathway. CCD associated with hemiataxia, demonstrated in patients with thalamic lesions, was presumed to result from retrograde deactivation of the cerebellar hemisphere via the dentatorubrothalamic pathway.
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PMID:Crossed cerebellar diaschisis accompanied by hemiataxia: a PET study. 153 16

Acute mountain sickness is a pathologic reaction as a result of bad adaptation to high altitudes (greater than 2.500 meters). The main symptoms are headache, nausea, vomits, and insomnia. When severe it can produce oliguria, retinal hemorrhage, ataxia and sometimes coma. Its etiology is not well known. It is considered that the first producer factor of the disease is tissular hypoxia secondary to low partial oxygen pressure existing in areas of high sea level. The treatment consists of descent and the use of dexametasone and acetazolamide.
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PMID:[Acute mountain sickness]. 210 53

As a possible preventive measure for brain dysfunction in Menkes disease, prenatal treatment by maternal administration of zinc, vitamin E and copper was examined in brindled mutant mice. During pregnancy and lactation, female heterozygous mice received 20 ppm zinc or 0.004% alpha-tocopherol acetate (vitamin E) throughout and 6 ppm copper from gestational day 13 in the drinking fluid, ad libitum. The maternal administration of zinc and vitamin E, as antioxidants, or copper resulted in decreased fetal and neonatal death of offspring, especially those of hemizygous males, as compared with the administration of water only. When offspring did not grow, maternal abnormal movements, which comprised rotatory movements of high speed with tremor and ataxia, were frequently observed. In the heterozygotes with abnormal movements, the level of lipid peroxidation in cerebrum and the concentration of copper in kidney were much higher than those in the heterozygotes with normal movement. Morphologically, in cerebellum of the heterozygotes with abnormal movements, the loss of Purkinje cells, abundance of lipofuscin granules and abnormal mitochondria or degenerative bodies of high electron density were frequently observed, as compared with heterozygotes with normal movement. These findings suggest that the development of hemizygous male mice may be influenced by both copper and oxygen radical metabolism.
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PMID:Abnormal movements in brindled mutant mouse heterozygotes: as related to the development of their offspring--biochemical and morphological studies. 216 11

Acute poisoning with organic solvents and other volatile compounds now usually follows deliberate inhalation (volatile substance abuse) or ingestion of these compounds. Solvents from adhesives, typewriter correction and dry cleaning fluids, cigarette lighter refills (butane) and aerosol propellants are commonly abused. The major risk is that of sudden death. Arrhythmias leading to cardiac arrest are thought to cause most deaths, but anoxia, respiratory depression and vagal stimulation leading to cardiac arrest may also contribute, as may indirect causes such as aspiration of vomit or trauma. In the United Kingdom (UK), 3.5 to 10% of young people have at least experimented with volatile substance abuse and mortality is more than 100 per annum. The products abused are cheap and readily available despite legislation designed to limit supply. Volatile substance abuse is not illegal and only a minority of abusers are known to progress to heavy alcohol or illicit drug use. Prevention of abuse by education, not only of children but also of parents, teachers, retailers and health care workers, is important in limiting the problem. However, volatile substance abuse-related deaths are still increasing in the UK despite many measures aimed at prevention. Clinically, volatile substance abuse is characterised by a rapid onset of intoxication and rapid recovery. Euphoria and disinhibition may be followed by hallucinations, tinnitus, ataxia, confusion, nausea and vomiting. It is important not to further alarm the patient if signs of serious toxicity are present, since a cardiac arrest may be precipitated. Further exposure should be prevented and the patient resuscitated and given supplemental oxygen if necessary. Cardiac arrhythmias should be treated conventionally and respiratory failure managed supportively. Long term exposure to n-hexane is associated with the development of peripheral neuropathy, while prolonged abuse (notably of toluene or chlorinated solvents) can cause permanent damage to the central nervous system, heart, liver, kidney and lungs. Knowledge of the routes of absorption, distribution and excretion of volatile compounds, and of the rates governing these processes, is important in understanding the rate of onset, intensity and duration of intoxication, and rate of recovery after volatile substance abuse. In addition, such knowledge is helpful when the clinician is attempting to interpret the results of toxicological analyses performed on samples (blood, other tissues, urine) from such patients. Many volatile substances are partly metabolised, the metabolites being eliminated in exhaled air or in urine. Although metabolism normally results in detoxification, enhanced toxicity may also result as with carbon tetrachloride, chloroform, dichloromethane, n-hexane, trichloroethylene and possibly halothane.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:An introduction to the clinical toxicology of volatile substances. 222 69

The patient was 56-year-old female, who suffered from ataxia and then fell into coma on the next day after she had moved from the sea level to an altitude of 4,200 m. After she was brought to lower altitude, consciousness recovered within several hours. For about 2 days thereafter, disorientation was observed, and she was diagnosed as AMS (acute mountain sickness). Only insomnia continued in chronic stage. The results of X-ray computed tomography (CT) on 25th day after the onset of the disease revealed no abnormal finding except the slightly increasing uptake of contrast material. Symmetrical low density regions were seen in bilateral basal ganglia after one year, and the globus pallidus lesions were confirmed by magnetic resonance imaging. In the past, cerebral edema has been reported in most cases of AMS, and the neurotic symptoms of AMS have been attributed to cerebral edema, while the essential condition of this disease is not yet elucidated. In the present case, the globus pallidus lesions could be identified through the following-up of the central nervous system by X-ray CT and MRI as the first attempt for the case of AMS. There has been no report of globus pallidus lesions in the cases of AMS. Whereas low oxygen partial pressure is the primary cause of AMS, and it is highly probable that the disorders in globus pallidus as reported in the cases of carbon monoxide poisoning, anesthetic accident, etc. are related to the occurrence of AMS.
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PMID:[A case of acute mountain sickness with bilateral lesion of pallidum]. 222 57

Ataxia is an occasional side effect of amitraz when used as a wash to treat dogs with demodectic mange. In the present study, successive doses of 0.5, 2, 5 and 10 mg kg-1 amitraz were given intravenously at intervals of nine minutes to thiopentone/methoxyflurane/oxygen anaesthetised dogs. The amplitude of the evoked muscle action potential to electrical stimulation of the right ulnar nerve and the muscle refractory period were unchanged by increasing doses of amitraz but there was a progressive and significant decrease in nerve conduction velocity. The minimum recorded nerve conduction velocity (50.7 +/- 1.5 m s-1) was still within an adequate range. From these results it appears that the ataxia following amitraz is unlikely to be attributable to peripheral mechanisms. The concurrent amitraz-induced rise in mean arterial pressure and bradycardia was consistent with previous findings in which alpha 2-adrenoceptors were shown to be the major mediators.
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PMID:Effects of amitraz on nerve conduction and neuromuscular transmission in anaesthetised dogs. 233 23

To assess the effects of moderate exercise [40-70% maximal oxygen uptake (VO2max)] on resting blood pressures, the presence of cerebrovascular lesions, and the life spans of stroke-prone hypertensive rats, nontrained and trained male and female rats were assigned to two experimental groups. The first (n = 48) were exercise trained after 38 days of age, whereas the second (n = 44) initiated exercise training when the animals were 134 days of age. To facilitate cerebrovascular lesions, the sodium concentrations in the rat chow and in the drinking solutions were increased. Symptoms utilized to denote the presence of cerebrovascular lesions were irritability, hyperresponsiveness, ataxia, lethargy, unwillingness to run, and combinations thereof. All brains were removed immediately after death, fixed, and evaluated grossly and microscopically for lesions. In the study with the younger animals, training was associated with a 7-9% increase in VO2max that was statistically significant only in animals with no histological evidence of cerebrovascular lesions. For the older animals, a significant 5-8% increase in VO2max was noted for animals with or without lesions. After 42 days of training for both groups, resting blood pressures for the trained groups with histological lesions were significantly lower. However, this trend did not continue, and the older trained rats appeared to have strokes earlier and to die sooner than their nontrained controls. Although 83% of the older animals had subjective evidence for a stroke before they died, the percentage of animals with lesions ranged from 42 to 58%, with the trained groups having higher percentages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise training and incidence of cerebrovascular lesions in stroke-prone spontaneously hypertensive rats. 234 35

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


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