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 administration of single oral doses of delta-9-tetrahydrocannabinol (THC) to patients with cancer pain demonstrated a mild analgesic effect. At a dose of 20 mg, however, THC induced side effects that would prohibit its therapeutic use including somnolence, dizziness, ataxia, and blurred vision. Alarming adverse reactions were also observed at this dose. THC, 10 mg, was well tolerated and, despite its sedative effect, may analgesic potential.
Clin Pharmacol Ther 1975 Jul
PMID:The analgesic properties of delta-9-tetrahydrocannabinol and codeine. 5 Jan 59

Chronic bipolar electrodes were implanted in cortical, limbic, diencephalic and mesencephalic regions of the rat. Following recovery from surgery the rats were maintained for 14--26 days on a liquid diet in which 35--42% of total calories were provided by ethanol. Following ethanol withdrawal, electrographic and behavioral monitoring was continued for 8--10 h. The withdrawal of ethanol resulted in the time-dependent appearance of a variety of withdrawal signs including tail arching, ataxia, rigidity, tremor and spontaneous and audiogenic convulsions. These behavioral signs were accompanied by the development of epileptiform abnormalities across wide-spread brain regions. Analysis of preconvulsive spike activity revealed a greater spike frequency in limbic, mesencephalic and non-specific diencephalic regions, as compared to those in cortex and specific diencephalon. Seizure discharge during the tonic-clonic phase of the primary audiogenic convulsion was initiated in the mesencephalon or amygdala, but spread rather extensively to the remainder of the brain. In those instances, however, where multiple convulsions occurred following the audiogenic convulsions, there was a marked decline in spread of seizure discharge to the cortex. These results were interpreted to support the notion that some degree of neuroanatomical specificity exists in the genesis of epileptiform abnormalities during ethanol withdrawal. A comparison of these results with those studying the neural mechanisms underlying other forms of generalized epilepsy was made. It is hypothesized that central pacemaking regions such as medial thalamus or reticular formation may serve to organize isolated epileptiform activity into coherent patterns of paroxysmal activity throughout the brain during the ethanol withdrawal syndrome.
Electroencephalogr Clin Neurophysiol 1978 Oct
PMID:Ethanol dependence in the rat: role of non-specific and limbic regions in the withdrawal reaction. 8 50

Congenital enzymopathic hyperlactacidemia results from a defect of utilisation of pyruvate either at the level of the pyruvate junction (pyruvate-carboxylase, pyruvate-dehydrogenase and Kreb's cycle), or at the level of the unidirectional enzymes on neo-glucogenesis and of neo-glycogenogenesis, e.g. glucose-6-phosphatase, phosphoenol-pyruvate-carboxykinase and glycogen synthetase. The enzymopathies which affect neoglucogenesis associate hyper-lactacidemia and fasting hypoglycemia and more or less marked hepatomegaly. Type I glycogenesis (von Gierke's disease) is the best known example. Enzymopathies which affect the pyruvate junction and the Krebs cycle, may be manifested in addition by: --either chronic neuropathies, e.g. Leigh's disease, recurrent ataxia, and moderate hyperalactacidemia,--or, as in congenital lactic acidoses, which have a rapid and severe prognosis with major hyperlactacidemia. Functional investigation, in particular, loading tests are of great value in orientation and justify the practice of tissue biopsy which permits the enzyme diagnosis. Recent, still unconfirmed knowledge of the pathogenesis of these diseases emphasizes the considerable importance of estimation of blood lactic acid in the investigation of metabolic acidoses of hereditary origin.
Ann Biol Clin (Paris) 1976
PMID:[Enzymopathic congenital hyperlactacidemia]. 18 25

The effects of weekly doses of transfer factor in four patients with ataxia--telangiectasia were investigated following a total course of 2 months therapy. Transfer factor administration showed no influence on the absolute lymphocyte counts, T-cell rosettes or antibody titres to EBV, but it caused conversion of skin-test reactivity and production of MIF to various antigens. There was a dissociation in blastic transformation response, the skin-test responses and MIF production. Serum interferon levels were low before, and 2, 6 and 24 hr after, therapy. Clinically no improvement in infections was observed following transfer factor therapy.
Clin Exp Immunol 1977 Sep
PMID:Transfer factor therapy in ataxia--telangiectasia. 20 9

The value of evoked potentials in studying conduction in the somatosensory pathway was assessed in patients with various neurological disorders. In patients with multiple sclerosis (MS) abnormalities of the cervical response (N14) were found particularly in longstanding cases but also in the early stages of the disease, even in patients without sensory symptoms or signs, and were reversible in some patients. The cortical response was also abnormal in some cases but the two were not always affected together. In Friedreich's ataxia both the cervical and cortical responses were usually abnormal. Subclinical abnormalities of the cervical responses were found in some patients with hereditary spastic paraparesis or mixed forms of spinocerebellar ataxia. The cervical responses were also abnormal in patients with peripheral neuropathy and cervical radiculopathy, and in some patients with brain-stem or thalamic lesions. Cervical and cortical responses were normal in the lateral medullary syndrome, whereas the cortical response was markedly abnormal in patients with high brain-stem or cerebral hemisphere vascular lesions. Cortical and subcortical responses were abnormal in some patients with stereotactic thalamic lesions. Enhanced cortical responses were found in patients with lesions at different levels in the CNS. The most marked enhancement was observed in patients with familial myoclonic epilepsy. Lesser degrees were found in some patients with MS, progressive supranuclear palsy, thalamic lesions, brain-stem encephalitis and syringomyelia. Enhanced responses were usually found in patients with minimal or no clinical sensory involvement. It is postulated that this type of abnormality results from an interference to the inhibitory mechanisms which normally operate at various levels in the somatosensory pathway. It is concluded that evoked potential studies are a valuable adjunct to the clinical evaluation of sensation, and that they may provide useful information on the pathophysiology of conduction in the somatosensory pathway.
Clin Exp Neurol 1978
PMID:The contribution of evoked potentials in the functional assessment of the somatosensory pathway. 22 50

In a 36-week controlled study, the efficacy of clonazepam administered with phenytoin and phenobarbital was evaluated in twenty-four epileptic mental patients suffering from major motor seizures. The patients were distributed in two strata according to the presence or the absence of chlorpromazine. As compared with placebo treatment in the chlorpromazine-free patients, a significant reduction in the frequency of the tonic-clonic seizures was observed during the 24-week clonazepam treatment. This effect could not be observed in the patients requiring the antipsychotic drug. The EEG performed before and at the end of the experimental period did not show any significant change. The most common adverse reactions to clonazepam were drowsiness and ataxia; they diminished with continued treatment.
Int J Clin Pharmacol Biopharm 1978 Jun
PMID:Clonazepam: its efficacy in association with phenytoin and phenobarbital in mental patients with generalized major motor seizures. 35 72

The case is reported of a 64-year-old woman with ataxia and dementia progressing to a state of extrapyramidal rigidity and death in 10 months. The neuropathological changes characterised by severe nerve cell degeneration and loss, a hypertrophic astrocytic gliosis and a status spongiosus were widespread in the cerebral cortex, corpus striatum and cerebellum and confirmed the clinical diagnosis of Creutzfeldt-Jakob disease.
Clin Exp Neurol 1977
PMID:A case of Creutzfeldt-Jakob disease. 35 85

Patients from a polydrug abuse treatment program were titrated with either secobarbital or methaqualone, their primary drug of abuse, to a state of mild intoxication, consisting of lateral and vertical nystagmus, ataxia, slurred speech, and drownsiness. The mean dose required to produce each sign was compared to that determined in a similarly treated control group. Tolerance to secobarbital was more easily demonstrated than tolerance to methaqualone, and nystagmus was the least sensitive indicator of patient tolerance. The individual signs were also cumulated into a graded rating scale of central nervous system depression which would be related to the dose administered. Tolerence was easily demonstrated at the higher stages of toxicity for secobarbital in the overall patient population, but tolerance to methaqualone was only unequivocal in the subjects indicating a relatively high frequency of abuse. Tolerance to methaqualone occurred at the lower stages of toxicity, suggesting that there is a difference between tolerance to secobarbital and tolerance to methaqualone. There was no indication that patients who also abuse alcohol are more tolerant than their patient counterparts. The patients who also had a history of amphetamine abuse, however, were less tolerant than the nonusers of these drugs.
Clin Toxicol 1979
PMID:Dose-response studies on tolerance to multiple doses of secobarbital and methaqualone in a polydrug abuse population. 49 34

The clinical details and results of some laboratory investigations are described in 4 patients who initially presented with severe external ophthalmoplegia, ataxia and areflexia. In 3 of these patients paresis of the limbs was restricted and minimal as in the syndrome first described by Fisher (1956). The fourth patient initially presented with similar symptoms but his illness progressed to a more typical form of acute idiopathic polyneuropathy, confirming Fisher's (1956) contention that this syndrome is an unusual variant of acute idiopathic polyneuritis.
Clin Exp Neurol 1977
PMID:Syndrome of ophthalmoplegia, ataxia and areflexia. 61 11

Clonazepam, a new anticonvulsant, appears to be useful for childhood minor motor seizures and for petit mal refractory to Ethosuximide and Trimethadione. It appears less effective in infantile spasms though may be beneficial when there is no response to steroids. It is variably effective in partial complex and focal epilepsy and may exacerbate tonic seizures. A transient disadvantage is the high incidence of side effects, especially lethargy and ataxia, though these may be transitory. Aggressivity and hyperkinesis may necessitate medication withdrawal. Some children who initially respond to therapy and then relapse may respond again to a higher dosage.
Clin Pediatr (Phila) 1978 Jan
PMID:The utility of clonazepam in epilepsy of various types. Observations with 22 childhood cases. 61 1


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