Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical examinations, questionnaires, and 24- or 36-hour polygraphic recordings were performed on 21 adult patients with the narcolepsy syndrome to investigate the short- and long-term effects of clomipramine HCL. Cataplexy was improved by the medication, but tolerance was observed 4 1/2 months of treatment. Clomipramine HCL induced significant changes in the sleep EEG, chin EMG, and EOG. In two patients, clomipramine HCL caused a nocturnal myoclonia that produced insomnia. Sexual side effects were seen with clomipramine HCL, particularly in males. A combination of clomipramine HCL and L-Dopa apparently prevented this difficulty in one patient. A rebound of cataplexy was seen during the 15 days following withdrawal of the drug. Methysergide maleate was found to be ineffective on cataplexy in four patients.
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PMID:Evaluation of short-term and long-term treatment of the narcolepsy syndrome with clomipramine hydrochloride. 93 75

Two sporadic cases of striato-nigral degeneration were characterized by the onset at the age of 61 of an akinetic-hypertonic syndrome and of a minimal or absent rest tremor, with a pyramidal syndrome, sphincter disorders, dysphonia, difficulty in swallowing and an unfavorable development in the space of two or three years not affected by L-Dopa. In one case, total insomnia was demonstrated by means of 3 polygraphic recordings during the night, two of them consecutive, and aprobenecide test showed a definite fall in H.V.A. and 5 H.I.A.A. in the lumbar cerebrospinal fluid. Anatomical verification showed, in one case, isolated putamino-nigral degeneration, and in the other associated with lesions of the olivo-cerebellopontine system. Much of the excess pigmentation found only in the putamen was melanotic in character and resulted perhaps from the striato-nigral degeneration, making it possible to classify this more accurately among the other multisystem degenerations, especially olivo-ponto-cerebellar atrophy and Shy-Drager syndrome
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PMID:[Striato-nigral degeneration. A propos of 2 anatomo-clinical cases]. 96 12

Sixteen patients with symptoms of restless legs syndrome and resulting insomnia are included in this study. They were nine women and seven men with a mean age of 50.8 years and with a mean duration of symptoms of 6.3 years. The purpose of the study is to determine the drugs that are useful for the treatment of restless legs syndrome. In 13 patients L-Dopa plus benserazide, in two patients bromocriptine, and in the remaining one patient piribedil were used orally at night approximately 1 h before bedtime. Compared with placebo these dopaminergic drugs decreased the times of waking up and staying awake periods at a statistically significant level (p changed between 0.025 and 0.01, t test). In this susceptibility of CNS there is dysfunction of the dopamine system triggered by sleep, and resting and dopaminergic potentiation by drugs affect the symptoms.
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PMID:Restless legs syndrome treatment with dopaminergic drugs. 354 61

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

A woman and her son had progressive dystonia and chronic insomnia at 32 and 19 years of age respectively. Levodopa was markedly effective at low dose both for dystonia and insomnia without dyskinesia over a 5-year follow-up period.
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PMID:[L-dopa-responsive dystonia: 2 familial cases of adult onset with sleep disorders]. 748 95

Twenty patients with problematic restless legs syndrome (RLS) were treated with pergolide. Efficacy, dosage, side effects, and tolerance were analyzed. Fifteen patients continued treatment for a median study time of 2 years. Five patients discontinued treatment after a mean of 4.2 months. Pergolide resulted in complete or near complete control of symptoms in 45% and moderate control in 50% of patients studied. Levodopa-induced daytime augmentation resolved in all patients in whom it had been present. The mean total daily maintenance dose of pergolide was 0.23 mg. Forty percent required an additional afternoon dose. Side effects developed in 12 patients (60%) and necessitated discontinuation of treatment in five. Common side effects were nausea, dizziness, and insomnia. Daytime augmentation occurred in 27% of patients, but this was mild and usually easily controlled with a supplementary afternoon dose of pergolide. Tolerance did not develop. We conclude that pergolide is an effective second-line agent for RLS, especially following levodopa-induced daytime augmentation.
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PMID:Pergolide in the management of restless legs syndrome: an extended study. 941 48

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

Semen Zizhiphi Spinozae has been used extensively for the treatment of insomnia. This study investigated the effect and possible mechanism of action of spinosin (also known as 2''-beta-o-glucopyranosyl swertisin), a major constituent of semen Zizhiphi Spinozae, on sleep in mice. The present results showed that spinosin significantly and dose-dependently augmented pentobarbital (45 mg/kg, i.p.)-induced sleep, reflected by increased sleep time and reduced sleep latency assessed with the loss-of-righting reflex, and these effects were potentiated by the 5-hydroxytryptamine (serotonin) precursor 5-hydroxytryptophan (5-HTP, 2.5 mg/kg,i.p.). With a subhypnotic dose of pentobarbital (28 mg/kg, i.p.), spinosin significantly increased the rate of sleep onset and exhibited a synergistic effect with 5-HTP (2.5 mg/kg, i.p.). Pretreatment with p-chlorophenylalanine (PCPA, 300 mg/kg, s.c.), an inhibitor of tryptophan hydroxylase, significantly decreased pentobarbital-induced sleep time, and spinosin significantly reversed this effect. The dopamine precursor L-3-(3, 4-dihydroxyphenylalanine (L-DOPA) reduced pentobarbital-induced sleep, an effect not significantly affected by spinosin. These results suggest that spinosin potentiated pentobarbital-induced sleep via a serotonergic mechanism.
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PMID:Spinosin, a C-glycoside flavonoid from semen Zizhiphi Spinozae, potentiated pentobarbital-induced sleep via the serotonergic system. 1846 60

Levodopa has been the gold standard therapy for the motor symptoms of Parkinson's disease for more than three decades. Although it remains the most effective treatment, its long-term use is associated with motor fluctuations and dyskinesias that can be disabling for patients and difficult for physicians to manage medically. In the last 10 years, the catechol-O-methyltransferase (COMT) inhibitor tolcapone has been studied for its efficacy as an adjunctive treatment to levodopa plus a dopa decarboxylase inhibitor. Adjunctive therapy with tolcapone can significantly reduce the dose of levodopa required. Moreover, treatment with tolcapone significantly reduces wearing off and on-off periods in fluctuating patients and improves 'on' time in patients with stable disease. Tolcapone has assumed a new place in the arsenal of medications for Parkinson's disease. This paper reviews the pharmacology, safety and efficacy of tolcapone in patients with advanced Parkinson's disease. After some initial concerns about its safety, tolcapone has been shown to be safe if used and monitored according to guidelines regarding liver function. Tolcapone produces expected dopaminergic side effects, including headache, nausea, insomnia, as well as diarrhea; however, these side effects are generally mild and as a rule do not result in discontinuation of therapy.
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PMID:Tolcapone: review of its pharmacology and use as adjunctive therapy in patients with Parkinson's disease. 1950 73

Levodopa-induced dyskinesia can result in significant functional disability and reduced quality of life in patients with Parkinson's disease (PD). The goal of this study was to determine if the addition of once-daily ropinirole 24-hour prolonged-release (n = 104) in PD patients not optimally controlled with levodopa after up to 3 years of therapy with less than 600 mg/d delays the onset of dyskinesia compared with increasing doses of levodopa (n = 104). During the study, 3% of the ropinirole prolonged-release group (mean dose 10 mg/d) and 17% of the levodopa group (mean additional dose 284 mg/d) developed dyskinesia (P < 0.001). There were no significant differences in change in Unified Parkinson's Disease Rating Scale activities of daily living or motor scores, suggesting comparable efficacy between the two treatments. Adverse events were comparable in the two groups with nausea, dizziness, insomnia, back pain, arthralgia, somnolence, fatigue, and pain most commonly reported. Ropinirole prolonged-release delayed the onset of dyskinesia with comparable efficacy to increased doses of levodopa in early PD patients not optimally controlled with levodopa.
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PMID:Onset of dyskinesia with adjunct ropinirole prolonged-release or additional levodopa in early Parkinson's disease. 2046 3


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