Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 9-year-old boy developed ataxia, right transient hemiparesis, left transient hemichorea, dysarthria and swallowing difficulties with left velar paralysis following two transient episodes of vomiting, headache and dizziness. Angiography demonstrated an occlusion of the distal part of the basilar artery. Thirty-six previously reported cases of vertebro-basilar arterial occlusion in children were reviewed, with particular regard to possible etiologies.
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PMID:Vertebro-basilar arterial occlusion in childhood--report of a case and review of the literature. 667 Jul 13

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

Twenty-two profoundly deafened adults, implanted with the single-electrode cochlear implant, were involved in a study to observe the effects of cochlear electrical stimulation on the vestibular system. Previous investigators had found evidence that the implant might disrupt postural stability. As there had been no general complaints of dizziness or dysequilibrium by the implant subjects, a study was undertaken to replicate the earlier study and to compare the results to more standardized procedures. A Sono-postural Test was devised from the Ataxia Test Battery for the testing of balance with and without an auditory prosthesis. Electronystagmography was also performed on the subjects before and after surgery as a means of monitoring vestibular status over time. Results from the these tests indicate that the single-electrode implant does not disrupt the balance system to any significant degree. In fact, evidence indicates that postural stability may actually improve with the cochlear implant activated.
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PMID:Effects of the single-electrode cochlear implant on the vestibular system of the profoundly deaf adult. 680 97

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

A short review is given of the pharmacokinetic characteristics and side effects of the nitroimidazoles: metronidazole, tinidazole and ornidazole. The drugs are well absorbed from the gastrointestinal tract, maximum plasma levels generally being obtained 1 to 4 h after oral intake. Metronidazole has been shown to be absorbed after rectal administration; vaginal absorption is documented for all three drugs. The nitroimidazoles are widely distributed in the body, cross the placenta and appear in breast milk. Therapeutically effective concentrations of e.g. metronidazole have been demonstrated in e.g. the central nervous system, middle ear discharges, bile, peritoneal fluid, and fluids and tissues of the female genital tract. The binding to plasma proteins is less than 20%. Available data suggest that the elimination half-lives of these drugs differ, being 7-8 h for metronidazole, about 12 h for tinidazole and 14-15 h for ornidazole. Both metronidazole and ornidazole, but not tinidazole, seem to be extensively metabolized before elimination. The nature and frequency of adverse reactions to this drug include encephalopathy in a few patients treated with doses between 5 and 10 g daily as an adjunct to radiotherapy, and peripheral neuropathy observed in patients treated for prolonged periods with high doses. Among the common side effects of the nitroimidazoles are symptoms from the gastrointestinal tract such as nausea, anorexia, vomiting and metallic or bitter taste. Dizziness, ataxia and headache have been reported. When given together with alcohol, a disulfiram-like intolerance reaction can be obtained.
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PMID:Pharmacokinetics of nitroimidazoles. Spectrum of adverse reactions. 694 57

Toluene appears to produce reversible effects upon liver, renal and nervous systems. Its usual route of intake is via respiration. The nervous system appears to be the most sensitive to the effects of toluene. Although there are few studies of toluene's neurotoxicity, some tenuous results can be cited. High level toluene exposures produced incoordination, ataxia, unconsciousness and eventually, death. Lower level acute exposures in man produce dizziness, exhilaration and confusion. Activity level has been inadequately studied. Schedule controlled behaviors have been reported to produce inverted U-shaped concentration-effect curves on response rate measures. Alterations at levels as low as 150 ppm have been reported when appetitive contingencies are used. Very few studies of the nervous system have been performed at levels below 1000 ppm and most of the results were inconclusive. The TLV (threshold limit value) of toluene has been set at 100 ppm for 8 hrs. No exposures on possible groups at special risk, such as perinatal, aged or impaired subjects have been made. Few studies of reversibility of effects in the nervous system have been reported. Much more work is needed before strong conclusions can be drawn.
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PMID:Neurobehavioral effects of toluene: a review. 703 26

Eight patients were evaluated for severe vertebrobasilar insufficiency (VBI). There were five males and three females, with an average age of 60.2 years (range 42 to 67 years). Three were diabetic and five hypertensive, including two patients who had both diseases. Seven of the eight had ongoing episodes of VBI refractory to anticoagulant and/or antiplatelet agents. Symptoms included two or more of the following in all patients: dizziness, diplopia, hemiparesis, hemihypesthesia, perioral numbness, bilateral visual blurring, dysarthria, and ataxia. Angiography revealed severe atherosclerotic stenosis of the proximal or midsection of the basilar artery in all patients. A 10-cm segment of the anterior or posterior division of the superficial temporal artery (STA) was anastomosed to a proximal segment of the superior cerebellar artery (SCA) through a right subtemporal approach. Seven of eight (87%) postoperative angiograms demonstrated patency as evidenced by filling of the SCA and, in most cases, of the basilar artery. Six of the eight patients were improved or asymptomatic after the operation, one was unchanged, and one died. The average follow-up period was 14 months, with a range of 4 to 23 months. Transient morbidity included temporal lobe swelling in four patients and a subdural hematoma in one. Anastomosis of the STA to the SCA is a feasible therapeutic option in the patient with VBI secondary to stenosis of the proximal or midsection of the basilar artery.
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PMID:Posterior circulation revascularization. Superficial temporal artery to superior cerebellar artery anastomosis. 707 75

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16


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