Insomnia clinical presentation

BW, a 50-year-old woman with a history of osteoarthritis and hypothyroidism, presents to the clinic complaining of hot flashes, vaginal dryness, and insomnia. She states that she experiences approximately two hot flashes per day and is awakened from sleep at least three to four times a week in a "pool of sweat" requiring her to change her clothes and bed linens. Her symptoms began about 3 months ago, and over that time, they have worsened to the point where they have become very bothersome. On questioning, she states her last menstrual period was 1 year ago. 

Withdrawal delirium (delirium tremens), which usually appears 1 to 4 days after abstinence and peaks at about 72 to 96 hours. The mortality rate may be as high as 15% if serious complicating medical problems are also present. Clinical signs and symptoms include profound confusion, illusions, delusions, vivid hallucinations, agitation, insomnia, and autonomic hyperactivity. Death results from infection, cardiac arrhythmias, fluid and electrolyte abnormalities, or suicide (e.g., in response to hallucinations, illusions, or delusions). 

As for most behavioral therapies, the success of SRT is entirely dependent on the patient s compliance with the prescribed sleep window (7,22). Despite the apparent simplicity of this clinical procedure, therapist guidance is often essential to optimize compliance with the clinical recommendations (16). The first hurdle is making it clear to the patient what is expected and why. Indeed, the idea of curtailing even further the sleep of someone who presents with insomnia is somewhat paradoxical. For many patients, it is counterintuitive when sleep quality is unsatisfactory—from their vantage point, time in bed should be increased to obtain more satisfactory sleep. Thus, it is essential to explain the basic principles of sleep homeostasis and the rationale behind SRT, which should help patients better understand why time in bed should be restricted (27). The addition of sleep education is also useful for elderly individuals to explain the nature and extent of sleep changes associated with aging (16,18,22,25). 

Since 1987 when zopiclone was introduced into clinical practice, extensive evaluations have shown that some rebound changes can be detected in healthy individuals [22-24], In patients with insomnia more than 20 studies have assessed rebound. Rebound can be found in such patients [25,26], but is usually more frequent and present in greater intensity in comparison groups given triazolam. 

From the published clinical studies, it would appear that the partial agonists bretazenil and abercamil are less likely to cause physiological dependence, have lower reinforcing effects and a lower incidence of subjective effects associated with abuse liability than the conventional 1,4-benzodiazepine sedative-hypnotics. It is presently unclear whether the full agonists for the GABA-A receptor, zolpidem and zopiclone, offer a real advance in the treatment of insomnia although their adverse effect profiles and abuse liability may be lower than that of the conventional benzodiazepines. 

Herbal preparations. Randomised clinical trials have shown some effect of valerian in mild to moderate insomnia, and hops, lavender and other herbal compounds show promise in pilot studies that are presently being pursued more fully. 

Similar to the clinical efficacy of theophylline, side effects are also closely related to sernm concentrations. No critical side effects have been observed at sernm theophylline levels np to 20 pg/ml. However, transient comparatively slight side effects similar to those of caffeine, including nausea, vomiting, headache, diarrhea, and insomnia, occnr in some patients at theophylline sernm concentrations below 20 pg/ml. These side effects may be present in np to 50% of patients when serum concentrations of 10 to 20 pg/ml are rapidly achieved, bnt they are usually much less frequent when the initial dose is low and the hnal drng concentration is gradually achieved by increasing doses in intervals of at least 3 days. 

A meta-analysis of 879 patients taking moclobemide is reported to have found that insomnia, restlessness, agitation and anxiety occurred twice as often in the 467 patients taking one or more benzodiazepines than in those not taking concurrent benzodiazepines. However, these adverse events were often already present when moclobemide was started, so it is suggested that the patient groups were probably different. Apart from this difference between the patient groups, there was no evidence of any relevant pharmacokinetic or pharmacodynamic interaction. Another review briefly reported that no clinically relevant interaction was noted between moclobemide and benzodiazepines in clinical studies. ... 

High intakes of thiamin administered orally are nontoxic. The rapidly saturable thiamin absorption mechanism limits the amount taken up from a single dose to 2.5 mg, and thiamin present in excess of protein binding capacity is excreted. However, there are reports of toxicity from chronic intakes in excess of 50mg/kg or >3 g/day with a wide variety of clinical signs, including headache, irritability, insomnia, rapid pulse, weakness, rapid pulse contact dermatitis, pruritus, and, in one case, death. 

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