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)

Bupropion SR was introduced for smoking cessation in the US in 1997. This review assesses the efficacy and safety of bupropion SR for treatment of tobacco dependence based on data from clinical trials and five years of postmarketing experience. Through June 2001, there were approximately 32 million patient exposures to bupropion (9 million for smoking cessation) in clinical practice, and more than 8000 patients have been studied in clinical trials for tobacco dependence. In clinical trials, bupropion SR was more effective than placebo at improving initial and long-term abstinence rates and preventing relapse. Bupropion SR is generally well tolerated. The most common adverse event in clinical trials or clinical practice is insomnia, which can also be a symptom of nicotine withdrawal. The two main risks of treatment with bupropion SR are major motor seizure and hypersensitivity reaction. Clinical trials data suggest that the incidence of seizure is approximately 0.1%, and that of serious cases of hypersensitivity approximately 0.12%. Benefit-risk assessment, assuming a 30% one-year quit rate demonstrates that for every 10,000 smokers treated with bupropion SR, 19 lives are saved and 86 cases of smoking-attributed morbidity are averted in a five-year period while the risk of experiencing one of the two potentially serious adverse events during treatment is 0.22%. These data further establish both the efficacy and safety of bupropion SR and its use in preventing the adverse health effects of chronic tobacco use.
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PMID:Efficacy and safety of bupropion SR for smoking cessation: data from clinical trials and five years of postmarketing experience. 1272 28

The advent of bupropion hydrochloride sustained release (Zyban) has heralded a major change in the options available for smoking cessation pharmacotherapy. Bupropion is a selective re-uptake inhibitor of dopamine and noradrenalin which prevents or reduces cravings and other features of nicotine withdrawal. Bupropion is a useful oral and non-nicotine form of pharmacotherapy for smoking cessation. For this review a total of 221 papers were reviewed plus poster presentations. This review examines in detail original clinical trials on efficacy, categorised according to whether they were acute treatment trials in healthy smokers; studies in specific populations such as people with depression, chronic obstructive pulmonary disease (COPD) or cardiovascular disease; or relapse prevention studies. Overall, these studies in varying populations comprising over four thousand subjects, showed bupropion consistently produces a positive effect on smoking cessation outcomes. The evidence highlights the major public health role that bupropion has in smoking cessation. The methodological issues of published clinical trials reporting one year outcomes were examined in detail including: completeness of follow-up; loss to follow-up; intention to treat analysis; blindness of assessment; and validation of smoking status. The review discusses contraindications, adverse effects, dose and overdose, addictive potential, and the role of bupropion in reducing cessation-related weight gain. Bupropion combined with or compared to other pharmacotherapies (nicotine patch; nortriptyline) is considered. Impressive evidence exists for the use of bupropion in smoking cessation among difficult patients who are hard-core smokers such as those with cardiovascular disease, chronic obstructive pulmonary disease (COPD) and depression. Bupropion reduces withdrawal symptoms as well as weight gain and is effective for smoking cessation for people with and without a history of depression or alcoholism. Serious side effects of bupropion use are rare. The major safety issue with bupropion is risk of seizures (estimated at approximately 0.1%) and it should not be prescribed to patients with a current seizure disorder or any history of seizures. In clinical trials of bupropion for smoking cessation no seizures were reported. Allergic reactions occur at a rate of approximately 3% and minor adverse effects are common including dry mouth and insomnia.
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PMID:Review of bupropion for smoking cessation. 1285 Sep 7

Bupropion hydrochloride is a monocyclic antidepressant which is used in a slow-release formulation as a smoking cessation aid. Its side effects include insomnia and dry mouth with seizures occurring in 1 in 1000 patients. In overdose, it can cause tachycardia, conduction defects and convulsions. It is, however, effective in smoking cessation in approximately 20% of patients and may be more effective if combined with nicotine replacement therapy. The key question is whether the risks associated with the drug are justified by the obvious benefits to health from smoking cessation.
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PMID:Zyban-- is there a cause for concern? 1290 29

Liposteroid was administered intravenously to 6 patients with refractory epileptic spasms. In one case, the spasms initially disappeared but then reappeared after three months. Another case had a transient and slight decrease of epileptic spasms. In the only patient in whom spasms disappeared, EEG abnormalities were greatly improved with diffuse spikes and waves changing into focal spikes. Two cases displayed hyperexcitability, insomnia and acting out behavior, and the therapy was discontinued in one of them. One case had appetite loss and another showed an increase in tonic seizures. No patient had serious adverse effects such as infection, edema, subdural hematoma and brain shrinkage. Although liposteroid therapy has been recommended as an easy, useful and safe alternative for ACTH, we found considerable adverse effects and only a small effect on refractory spasms, and conclude that the regimen should be modified.
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PMID:[Liposteroid therapy for refractory epileptic spasms]. 1463 51

The objective of this study was to evaluate sleep macrostructure and sleep disturbance in a group of 39 patients with temporal lobe epilepsy (TLE). Patients completed questionnaires to evaluate their sleep and subjective daytime sleepiness (Epworth Sleepiness Scale [ESS]) and undergone Polysomnography and Multiple Sleep Latency Test (MSLT). Daytime sleepiness was the most frequent complaint (85%), followed by wakefulness during sleep, history of seizures during sleep (75%) and initial insomnia (26%). Parasomnias (67%), obstructive sleep apneas (13%), restless legs syndrome (15%) and periodic limb movements (5%) were the most frequent sleep disorders. The most frequent changes of sleep patterns were: sleep architecture fragmentation (100%), decreased amount of REM sleep (92%) and increase in time awake after sleep onset (77%). There were significative correlations between the ESS and the MSLT (p<0,05). In conclusion, TLE patients have fragmented sleep with increased sleep stages shifts, increased number of awakenings and in time awake after sleep onset. REM sleep was decreased. Daytime sleepiness was the most frequent complaint in TLE patients.
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PMID:[Sleep disorders in temporal lobe epilepsy]. 1476 2

The spectrum of alcohol withdrawal symptoms ranges from such minor symptoms as insomnia and tremulousness to severe complications such as withdrawal seizures and delirium tremens. Although the history and physical examination usually are sufficient to diagnose alcohol withdrawal syndrome, other conditions may present with similar symptoms. Most patients undergoing alcohol withdrawal can be treated safely and effectively as outpatients. Pharmacologic treatment involves the use of medications that are cross-tolerant with alcohol. Benzodiazepines, the agents of choice, may be administered on a fixed or symptom-triggered schedule. Carbamazepine is an appropriate alternative to a benzodiazepine in the outpatient treatment of patients with mild to moderate alcohol withdrawal symptoms. Medications such as haloperidol, beta blockers, clonidine, and phenytoin may be used as adjuncts to a benzodiazepine in the treatment of complications of withdrawal. Treatment of alcohol withdrawal should be followed by treatment for alcohol dependence.
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PMID:Alcohol withdrawal syndrome. 1505 9

Zolpidem is a sedative and hypnotic drug belonging to imidazopyridine family. Zolpidem facilitates GABAA function more selectively than benzodiazepines, and produces a selective hypnotic effect. In comparison with benzodiazepines this mechanism could be reduce liability to induce dependence. Recently, some cases of zolpidem abuse and dependence have been published. The Authors report 2 cases of addiction to high dose of zolpidem and compare them with others described in the literature. Both patients had been reknown drug addicts before their first prescription of zolpidem and a borderline personality disorder was diagnosed. The patients rapidly developed over consumption and dependence of the molecule, when taking doses as high as 240 and 400 mg daily. To get zolpidem, one patient falsifies prescriptions. They don't suffer from the sedative effects while searching for anxiolytic and stimulating effects. They were also dysarthric, confused, high energy for mental and physical activity. The cases of zolpidem abuse and dependence in the literature describe these symptoms and others such as losing sense of orientation in time and space, amnesia and visual hallucinations. The most typical withdrawal symptom is high levels of anxiety. Moreover, one patient presents an epileptic seizure whereas the other display a severe psychiatric complication such a psychosis. In the literature, withdrawal was accompanied by confusion, suicidal ideas, nausea, vomiting, sweat, tremors, tachycardia and insomnia rebound. The epileptic seizures are described but acute psychosis complication is rare. Pharmacological hypotheses are described. The effects of zolpidem on GABAA receptor gene expression are consistent with the reduced tolerance liability of this drug as well as with other ability to induce both physical dependence and withdrawal syndrome. Through the review of the literature, the Authors noted that 50% of the cases of dependence on zolpidem are drug addicts, therefore concluding that drug addicts are more likely to become dependent on zolpidem.
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PMID:[Dependence on zolpidem: a report of two cases]. 1510 18

Adenosine is a purine nucleoside and modulates a variety of physiological functions by interacting with cell-surface adenosine receptors. Under several adverse conditions, including ischemia, trauma, stress, seizures and inflammation, extracellular levels of adenosine are increased due to increased energy demands and ATP metabolism. Increased adenosine could protect against excessive cellular damage and organ dysfunction. Indeed, several protective effects of adenosine have been widely reported (e.g., amelioration of ischemic heart and brain injury, seizures and inflammation). However, the effects of adenosine itself are insufficient because extracellular adenosine is rapidly taken up into adjacent cells and subsequently metabolized. Adenosine uptake inhibitors (nucleoside transport inhibitors) could retard the disappearance of adenosine from the extracellular space by blocking adenosine uptake into cells. Therefore, it is expected that adenosine uptake inhibitors will have protective effects in various diseases, by elevating extracellular adenosine levels. Protective or ameliorating effects of adenosine uptake inhibitors in ischemic cardiac and cerebral injury, organ transplantation, seizures, thrombosis, insomnia, pain, and inflammatory diseases have been reported. Preclinical and clinical results indicate the possibility of therapeutic application of adenosine uptake inhibitors.
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PMID:Adenosine uptake inhibitors. 1521 15

The relationship of sleep and epilepsy demonstrates the delicate association of brain physiology and dysfunction. Sleep affects the distribution and frequency of epileptiform discharges in humans and influences the rate of kindling in animals. Epileptic discharges, on the other hand, alter sleep regulation and provoke sleep disruption. This effect on sleep appears to carry over to sleep complaints in patients with epilepsy. Individuals with epilepsy frequently complain of symptoms suggestive of disturbed sleep, such as excessive daytime sleepiness, insomnia, or with more subtle complaints such as an increase in seizure frequency. More commonly, these symptoms indicate an underlying sleep disorder rather than the effect of epilepsy or medication on sleep. Clinicians must be able to identify and differentiate between potential sleep disorders and sleep dysfunction related to epilepsy and direct therapy to improve the patient's symptoms. The reciprocal relationship of sleep and epilepsy and the management of sleep complaints in the patient with epilepsy will be reviewed.
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PMID:Sleep and epilepsy. 1544 23

We describe the clinical and genetic characteristics of the 85 definite or probable human prion diseases cases died between January 1993 and December 2002 in Catalonia (an autonomous community of Spain, 6 million population). Seventy-three (86%) cases were sporadic Creutzfeld-Jakob diseases (sCJD) (49 definite, 24 probable), with a median age at onset of 66 years. The clinical presentation was dementia in 29 cases, ataxia in 14 and visual symptoms in five. The median survival was 3 months. The 14-3-3 assay was positive in 93% cases, 62% presented periodic sharp wave complexes (PSWC) in EEG but only 18% the typical signs on MRI. Forty-eight sCJD were studied for codon 129 PRNP polymorphism: 69% were methionine/methionine (M/M), 14.5% valine/valine (V/V) and 16.5% M/V. Six out of seven V/V cases did not present PSWC and in two survival was longer than 20 months. Eleven cases (13%) were genetic: five familial fatal insomnia and six familial CJD (fCJD). Up to four (67%) fCJD lacked family history of disease, two presented seizures early at onset and one neurosensorial deafness. The only iatrogenic case was related to a dura mater graft. No case of variant CJD was registered. The study confirms in our population the consistent pattern reported worldwide on human prion diseases. Atypical features were seen more frequently in sporadic 129 V/V CJD and fCJD cases.
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PMID:Clinical and genetic features of human prion diseases in Catalonia: 1993-2002. 1546 48


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