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)

Five female inpatients with major depression (melancholic type, DMS-III-R) were treated with the beta-adrenergic agonist clenbuterol for three weeks, with doses ranging from 100 micrograms to 150 micrograms. Remission of depressive symptomatology during treatment was observed in only one patient. All patients complained of side effects, especially tremor, agitation and restlessness. The sleep EEG showed no consistent effects on sleep parameters, including REM latency and percentage of REM sleep. Thus, the impact of clenbuterol on sleep clearly differs from that of most classical antidepressants. Regarding the lack of therapeutic efficacy, the data are compatible with the hypothesis of a relationship between REM sleep suppression and an antidepressant drug effect. Despite the small sample size, it can be concluded that clenbuterol is not likely to be a promising alternative to proven antidepressants in the treatment of major depression.
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PMID:The action of clenbuterol on sleep and symptomatology in depressives. 189 86

Three aged patients (age 63-78 years) had 3-15-year histories of abnormal behaviors during nocturnal sleep. These three patients presented no other psychiatric problems. Polysomnographic recordings were carried out from 1-3 nights after adaptation. The patients were simultaneously monitored via a video system during the recording period. Various nocturnal behaviors, including laughing, weeping, the shaking of arms and getting up were detected during these recordings. These behaviors appeared exclusively during REM periods which were associated with a large amount of abnormal REM sleep lacking muscle atonia (d-STREM with EMG). NREM sleep architecture was intact and %SWS was within the normal limits per age for all the patients. The patients, manifesting such abnormal behaviors during sleep, could be aroused completely with awakening stimuli, and could recall in detail their unpleasant dreams. Two of the three were treated with clonazepam (0.5-1 mg/day) which immediately decreased the abnormal behaviors during sleep. Polysomnographic studies after the treatment showed a marked decrease in the d-STREM with EMG. The above results indicate that these abnormal behavior during nocturnal sleep were closely linked to d-STREM with EMG. And the administration of clonazepam not only led to an amelioration in the abnormal behaviors but also in the polysomnographic pathology. It is concluded that parasomnia in the aged is characterized by behavioral manifestations of the dreaming due to dysfunctions of the muscle atonia system.
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PMID:[Parasomnia associated with abnormal REM sleep in the aged]. 237 83

Twenty male adult Wistar rats were unilaterally lesioned in the substantia nigra (SN) with 6-hydroxydopamine (6-OHDA), and prepared with chronic cortical (ECoG) and neck muscle (EMG) electrodes. Longitudinal study over a period of up to 18 months demonstrated the emergence, in about two-thirds of the rats, of spontaneous repetitive episodes of head and neck tremor during awake at rest, of up to 20 seconds duration each, that were associated with spike and wave-like ECoG activities. These episodes of tremor at rest disappeared during sleep and REM sleep episodes, and also following the i.p. administration of L-DOPA. It is assumed that these tremor at rest episodes are analogous to those reported to occur in primates after experimentally induced dysfunction of the nigro-striatal, extrapyramidal system.
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PMID:Tremor at rest episodes in unilaterally 6-OHDA-induced substantia nigra lesioned rats: EEG-EMG and behavior. 308 91

The present work studied the effects of REM sleep deprivation on the responses to cholinomimetic drugs in rats. Cataleptic behavior induced by pilocarpine, oxotremorine and eserine was not modified by previous REM sleep deprivation. On the other hand, the intensity of oxotremorine- and eserine-induced tremors, but not that of pilocarpine, was clearly augmented in the REMd rats and latency to the first tremor was shorter. REM sleep deprivation also potentiated the convulsions induced by nicotine. Two hypothetical mechanisms through which REM sleep deprivation could lead to the described hyperresponsiveness to cholinomimetic drugs are discussed.
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PMID:Central responses to cholinergic drugs of REM sleep deprived rats. 336 16

A pharmacological study was carried out of a case of severe insomnia following brain-stem lesions; several polygraphic controls were used. Initially total duration of sleep was brief (less than 4 h) with a high REM/NREM ratio and a short paradoxical sleep (PS) latency. In addition, periodic breathing and tremor were observed. Slow injection of delta-sleep-inducing peptide (DSIP) improved sleep both quantitatively and qualitatively, although PS latency remained short. These effects were reversible. The effects of 5-HTP + benzerazide, of L-DOPA + benzerazide (Modopar) and of clonazepam (Rivotril) were compared.
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PMID:Sleep disturbances in a case of brain-stem lesions; pharmacological study. 619 41

Several authors have recommended [1, 3, 8, 12] that the fetus be mechanically stimulated if the abdominal pregnancy CTG shows no accelerations. One expects the fetus to show a motor response to mechanical stimulation. Fetal movements expressed as accelerations in the abdominal CTG are considered to reflect "arousal" of the previously asleep fetus and are thought to be normal. An absence of such a response in considered by some as a sign of pathological fetal changes [3, 8, 12]. Others, however, have found that the normal non-stressed fetus need not change its sleep-arousal state after mechanical stimulation [5, 14]. An attempt was made to clarify this in the present work. We studied the CTG recordings and the ultrasound pictures in 63 pregnancies in a total of 83 cases for an average of 56 minutes. Fetal movements were marked by pressing a lever on the labor pressure chart. The fetus was mechanically stimulated by shaking its head manually for 5 seconds. Control recordings were also made, when the fetus was not so stimulated. The following results were obtained: With a normal CTG (reactive nonstress test, FISCHER score 8-10 points) Mechanical stimulation led to no changes in 87% of NREM sleep and in 93.9% of REM sleep. A change to a more active state (REM sleep + arousal) due to stimulation was found in 13% of NREM sleep, which is significantly more frequent than the 2.9% found when no stimulation occurred. A change from REM sleep to arousal was found in 6.1%, not significantly different from 1.8% found without stimulation. Short-lasting reactions to mechanical stimulation included movements, acceleration of fetal heart rate and dip 0. These reactions were equally frequent in REM and NREM sleep, i.e. 75% and 68.5% respectively. These reactions occurred by chance less frequently, in 14.5% of cases in REM and in 3% of cases in NREM sleep (Tab. II). The occurrence is significantly higher in REM than in NREM sleep. In a pathological CTG (Fischer score 7 points or less) our technique does not permit us to distinguish the different sleep-arousal states. Only the short-lasting response to mechanical stimulation of the fetus was hence evaluated. Mechanical stimulation resulted in a fetal response in 19% with decelerations of variable expression (Figs. 1a, 1b, 2, 3) similar to the variable decelerations observed during labor. These decelerations occurred only together with other signs of fetal distress in the CTG.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Fetal response to external mechanical stimuli. 664 17

This is a first report on the investigation of the antidepressant activity of MCI-225 (4-(2-fluorophenyl)-6-methyl-2-(1-piperazinyl)thieno[2,3-d]pyrimidine monohydrate hydrochloride, CAS 99487-26-0) in comparison with maprotiline (CAS 10347-81-6), desipramine (CAS 58-28-6), imipramine (CAS 113-52-0) and trazodone (CAS 25332-39-2). MCI-225 inhibited the synaptosomal uptake of noradrenaline (NA, Ki = 35.0 nmol/l), serotonin (5-HT, Ki = 491 nmol/l), and dopamine (Ki = 14,800 nmol/l), although it did not inhibit MAO-A and MAO-B activities. MCI-225 showed high affinity only for the 5-HT3 receptor (Ki = 81.0 nmol/l) among all receptors tested including M1, M2, alpha 1, and H1 receptors. The inhibition of the von Bezold-Jarisch reflex by MCI-225 (ID50 = 22.2 mg/kg, p.o.) suggests its antagonistic action on the 5-HT3 receptor. MCI-225 dose-dependently reduced reserpine-induced hypothermia (0.3-10 mg/kg, p.o.) and potentiated yohimbine-induced lethality (3-100 mg/kg, p.o.) in mice. These effects of MCI-225 were as potent as desipramine and more potent than maprotiline, imipramine and trazodone. MCI-225 and desipramine did not change either 5-HTP-induced head movements or p-CA-induced hyperactivity in rats. In forced swimming tests in rats, the minimum effective doses of MCI-225, maprotiline, desipramine, and imipramine were 1, 30, 10 and 30 mg/kg, p.o., respectively, for 5-days administration. Only MCI-225 had shown its full activity with this short term treatment. MCI-225 (10 mg/kg, p.o.) decreased the REM sleep period without affecting slow-wave sleep or wakefulness in rats. Even at 100 mg/kg, p.o. MCI-225 and trazodone did not inhibit oxotremorine-induced tremor, lacrimation or salivation in mice in contrast with imipramine. These results suggest that MCI-225, which selectively inhibits NA uptake and antagonizes the 5-HT3 receptor, has potential as a new type of potent antidepressant.
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PMID:Pharmacological profile of the novel antidepressant 4-(2-fluorophenyl)-6-methyl-2-(1-piperazinyl)thieno-[2,3-d]pyrimidine monohydrate hydrochloride. 945 Jan 61

Patients suffering from Parkinson's disease (PD) often report about sleep disorders and excessive daytime sleepiness. To some extent, motor disabilities or neural degeneration of sleep modulating structures may be responsible for these effects. Depressive disorders also contribute to the occurrence of insomnia and daytime sleepiness. Nevertheless, dopaminergic, anticholinergic, and other drugs used in PD have a great impact on sleep/wakefulness mechanisms. They may indirectly improve or worsen sleep by changing motor symptoms such as akinesia, hyperkinesia, or tremor. Although their is only little information on the complex regulation of vigilance, it is well known that monoaminergic and cholinergic drugs could influence it directly. Data from animal experiments and clinical experiences led to the hypothesis of a biphasic influence on sleep by dopaminergic substances: small doses of L-Dopa e. g. appear to improve sleep whilst higher doses led to insomnia. Different dopaminergic receptor types or changes in receptor sensitivity may explain these phenomena. Dopaminergic and anticholinergic drugs suppress REM sleep. Recently, initial data on 'sleep attacks' after pramipexole or ropinirole treatment were published. Our preliminary results using 24 h polygraphic recordings showed excessive daytime sleepiness in patients taking ropinirole and L-Dopa which disappeared when changed to ropinirole monotherapy. Sleepiness did never appear as an irresistible attack. Current hypotheses on this topic are reviewed.
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PMID:Effects of parkinsonian medication on sleep. 1119 13

This study examined the effects of acute and chronic desipramine, 24-h total sleep deprivation (TSD) and 96-h REM sleep deprivation (REMSD) on physostigmine-induced hypothermia, analgesia and behaviour. The effects of acute and chronic desipramine treatment on oxotremorine-induced hypothermia were also examined. Intraperitoneal administration of physostigmine (0.5 mg/kg i.p.) induced hypothermia, analgesia, purposeless chewing movements (chewing) and head tremors. While atropine given in a low dose (1.0 mg/kg i.p. 15 min prior) did not antagonize the hypothermia, chewing and head tremor associated with physostigmine (0.5 mg/kg i.p.), a higher dose of atropine (10 mg/kg i.p. 15 min prior) decreased physostigmine-induced hypothermia, chewing and head tremor behaviour. Chronic (10 or 20 mg/kg i.p. daily for 10 days and withdrawn 24 h prior, chronic DMI) and acute (10 mg/kg, i.p. + 60 min prior, acute DMI) desipramine treatments abolished physostigmine (0.5 mg/kg i.p.)-induced hypothermia compared with saline pretreatment. Interestingly atropine (1 mg/kg i.p. 15 min prior) reversed the inhibitory effect of chronic DMI on hypothermia induced by physostigmine. Acute but not chronic DMI decreased physostigmine-induced chewing and head tremor behaviour. Atropine (1 mg/kg i.p. 15 min prior) increased the inhibitory action of acute DMI on physostigmine-induced chewing behaviour. Acute DMI (10 mg/kg i.p.) decreased oxotremorine (0.1 mg/kg i.p.)-induced hypothermia, while chronic DMI increased the hypothermic effect of oxotremorine. TSD and REMSD did not alter physostigmine (0.5 mg/kg i.p.)-induced hypothermia; however, REMSD and stress decreased physostigmine-induced analgesia and chewing.It is suggested that chronic desipramine treatment decreased physostigmine-induced hypothermia by causing hypersensitivity of pre-synaptic muscarinic receptors, whereas acute desipramine decreased the sensitivity of post-synaptic muscarinic receptors
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PMID:Functional reactivity of central cholinergic systems following desipramine treatments and sleep deprivation. 1368 87

Patients affected by Parkinson's disease (PD) often complain of disturbed sleep resulting from nighttime motor disabilities such as nocturnal akinesia, tremor and rigidity, motor behaviour during REM sleep or periodic leg movements (PLM) during sleep. Sleep may also be affected by dopaminergic and anticholinergic drugs or coexisting depressive syndrome. Deep brain stimulation (DBS) of subthalamic nucleus (STN) effectively reduces PD motor disability. The aim of this study is to evaluate the sleep architecture modifications after STN DBS. We assessed five patients (two men and three women, mean age 63.8+/-3.3 years, with a mean history of PD of 13.8+/-4.9 years) who underwent STN DBS. The mean levodopa equivalent dosage (LED) was 1010+/-318 mg before surgery and 116+/-93 mg 3 months after surgery. Polysomnography (PSG) with audiovisual recordings was performed on two separate nights, the first assessment in the week before surgery and the second 3 months after surgery. Three months after surgery, PSG showed an increase in total sleep time, in the longest period of uninterrupted sleep, and in the percentage of stage 3-4 NREM sleep, while there was a reduction of wakefulness after sleep onset. PLM, apnea-hyopnea index and REM sleep behaviour disorder were unaffected by STN DBS. STN DBS seems to be an effective therapeutic option for the treatment of advanced Parkinson's disease because it improves the cardinal symptoms and also seems to improve sleep architecture.
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PMID:Effects of deep brain stimulation of the subthalamic nucleus on sleep architecture in parkinsonian patients. 1503 45


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