Insomnia duration

A class of sedative/hypnotic type drug that exert their effects through the benzodiazepine binding site on GABAa receptors. The class consists both of molecules that contain the benzodiazepine moiety, for example diazepam, lorazepam and flunitrazepam, and the newer, non-benzodiazepine compounds such as zolpidem, zopiclone, indiplon and zaleplon. BzRAs are primarily used for the treatment of anxiety, insomnia and to elicit varying levels of sedation. The wide selection of compounds currently available affords the prescribing clinician extensive options in terms of relative efficacies and durations of action. 

Pain is described based on the following characteristics onset, duration, location, quality, severity, and intensity. Other symptoms may include anxiety, depression, fatigue, anger, fear, and insomnia. 

On discontinuation of hypnotic BZDRAs, patients can experience rebound effects, specifically rebound insomnia that may last for one to two nights. Rebound insomnia occurs more frequently after discontinuation of shorter-duration BZDRAs compared with long-duration BZDRAs. Intermittent hypnotic therapy with the lowest dose possible reduces the likelihood of tolerance, dependence, and withdrawal when therapy is stopped. Patients should be counseled that rebound insomnia is not necessarily a return of their original symptoms, and it may take a few nights for rebound symptoms to subside. 

The importance of adenosine deaminase in the duration and intensity of sleep in humans has been noted recently (Retey et al. 2005). Animal studies suggest that sleep needs are genetically controlled, and this also seems to apply in humans. Probably, a genetic variant of adenosine deaminase, which is associated with the reduced metabolism of adenosine to inosine, specifically enhances deep sleep and slow wave activity during sleep. Thus low activity of the catabolic enzyme for adenosine results in elevated adenosine, and deep sleep. In contrast, insomnia patients could have a distinct polymorphism of more active adenosine deaminase resulting in less adenosine accumulation, insomnia, and a low threshold for anxiety. This could also explain interindividual differences in anxiety symptoms after caffeine intake in healthy volunteers. This could affect the EEG during sleep and wakefulness in a non-state-specific manner. 

Systemic effects of methamphetamine are similar to those of cocaine. Inhalation or IV injection results in an intense rush that lasts a few minutes. Methamphetamine has a longer duration of effect than cocaine. Pharmacologic effects include increased wakefulness, increased physical activity, decreased appetite, increased respiration, hyperthermia, euphoria, irritability, insomnia, confusion, tremors, anxiety, paranoia, aggressiveness, convulsions, increased heart rate and blood pressure, stroke, and death. 

Insomnia can be a common problem for people when first changing a drug problem. Sleeping problems can be related to the rebound effects of the drugs, or may be related to rumination and regret. Since insomnia is common, therapists and counselors will likely want to teach their clients how they can reduce the duration of this potentially uncomfortable problem. To orient the client, the counselor or therapist will want to emphasize to the client that insomnia is not life threatening, and that eventually he or she will sleep. This orientation is meant to put the client at ease... 

Having observed a decrease in appetite and thirst when testing BZ, we decided to measured caloric and fluid intake more precisely in the EA 3443 series. At the incapacitating dose, calories ingested and fluid consumed both dropped by about 40%. Sleep duration, also measured, increased at the lower doses but seemed to drop precipitously at the incapacitating dose. This seeming insomnia, however, was illusory. Delirious subjects appeared physically awake, but were asleep in terms of brain electrical activity - the so-called pseudowakeful state. ... 

In general, caloric and fluid intake both tend to decrease as the dose of EA 3443 is increased (Table 8). Sleep duration per 24 hours increases at lower doses (reflecting its sedative effect) but then declines as delirium takes over. The apparent insomnia during delirium often referred to as the pseudowakeftil state, in which the subject is active and seems to be awake, but is actually asleep in terms of EEG activity. 

Ultimately, it is a drug s half-life combined with its potency that dictates its utility as a sedative-hypnotic. Like other benzodiazepines, clonazepam (Klonopin) can be used to treat insomnia, but its long duration of action renders it prone to hangover effects at doses needed to treat insomnia. Nevertheless, low doses of clonazepam (0.25-2 mg) are a treatment for PLMD and are also used to treat RLS. When hangover effects of even low doses of clonazepam are a problem, other benzodiazepines can be used. 

Benzodiazepines have similar pharmacological properties and are used in anxiety and insomnia. The choice of which benzodiazepine to use usually lies with the pharmacodynamic and pharmacokinetic properties, which vary across the class. For example, diazepam, flurazepam and nitrazepam have a prolonged duration of action whereas lorazepam and temazepam have a shorter duration of action. 

Duration of therapy Because sleep disturbances may be the presenting manifestation of a physical or psychiatric disorder, initiate symptomatic treatment of insomnia only after careful evaluation of the patient. The failure of insomnia to remit after 7 to 10 days of treatment may indicate the need for evaluation of a primary psychiatric or medical illness. Do not prescribe zaleplon in quantities exceeding a 1-month supply. 

All these drugs reduce sleep duration, decrease SWS and REM sleep, increase sleep latency and increase sleep fragmentation. They can cause a dose-related insomnia during use, and hypersomnia with increased dreaming and nightmares on withdrawal after chronic use. 

Mirtazapine is an antidepressant with a novel mechanism of action affecting both 5-HT and noradrenergic function. A recent systematic, open-label study found that 9 (34.6%) of 26 subjects (5 females, 21 males mean age, 10.1 +/— 4.8 years, age range 3.8-23.5 years) with autistic disorder and other PDDs were much improved or very much improved on the CGI after a mean duration of treatment of 5 months (Posey et al., 2001). The dosage range for mirtazapine was 7.5 to 45 mg/day with a mean daily dose of 30.29 mg +/— 12.64 mg. Target symptoms of aggression, self-injury, irritability, hyperactivity, anxiety, depression, and insomnia showed improvement. Adverse effects were transient and minimal and included increased appetite, irritability, and sedation. Based upon these preliminary data, a double-blind, placebo-controlled trial appears warranted. 

GAD differs from other types of anxiety disorders because, although the anxiety is present most of the time, GAD patients do not fear specific events such as social situations or having a panic attack (as in social anxiety or panic disorder). GAD is distinguished from normal worry or anxiety because of its long-term duration. GAD is frequently the underlying cause of many symptoms, including irritability, insomnia, headache, and muscle tension. This can often make it very hard to diagnose. A person with GAD will often go to his or her family physician and complain of nerves. ... 

This non-BZD hypnotic, cyciopyrroione, is indicated for short-term management of insomnia. Zopiclone has a BZD-like profile, a short half-life of 3.5 to 6.5 hours, no active metabolites, minimal rebound effects, and less abuse potential than BZDs. The usual therapeutic dose is oral 7.5 mg administered 30 to 60 minutes before bedtime. Zopiclone has a well-documented capacity to reduce sleep latency, improve quality and duration of sleep, and reduce the frequency of nighttime awakenings. In clinical trials, 7.5 mg doses of zopiclone have been found to be as effective as triazolam 0.5 mg, temazepam 20 mg, flurazepam 15-30 mg, and nitrazepam 5 to 10 mg for the short-term treatment of insomnia (136). 

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