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Sleep benzodiazepines

Sleeplessness in ALS has numerous causes. Respiratory insufficiency, difficulty repositioning in bed, anxiety and depression can all contribute to poor sleep. Treatment of depression with sedating antidepressants such as mirtazapine, tricyclic antidepressants, or trazadone can help promote sleep. Zolpidem, a non benzodiazepine sleep aid, is effective and carries a low risk of respiratory depression. Other medications that can be helpful include anithistamines, chloral hydrate and selective use of benzodiazepines (Gordon and Mitsumoto, 2006). Non-invasive positive pressure ventilation can help relieve orthopnea in those with respiratory muscle weakness, and special equipment, such as a hospital bed, can reduce nighttime discomfort. [Pg.572]

Substance misuse, especially alcohol, benzodiazepines/sleeping tablets / ... [Pg.557]

A medication that causes induction of sleep. The majority of currently available hypnotics (for example benzodiazepine receptor agonists) act via potentiating the brain s inhibitory GABAergic systems, in turn reducing the activity of arousal (i.e. wake promoting) neurotransmitter systems. [Pg.608]

Valerian Valeriana officinalis Restlessness, sleep disorders Rare if used as directed. May interact with the barbiturates (eg, phenobarbital), the benzodiazepines (eg, diazepam) and the opiates, (eg, morphine). [Pg.661]

Benzodiazepines and other anxiolytics. Although benzodiazepines are widely used in the treatment of acute alcohol withdrawal, most nonmedical personnel involved in the treatment of alcoholism are opposed to the use of medications that can induce any variety of dependence to treat the anxiety, depression, and sleep disturbances that can persist for months following withdrawal. Researchers have debated the pros and cons of the use of benzodiazepines for the management of anxiety or insomnia in alcoholic patients and other substance abuse patients during the postwithdrawal period (Ciraulo and Nace 2000 Posternak and Mueller 2001). [Pg.36]

A rebound sleep disturbance has been found after only 7—10 days of treatment with therapeutic doses of triazolam (Greenblatt et al. 1987). Others have described a withdrawal syndrome after substitution of a short-acting benzodiazepine for a long-acting benzodiazepine (Conell and Berhn 1983). Rebound insomnia may occur with zolpidem. [Pg.129]

Sporadic use (e.g., for the induction of sleep after a psychostimulant binge) does not require specific detoxification. Sustained use can be treated as described in the previous sections on detoxification from therapeutic or high dosages but with added caution. In mixed opioid and benzodiazepine abuse, the patient should be stabilized with methadone (some clinicians use other oral preparations of opioids) and a benzodiazepine. Buprenorphine should not be administered with benzodiazepines, because a pharmacodynamic interaction is possible (Ibrahim et al. 2000 Kilicarslan and Sellers 2000) and fatalities have been reported with the combination (Reynaud et al. 1998). Sedative-hypnotic withdrawal is the more medically serious procedure, and we usually... [Pg.133]

Setting aside the general anaesthetics, which do not directly modify the function of any particular neurotransmitter, all the drugs that are used to induce sleep, i.e. the hypnotics , augment the function of GABA and so directly depress neuronal function and probably facilitate cortico-thalamic synchrony. Most of them are benzodiazepines... [Pg.495]

Benzodiazepines which can be possessed by those above and also others as long as they are a medicinal product (use for epilepsy, anxiety and sleeping pills)... [Pg.501]

Table 32.1 describes 30 persons who have been observed to use one of four available therapeutic compounds for the treatment of one of three possible disorders. The four compounds in this measurement table are the benzodiazepine tranquillizers Clonazepam (C), Diazepam (D), Lorazepam (L) and Triazolam (T). The three disorders are anxiety (A), epilepsy (E) and sleep disturbance (S). In this example, both measurements (compounds and disorders) are defined on nominal scales. Measurements can also be defined on ordinal scales, or on interval and ratio scales in which case they need to be subdivided in discrete and non-overlapping categories. [Pg.161]

Benzodiazepines are recommended for acute treatment of generalized anxiety disorder when short-term relief is needed, as an adjunct during initiation of antidepressant therapy, or to improve sleep. [Pg.605]

Side effects associated with benzodiazepines in PD patients are similar to those observed in other disorders. Sedation, fatigue, and cognitive impairment are the most commonly reported side effects.49 Benzodiazepines should be avoided in patients with current substance abuse, a history of such, dependence, or sleep apnea. Additionally, caution should be used in older adults because they have more pronounced psychomotor and cognitive effects. [Pg.616]

FIGURE 38-1. Primary assessment and initial treatment for complaint of excessive daytime sleepiness. RLS, restless-legs syndrome NPSG, nocturnal polysomnography OSA, obstructive sleep apnea DA, dopamine agonist MSLT, multiple sleep latency test BZDRA, benzodiazepine receptor agonist SNRI, serotonin and norepinephrine reuptake inhibitor TCA, tricyclic antidepressant CPAP, continuous positive airway pressure. [Pg.627]

Non-REM parasomnias usually do not require treatment. If needed, low-dose benzodiazepines such as clonazepam can be prescribed for bothersome episodes. Clonazepam reduces the amount of sleep time spent in stages 3 and 4 of non-REM sleep, where most non-REM parasomnias occur. For treating RBD, clonazepam 0.5 to 2 mg at bedtime is the drug of choice, although melatonin 3 to 12 mg at bedtime also may be effective. Patients with RBD also should have dangerous objects removed from the bedroom and cushions placed on the floor to reduce the chance of injury from breakthrough episodes. [Pg.630]

Gandolfo G., Scherschlicht R., Gottesmann C. (1994). Benzodiazepines promote the intermediate stage at the expense of paradoxical sleep in the rat. Pharmacol. Biochem. Behav. 49, 921 7. [Pg.454]


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See also in sourсe #XX -- [ Pg.163 ]




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