Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(+)-4-propyl-9-hydroxynaphthoxazine (PHNO) is a novel selective D2 agonist. The efficacy and safety of PHNO was studied in 10 Parkinsonian patients (Hoehn and Yahr Stage II or III) who continued to receive levodopa/carbidopa. At the lowest dose administered (0.25 mg tid), nine of the 10 patients improved with respect to rigidity, bradykinesia and tremor. At this dose there was one dropout because of severe orthostasis. Although there was a trend towards improvement in motor scores with the higher doses (0.5-1.0 mg tid), this was not statistically significant. At higher doses there were a total of four dropouts because of adverse effects such as nausea, vomiting and orthostatic hypotension. It appears that PHNO may prove to be efficacious in the treatment of Parkinson's disease.
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PMID:The efficacy of (+)-4-propyl-9-hydroxynaphthoxazine as adjunctive therapy in Parkinson's disease. 274 65

Primidone was compared to the unselective beta adrenoceptor antagonist propranolol in the suppression of essential tremor. In a 4-week single-blind placebo-controlled study primidone was given in increasing doses from 62.5 mg X 1 up to 250 mg X 3 daily and propranolol 20 mg X 3 daily. The drugs produced a similar reduction in the degree of tremor after 2 and 1 weeks' medication respectively. This indicates that primidone can be an alternative to propranolol when beta-blockers are contraindicated. However, primidone was significantly even more effective in the beginning after only 2 doses, when at the same time 10 of 13 patients showed a maximum of acute toxic side-effects producing nausea, vomiting, giddiness and/or sedation. Correlation analysis between the individual tremor amplitude reductions and plasma primidone concentrations showed on the second day a tendency towards a greater reduction in tremor in those patients with the highest primidone plasma concentration. By the fourteenth day tremor had increased compared with the second day and correlation analysis between individual increase in tremor amplitude and plasma phenobarbital concentrations showed the highest degree of tremor increase in those patients who had the highest levels of phenobarbital. These and other data suggest that after the first doses, tremor suppression and acute toxicity is related to the initial exposure to primidone and the plasma level of the drug itself rather than its metabolites phenobarbital and phenylethylmalanomide. The individual tremor frequency spectrums did not change significantly during the placebo and propranolol periods, whereas the frequency tended to decrease during the primidone period.
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PMID:Primidone and propranolol in essential tremor: a study based on quantitative tremor recording and plasma anticonvulsant levels. 288 81

Flumazenil (Ro 15-1788) proved to be a very efficacious competitive antagonist of benzodiazepines that reliably counteracts their pharmacological actions within 1-2 min as could be demonstrated in clinical and EEG studies. In general, a total dose of 0.3-0.8 mg will be sufficient in clinical practice, avoiding side effects like nausea, tremor, sweating, or transient anxiety that could be observed when higher dosages were administered. Its therapeutic range is very high as could be demonstrated in experimental animal in which up to 8.000-fold the clinical dose was administered. The total volume of distribution (Vdes) amounts to nearly 1.000 ml/kg BW and the total clearance exceeds 1.200 ml/min, resulting in a biological half-life of less than 60 min. According to the benzodiazepine dosage and the rapid plasma concentration decline of flumazenil, in some cases a resedation could be observed. Hence, a careful observation of the antagonised patient on the ward is mandatory for 1.5-2 h, even if at first sight the antagonization seemed successful and the patient fully awake and cooperative. In anaesthesia, indications to administer flumazenil are adverse drug reactions and prolonged recovery after adequate benzodiazepine dosage. In intensive care medicine, the antagonist may be used in the treatment of benzodiazepine overdose as well as in the differential diagnosis of a coma of unknown origin. Additionally, the antagonist may be administered to interrupt benzodiazepine sedation e.g. for neurological examination.
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PMID:[Antagonism of the effects of benzodiazepines using flumazenil (Ro 15-1788)]. 289 85

In a double-blind placebo-controlled cross-over study the encephalotropic and psychotropic properties of sertraline--a new potent and highly selective inhibitor of synaptosomal serotonin uptake--were studied along with blood levels of the parent drug and main metabolite in ten normal healthy volunteers. They received randomized at weekly intervals oral single doses of placebo, 100, 200 and 400 mg setraline and 100 mg zimelidine as reference drug. Blood sampling, EEG recordings, psychometric tests and evaluation of pulse, blood pressure and side-effects were carried out at the hours 0, 2, 4, 6, and 8. Blood level investigations demonstrated that sertraline is slowly absorbed with dose-dependent blood concentrations peaking in the 4th to 6th hour and remaining high thereafter, while the main metabolite, CP-53261 exhibited an even slower rise in plasma concentration up to the 8th hour. Computer-assisted spectral analysis of the EEG demonstrated slight effects of 100 mg zimelidine and 100 mg sertraline on human brain function, but moderate to marked effects after 200 and 400 mg sertraline as compared with placebo. Changes after 100 mg sertraline and the reference compound resembled the pharmaco-EEG profiles of antidepressants of the desipramine type and were indicative of some vigilance-improving properties while higher doses of sertraline induced alterations reminiscent of those after antidepressants of the imipramine type, thereby reflecting vigilance changes of the dissociative type. This neurophysiological conclusion was supported by the psychometric and psychophysiological data showing partly after 100 mg sertraline and zimelidine an improvement in psychometric performance, while 200 and 400 mg sertraline induced a deterioration of noopsyche and thymopsyche of the normal volunteers. Psychophysiological variables exhibited a dose-dependent change in CNS activation and a widening of the pupillary size. Time-efficacy calculations based on pharmacodynamic changes demonstrated maximal encephalotropic effects after 100 mg zimelidine in the 2nd to 4th hour, and after setraline in the 4th to the 6th hour, which is in agreement with the blood level data. Pulse, systolic and diastolic blood pressure showed no clinically relevant findings. Side-effects were non-existent to minimal after 100 mg zimelidine and sertraline, but marked after 200 and 400 mg sertraline characterized by nausea, vomiting, diarrhea, giddiness, restlessness, tremor and trismus.
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PMID:On central effects of serotonin re-uptake inhibitors: quantitative EEG and psychometric studies with sertraline and zimelidine. 294 57

A case is reported in which tocainide, a relatively new cardiac antiarrhythmic for oral use, is believed to have caused a delirium. The patient had been admitted to a coronary intensive care unit for the treatment of ventricular arrhythmia and had developed confusion, impairment in concentration and severe anxiety. Her EEG was compatible with metabolic encephalopathy. The clinical picture varied with the use of tocainide so closely that it appeared to be the most likely cause of the delirium. Other factors were taken into consideration but did not seem to adequately disprove this impression. Tocainide has been known to cause minor, transient and treatable side effects in the form of gastrointestinal and central nervous symptoms--mainly nausea, tremor and dizziness. There have also been three case reports of paranoid psychoses. It is suggested that psychiatrists be aware of the above complications as they may have occasion to see patients taking tocainide, especially in consultation-liaison work. A table with the more common side effects and their frequencies is included.
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PMID:Mental changes associated with tocainide, a new antiarrhythmic. 310 61

In a randomized, prospective, double-blind trial we investigated the efficacy and safety of the benzodiazepine antagonist RO 15-1788 in 57 patients undergoing general surgery. Anesthesia was induced and maintained by a combination of Flunitrazepam-Fentanyl-Pancuronium. Inhalation anesthetics were excluded from the study. After reversal of any residual relaxant effect we titrated RO 15-1788 or placebo by repeated i.v. administration of 0.1 mg (= 1.0 ml) up to a maximum dosage of 1.0 mg or to a definite arousal reaction. Before as well as 5, 10, 15, 30, 60, and 120 min after injection of the trial substance we evaluated efficacy (sedation, comprehension and collaboration, orientation in time and space), presence of anterograde amnesia, side-effects, hemodynamics, and subjective patient assessment by a point scale. RO 15-1788 significantly improved the level of consciousness (P less than 0.005) at a dosage of 0.59 +/- 0.29 mg at 5, 15, 30, and 60 min after administration as well as orientation in time and space (P less than 0.005) after 30 min. There was significantly less anterograde amnesia (P less than 0.005) after 15, 30, and 60 min. Symptoms of a benzodiazepine rebound effect after 120 min indicate a short half-life time of RO 15-1788. We did not observe any hemodynamic side effects. Local tolerance was good. Side effects in terms of nausea (1 case), vomiting (4), euphoria or dysphoria (2), benign cardiac arrhythmias (1) or a state of excitation (1) occurred several times after RO 15-1788 as well as after placebo (nausea 2, vomiting 6, muscular tremor 1). Our results indicate the efficacy and safety of RO 15-1788.
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PMID:[Efficacy and safety of the benzodiazepine antagonist RO 15-1788]. 313 35

Three placebo-controlled double-blind and crossover trials were carried out to analyze the effects of oral yohimbine (YOH) 0.8 mg/kg on mood and performance in 16 healthy students. Subjective assessments (visual analogue scales, side-effects on questionnaire) and objective measurements (digit symbols, flicker fusion, tapping, heterophoria) were done at baseline, and post treatment. YOH shifted the healthy subjects' mood towards feeling panicked, elevated systolic blood pressure and plasma prolactin concentrations, reduced digit symbol substitution, and induced drowsiness and passiveness. Caffeine (CAF) 10 mg/kg raised plasma cortisol and rendered the subjects slightly panicked. Muzziness, clumsiness, tremor, chills and nausea were common after both YOH and CAF. Diazepam (DZ) 0.3 mg/kg given at 60 min antagonized some effects of CAF but failed to antagonize YOH. Clonidine (CLO) 100 micrograms counteracted YOH effects on blood pressure but less the subjective and hormonal effects. CLO 200 micrograms partly antagonized the pressor, sedative but not the hormonal responses of YOH. DZ counteracted YOH effects on plasma cortisol on panic but not on other subjective measures or plasma prolactin. Since CLO did not abolish YOH-induced prolactin increase, it is suggested that these effects of YOH are mediated not only via adrenergic alpha 2-receptors; other mechanisms made important contributions.
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PMID:Anxiogenic effect of yohimbine in healthy subjects: comparison with caffeine and antagonism by clonidine and diazepam. 315 10

A phase I study of recombinant human tumor necrosis factor (rHu-TNF:PT-050) given by intravenous infusion over 30 min or by intratumoral administration was performed in 53 patients with various types of malignant tumors. The dose of rHu-TNF was started with 0.1 x 10(6) U/body for both intravenous infusion and intratumoral administration and increased to 5 x 10(6) U/body for intravenous infusion and 2 x 10(6) U/body for intratumoral administration. The side effects of rHu-TNF given by intravenous infusion included fever, shaking chills, hypotension, general malaise, nausea, and vomiting, and clinical laboratory tests showed elevations of GOT, GPT, and ALP, etc. Among these, only hypotension was dose-related and was considered to be a dose-limiting factor. The maximum tolerable dose estimated was 1 x 10(6) U/body. The plasma concentration of rHu-TNF after completion of a 30-min infusion was dose-dependent, and the elimination half-life was 0.5-2.4 hr. When the rHu-TNF was administered intratumorally, the frequency of side effects was low compared with intravenous infusion.
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PMID:Phase I study of recombinant human tumor necrosis factor (rHu-TNF:PT-050). 318 Jan 46

Over 100 workers exposed to trichloroethylene (TRI) mostly at less than 50 ppm during the production or vapor degreasing operation and about an equal number of the non-exposed control workers were examined for subjective symptoms, hematology, serum biochemistry, and sugar, protein and occult blood in urine. Essentially all the clinico-laboratory tests stayed normal, and there was no significant differences in the findings between the exposed and the controls. Thus, no clinically significant effects of TRI exposure were found in the blood and liver functions among the exposed workers as compared with the controls. The prevalence of the subjective symptoms was, however, significantly higher in the exposed group than in the controls, and dose-response relationship could be established in some selected symptoms such as nausea, heavy feeling in the head, forgetfulness, tremor in extremities, cramp in extremities and dry mouth, although the exposure was low. The findings warrant further attention to the effects of TRI especially on the central nervous system at the concentration lower than e.g., 50 ppm.
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PMID:Increased subjective symptom prevalence among workers exposed to trichloroethylene at sub-OEL levels. 321 80

Heliox compression deeper than 16 ATA can lead to EEG changes associated with confusion and somnolence. In man the symptoms termed the high pressure neurologic syndrome (HPNS) can also include increased tremor, memory problems, dizziness, nausea, and vomiting. In a series of 3 dives at NUTEC, a compression profile developed for operational use down to 360 msw was evaluated. In each dive 6 different divers were compressed to 360 msw on heliox. Neuropsychologic and neurophysiologic testing were performed repeatedly. The HPNS testing revealed only mild effects of the compression. Only 3 divers had impairments of more than 2 SD in peripheral motor function compared to their predive average. Memory was impaired periodically in 2 divers. The same was found for perceptual speed and reasoning. Fifty percent of the divers had an increase of more than 2 SD in postural tremor, but that had minimal effect on their motor performance. Six of the 18 divers had an EEG power spectrum with both alpha band inhibition and theta increase. While the performance impairment was most marked around 240 msw, the EEG changes occurred mainly deeper than 300 msw. In only 1 of the 18 divers marked EEG changes, marked tremor increase, and marked cognitive performance impairment were observed at the same time. Although mild HPNS was observed, the divers were little impaired during the compression to 360 msw. The results confirm that using a compression profile with rates decreasing progressively with increasing depth, and with several intermediate stops, provides fit divers at depth. By using standard batteries of HPNS testing we were able to obtain evidence for the acceptability of this compression profile.
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PMID:HPNS effects among 18 divers during compression to 360 msw on heliox. 321 42


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