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 present study was undertaken in order to describe 16 more patients suffering from startle-induced epileptic seizures and to clarify further the possible therapeutic activity of benzodiazepines in this rare reflex epilepsy. The interictal and ictal electroclinical data of 16 epileptic children or adolescents have been detailed. A CT-scan was performed in 10 patients; six of them showed an atrophy of the mesial surface of one or both hemispheres ("mesial hypodensity"). Benzodiazepine was associated with the previous antiepileptic treatment in the 16 ineffectively treated patients. Clonazepam was administered in three patients; one of them was completely unresponsive and two became seizure-free for a mean of 16.5 months but complained of drowsiness or ataxia. Clobazam was administered in 13 patients; 15.4% of them were completely unresponsive, 23.1% experienced drug resistance, and 61.5% obtained a good control (91.5% reduction of the reflex seizures) for a mean of 22.75 months. In spite of a possible loss of therapeutic activity, the appearance of very few unfavorable side effects and the presence of favorable side effects ("psychomotor arousal") make clobazam therapy important in the treatment of patients suffering from startle epilepsy.
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PMID:Startle-induced epileptic seizures. 651 Mar 79

The photopalpebral reflex (PPR) is a useful method to assess level of arousal. Healthy males were given either brotizolam (0.0625, 0.125, 0.25 or 0.5 mg) or placebo within a double-blind, crossover design. Changes in PPR and subjective assessments were observed for 5 h after medication. Prolongation of the latencies of PPR were dose dependent, and the amplitude tended to be reduced. These effects appeared within 30 min, and lasted about 4 h. The dose-response curve of the maximum prolongation of the latencies was linear. Sleepiness and slight ataxia were observed after drug ingestion. Sleepiness was correlated with the prolongation of the PPR latencies. Brotizolam could be a potent hypnotic, with rapid onset and moderate duration of action, and it has no severe side-effects.
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PMID:Effect of brotizolam on the averaged photopalpebral reflex in man. 666 78

A case of a medial and caudal infarction of the midbrain in a 56 years old woman is reported. The clinical syndrome included a rapidly recovering sleepiness, an ophthalmoplegia related to damage to the caudal part of the oculomotor nuclear complex, a slow extrapyramidal dysarthria and a severe ataxia. The latter was characterized by the prevalent involvement of posture control, resulting from an axial hypotonia and the lack of balance reflexes. The CT scan showed a low density area in the central part of the midbrain. Electrophysiological investigations were carried out to study the impairment of the sensory and auditory tracts in the brainstem. In spite of the gravity of initial signs, recovery was good and the patient led a normal life 8 months later.
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PMID:[Regressing median peduncular infarction]. 669 25

A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3-4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.
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PMID:Acute trazodone poisoning: clinical signs and plasma concentrations. 671 57

The present study describes the interaction between carbamazepine (CBZ) and viloxazine, a recently synthesized antidepressant agent. Seven epileptic patients on chronic anticonvulsant therapy showed a significant (p less than 0.005) increase in steady-state serum CBZ levels (from 8.1 +/- 2.5 SD to 12.1 +/- 2.5 SD micrograms/ml) when viloxazine (300 mg/day) was added to the therapy. The effect was associated with the appearance of mild CBZ intoxication. The symptoms of this intoxication (i.e., dizziness, ataxia, fatigue, drowsiness) disappeared rapidly, and serum CBZ levels decreased to the basal values, when viloxazine administration was stopped.
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PMID:Effect of viloxazine on serum carbamazepine levels in epileptic patients. 674 18

Eight psychiatric patients with tardive dyskinesia (TD) were treated with single doses of the synthetic met-enkephalin analogue FK 33-824 (1, 2, and 3 mg IM) morphine (10 mg SC) and naloxone, an opiate receptor antagonist (0.8 mg IM). The drug effects were assessed by blind evaluation of randomly sequenced videotapes made before and during treatment. FK 33-824 (1, 2, and 3 mg IM) slightly reduced TD (P < 0.05) and increased preexisting bradykinesia. The effect on TD, however, was pronounced only in patients concurrently treated with neuroleptics in relatively high doses. Morphine had a similar although weaker antihyperkinetic effect, whereas naloxone had no effect. Side effects of FK 33-824 included dizziness, heaviness in the extremities, slurred speech, and dryness of mouth. Morphine caused drowsiness, dizziness, ataxia, and nausea, and naloxone had no side effects. The results do not point to a primary role of enkephalin in the pathophysiology of TD, but enkephalin may interact with dopamine functions and potentiate some of the effects of neuroleptic drugs.
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PMID:Enkephalin, morphine, and naloxone in tardive dyskinesia. 677 5

Acivicin, an L-glutamine antagonist, was administered to 37 evaluable patients with refractory advanced solid tumors in a phase I trial. A total of 67 evaluable 72-hr iv infusions were given at 3- to 4-week intervals. Doses ranged from 3.0 to 90 mg/m2/course. Reversible CNS toxicity was dose-limiting and included lethargy, somnolence, anxiety, hallucinations, and paranoid psychoses. Four of five patients experienced unacceptable CNS toxicity at 90 mg/m2. Three of eight patients experienced reversible diaphoresis and chills without fever at 75 mg/m2, and two had dizziness and ataxia. Hematopoietic toxicity, nausea, emesis, and diarrhea were mild and dose-related. One patient developed a blue-green discoloration of the infusion arm. Serial plasma and urine specimens from 13 patients were assayed for acivicin using a microbiologic method. Peak plasma levels at the end of the 72-hr infusions correlated with dose and ranged from 0.09 to 1.10 microgram/ml. When data from six patients were fitted to a two-compartment open model, alpha-half-life ranged from 1.1 to 63 mins, while beta-half-life ranged fro 338 to 629 mins. Renal clearance ranged from 6 to 24 mL/min, and nonrenal clearance accounted for 58%-83% of the total drug clearance. CNS toxicity correlated with plasma acivicin levels which exceeded 0.9 microgram/ml for greater than 16 hrs, but not with peak plasma levels or with the integrals of the concentration x time curves. Minor responses were seen in one patient with melanoma, in one with epidermoid pulmonary carcinoma, and in two with colon carcinoma. A starting dose of 60 mg/m2/course was recommended for phase II trials, with possible escalation to 75 mg/m2 in the second course if the drug was well-tolerated.
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PMID:Phase I trial and pharmacokinetics of acivicin administered by 72-hour infusion. 687 83

Methyl chloride is encountered in the chemical industry as a methylating agent in the production of butyl rubber, tetramethyl lead, and other products as well as a blowing agent for some polystyrene foams. It is a potent CNS depressant whose principal route of absorption is by inhalation, although it can be absorbed through the skin. Symptoms of the neurotoxicity include headache, drowsiness, giddiness, ataxia, convulsion, and coma. This review focuses on the human case reports of acute and chronic exposures as well as some of the more important inhalation studies conducted with animals. The chemical and physical properties and the more important industrial uses are also discussed.
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PMID:Neurotoxicity of methyl chloride. 703 27

Complications from mydriatic and cycloplegic drugs are rare compared with their extensive use. Adverse effects are often related to dosage or other factors. The ocular complications include increased intraocular pressure, pigmentation of the conjunctiva and cornea, pigment in the anterior chamber, lacrimal duct blockage, macular edema, corneal endothelium damage, hyperemia, allergy, discomfort, and blurred vision. The systemic complications are those common to sympathomimetic and parasympatholytic drugs and include tachycardia, hypertension, headache, faintness. pallor, trembling, excessive sweating, palpitations, arrhythmias, confusion, hallucinations, drowsiness, ataxia, flushed skin, high fever, dysarthria, thirst, dry mouth, convulsions, disorientation, nervousness, coma, and death. An understanding of all possible side effects is of paramount importance to those using these drugs in the treatment of anticholinesterase poisoning. This review is intended as a ready reference to the adverse effects of mydriatic and cycloplegic drugs.
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PMID:Mydriatic and cycloplegic drugs: a review of ocular and systemic complications. 703 29

Taurine was administered orally to 25 intractable epileptic children, ranging in age from 4 months to 12 years. All patients had been suffered from frequent seizures daily in spite of vigorous anticonvulsant medication. Daily taurine doses ranged from 0.05 to 0.3 g/kg. Twelve patients received probenecid additionally in doses ranging from 0.5 to 1.0 g/day. Complete control of seizures was achieved in a case of Lennox syndrome, over 50% decrease of seizure frequency in 1 case, less than 50% decrease in 4 cases, and no effects in 18 cases. The effects of taurine often manifest only temporarily. Electroencephalographic abnormalities did not improve by taurine in 21 cases examined except 1 in which EEG markedly ameliorated along with clinical seizure control. In 6 patients, the concentration of taurine in CSF and serum did not change but urinary excretion increased. Four patients exhibited side effects of drowsiness and ataxia.
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PMID:Therapeutic trial by taurine for intractable childhood epilepsies. 703 91


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