Insomnia, pharmacological treatment

Walsh JK, Schweitzer PK. Ten-year trends in the pharmacological treatment of insomnia. Sleep 1999 22 371-375. 

Chronic insomnia calls for careful assessment for a medical cause, non-pharmacologic treatment, and careful use of sedative-hypnotics (intermittently to prevent tolerance and dependence). 

Indeed, a pharmacological approach is the first line treatment in transient insomnia. Meanwhile, a behavioral or non-pharmacological approach is the recommended therapy for chronic insomnia, together with intermittent aid of pharmacological treatment [3]. 

GHB was hrst synthesized in the laboratory by the French biochemist Henri Lahorit (1914-1995) in 1961. In the succeeding four decades, extensive research has been conducted on the pharmacological uses and effects of GHB. In general, those studies appear to suggest that GHB has some valuable applications in the medical sciences. It functions well as an anesthetic with apparently few or no serious side effects. Based on this research, the drug has been adopted in many parts of the world for use as a general anesthetic, a treatment for narcolepsy and insomnia, a treatment for alcoholism, and an aid in childbirth. 

Neubauer DN New directions in the pharmacologic treatment of insomnia. Primary Psychiatry 2006 13 51. 

McCall WV. Pharmacologic treatment of insomnia. In Lee-Chiong TL, Sateia MJ, Carskadon MA, eds. Sleep Medicine. Philadelphia Hanley Belfus, 2002 169-176. 

Special considerations for pharmacological treatment of pediatric insomnia in children with children with special needs... 

When insomnia is not caused by, or fails to respond to treatment for, another medical or psychiatric condition in dementia, pharmacological treatment with sedating agents may be considered as symptomatic therapy. Controversies regarding the use of sedating medications in demented patients revolve around issues of efficacy and issues of potential toxicity, neither of which have been resolved by appropriately comprehensive empirical study. There is evidence, however, that sedative-hypnotics as a class may be inappropriately prescribed or overprescribed for demented patients. 

New pharmacological treatments have been developed for the treatment of obesity. These include the combination of phentermine and fenfluramine (phen-fen) and, alternatively, dexfenfluramine (Redux). Phentermine (Fastin, lonamin) is a stimulant and fenfluramine (Pondimin) is a serotonin agonist. In combination they have persistent appetite suppression and weight loss effects. These medications can cause anxiety and insomnia and must be used with extreme caution if taken with antidepressants, especially SSRIs. Dexfenfluramine works similarly, but avoids the side effect of increased anxiety, and instead tends to cause diarrhea, dry mouth, and somnolence. There have also been reports of pulmonary hypertension, a potentially fatal condition, especially when taken for longer than three months. Some researchers (Ricuarte et al. 1991 McCann et al. 1994) have expressed concern because rats given these medications showed evidence of neuronal toxicity. Thus, they are effective medications, but must be used with caution. 

In most individuals, some degree of distress after a disorder is normal and resolves without treatment, and education and counseling may be all that is necessary to reassure them. Therefore, primary care clinicians should avoid indiscriminate pharmacologic treatment and mental health referral for all patients experiencing distress following a disorder (30). However, patients suffering extreme distress, such as those with dissociative symptoms or insomnia, are candidates for symptomatic treatment. 

Insomnia caused by major psychiatric illnesses often responds to specific pharmacological treatment for that illness. In major depressive episodes with insomnia, for example, the selective serotonin reuptake inhibitors, which may cause insomnia as a side effect, usually will result in improved sleep because they treat the depressive syndrome. In patients whose depression is responding to the serotonin reuptake inhibitor but who have persistent insomnia as a side effect of the medication, judicious use of evening trazodone may improve sleep, as well as augment the antidepressant effect of the reuptake inhibitor. However, the patient should be monitored for priapism, orthostatic hypotension, and arrhythmias. 

Inhibition of serotonin reuptake from the neuronal synapse and the subsequent increase in its functionality is one of the mainstays of the pharmacological treatment of depression. Like many amino acids, tryptophan is commercially available as a nutritional supplement or as a so-called smart drug, claiming to reduce symptoms of depression, anxiety, obsessive-compulsive disorders, insomnia, fibromyalgia, alcohol withdrawal, and migraine. However, no convincing clinical data are available to support these... 

Pharmacological Profiles of Anxiolytics and Sedative—Hypnotics. Historically, chemotherapy of anxiety and sleep disorders rehed on a wide variety of natural products such as opiates, alcohol, cannabis, and kawa pyrones. Use of various bromides and chloral derivatives ia these medical iadications enjoyed considerable popularity early ia the twentieth century. Upon the discovery of barbiturates, numerous synthetic compounds rapidly became available for the treatment of anxiety and insomnia. As of this writing barbiturates are ia use primarily as iajectable general anesthetics (qv) and as antiepileptics. These agents have been largely replaced as treatment for anxiety and sleep disorders. 

BZD effects on human sleep are well characterized (Mendelson 2001) (a) decreased sleep latency (b) decreased awakenings (c) increased stage II sleep (d) suppressed stage III and IV sleep (e) increased REM sleep latency (f) initial reduction and fragmentation of REM sleep. Discontinuation of BZD treatment after three to four weeks produces a rebound of REM sleep as well as slow-wave sleep (SWS). BZD and non-BZD compounds are pharmacological agents indicated in the management of anxiety, insomnia, and other conditions in which anxiety is the main symptom, and should be considered as symptomatic medications (Nishino et al. 2004). 

Zolpidem (1) is an effective hypnotic agent indicated for the short-term treatment of insomnia. Zolpidem interacts with the GABAa receptor, and its pharmacological effect is blocked by the benzodiazepine-receptor antagonist fiumazenil (Sanger and Depoortere, 1998). Zolpidem displaces benzodiazepines more selectively from the cerebellum than the hippocampus or spinal cord, consistent with preferential interaction with the ajGABAA receptor subtype (sometimes referred to as the benzodiazepine coi receptor). Studies... 

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