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Treatment of insomnia should be individualized, based on the nature and severity of the symptoms, and should include two approaches. The first approach (the most adequate) is to eliminate the factors that cause insomnia, the second includes measures to normalize sleep itself. The general tactic is:

• 1) with early manifestations of sleep disorders, the first approach dominates;
• 2) with extensive and sufficiently long insomnia, a combination of both approaches;
• 3) in chronic insomnia, when the factor that caused them has become less relevant, the second approach dominates.

The first approach is associated with the prevention or mitigation of various stressful, psycho-traumatic factors, which is achieved by recommendations on the organization of work, rest, life in general, sleep hygiene, psychotherapeutic and psychopharmacological approaches. It is necessary to treat endogenous mental, organic neurological, somatic diseases, avoid the abuse of psychotropic drugs and alcohol, adequate therapy for sleep apnea and restless legs syndrome. The first way is undoubtedly a priority, but rather difficult and far from always effective due to the different curability of these conditions. In addition, in most cases, the identification of the etiological factor is difficult (or the causes of insomnia in a particular patient are numerous). It should also be taken into account that the pathology associated with insomnia can significantly modify insomnia disorders.

The second approach includes pharmacotherapy and non-pharmacological treatments. Non-drug methods are diverse: sleep hygiene, psychotherapy, phototherapy, encephalophony (“music of the brain”), acupuncture, biofeedback, physiotherapy (hydrotherapy, aeroionotherapy, electrotherapy, climatotherapy, devices that regulate the rhythm of breathing, creating pleasant noise (sea surf ), thermal effect on the nose area), homeopathy.

Sleep hygiene is an integral component of the treatment of any form of insomnia. Pharmacotherapy currently plays a leading role in the treatment of insomnia. Today in the world, about 3% of people constantly and 25-29% periodically take various sleeping pills, and the frequency of their use increases with age. The specificity of the pharmacotherapy of insomnia lies in the fact that if the treatment of most chronic diseases and syndromes requires a long-term (weeks and months) maintenance of the therapeutic concentration of the active form of the drug in the blood, then in case of insomnia, the effect of the drug should ideally begin immediately after administration, last only for sleep and stop upon awakening.

The following principles for prescribing sleeping pills are proposed, taking into account their diversity and for unifying their use.

• 1. It is preferable to start the treatment of insomnia with herbal sleeping pills, melatonin or doxylamine. These drugs create the least problems for patients and can be easily discontinued in the future.
• 2. The predominant use of short-lived drugs. These drugs usually do not create post-somnia problems, rarely cause lethargy and drowsiness during wakefulness, and do not adversely affect

Benzodiazepines

Benzodiazepines reduce the latent period of sleep, reduce the frequency of nocturnal awakenings, and increase the total sleep time. In addition, they reduce the time of REM sleep. Benzodiazepines relax skeletal muscles, have anticonvulsant and anxiolytic properties due to their non-selective binding to BDZ2 and BDZ3 receptors.

In the elderly, as well as in patients with impaired renal and hepatic function, it is more preferable to use benzodiazepines with a short half-life (triazolam) that do not produce active metabolites. This avoids excessive sedation due to the accumulation of active metabolites.

Benzodiazepines with a long half-life (flurazepam) are preferred in patients with daytime anxiety.

Drugs with an average half-life (temazepam, estazolam) can be used as a reasonable compromise in patients with early morning awakenings. Side effects of benzodiazepines include daytime sedation, anterograde amnesia, respiratory depression, and withdrawal syndrome. Tolerance may develop in 1-2 weeks.

Benzodiazepines are characterized by the phenomenon of "recoil" of insomnia, which can develop even if the drug was used for only 1 night. The risk of developing the phenomenon of "recoil" is higher, the greater the dose of benzodiazepines and the shorter the half-life, but does not depend on the duration of use of the drugs.

Due to the possibility of addiction to benzodiazepines, it is undesirable to prescribe (and if used, then with extreme caution) to patients with a tendency to abuse narcotic drugs.

The specificity of the pharmacotherapy of insomnia in the fact that if the treatment of most chronic diseases and syndromes requires a long-term (weeks and months) maintenance of the therapeutic concentration of the active form of the drug in the blood, then in case of insomnia, the effect of the drug should ideally begin immediately after administration, last only for sleep and stop upon awakening.

Zolpidem is a selective benzodiazepine (BDZ1) receptor agonist, highly selective for the GABA-chlorine channels of the BDZl receptors of the central nervous system. Modulating effects along the GABA line cause a sedative effect.

Zolpidem is characterized by a rapid onset of action, with a half-life of 1.5-2.5 hours. These characteristics make it possible to take zolpidem even late at night without worrying about residual cognitive impairment the next morning. Zolpidem reduces sleep latency and increases total sleep time.

Unlike non-selective benzodiazepines, zolpidem does not reduce REM sleep and A-rhythm. The usual dose of zolpidem is 10 mg immediately before bedtime. It is reduced to 5 mg in patients over 65 years of age, as well as in the presence of liver disease.

Side effects include drowsiness (5%), dizziness (5%), headache (3%), gastrointestinal symptoms (4%). Most of the side effects are dose-dependent and occur when the drug is administered at a dose of more than 20 mg per day. Approximately 1-2% of patients taking zolpidem complain of memory problems, nightmares, confusion, and isolated cases of sensory disturbances and psychotic symptoms are known.

Zolpidem instruction

Indications

Treatment of transient and situational insomnia in adults with clinically significant (severe) sleep disturbance, including difficulty falling asleep.

Contraindications

• Hypersensitivity to zolpidem or excipients of the drug.
• Acute and/or severe respiratory failure.
• Severe acute or chronic liver failure (more than 9 points on the Child-Pugh scale) (risk of developing encephalopathy).
• Sleep apnea syndrome.
• Pseudoparalytic myasthenia (myasthenia gravis).
• Age up to 18 years (lack of clinical data).
• Congenital galactosemia (galactose intolerance), glucose or galactose malabsorption syndrome, lactase deficiency.

Dosage and administration

Inside (just before going to bed) with a sufficient amount of liquid, in a single dose of 10 mg.

The use of the drug is not recommended if the expected duration of the forthcoming sleep is less than 8 hours.

For adults under the age of 65, a single dose is 10 mg.

In elderly or debilitated patients, with impaired liver function, treatment is started with a dose of 5 mg. If necessary (insufficient clinical effect) and good tolerability of the drug, the dose can be increased to 10 mg.

The maximum daily dose is 10 mg.

The course of treatment should not exceed 4 weeks. With transient insomnia, the recommended course of treatment is 2-5 days, with situational insomnia - 2-3 weeks.

A gradual dose reduction is recommended, the regimen for discontinuation of therapy is individual. The need for longer therapy is assessed at a second consultation with the doctor.

Side effects

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From the side of the nervous system.

Often - drowsiness, a feeling of intoxication, headache, dizziness, increased insomnia, anterograde amnesia (the effects of amnesia may be associated with behavioral reactions), the risk of which increases in proportion to the dose, hallucinations, agitation, nightmares; infrequently - confusion, irritability; frequency is unknown - impaired consciousness, dysphoria, aggressiveness, visual and auditory hallucinations, irritability, behavioral reactions, somnambulism, drug dependence (may develop even when using therapeutic doses), when the drug is discontinued - "withdrawal" syndrome or "rebound" insomnia, decrease libido, gait disturbance, ataxia, falls (mainly in elderly patients), addiction to the drug (decrease in sedative and hypnotic effect when used for several weeks). Most side effects on the part of the psyche are paradoxical reactions.

From the digestive system

Often - diarrhea, nausea, vomiting, abdominal pain; frequency unknown - increased activity of "liver" enzymes.

From the side of the musculoskeletal system

Frequency unknown - muscle weakness.

From the side of the skin

Frequency unknown - rash, itching, urticaria, hyperhidrosis.

Allergic reactions

Frequency unknown - angioedema.

Other

Often - a feeling of fatigue; infrequently - diplopia.

Drug interactions

Alcohol enhances the sedative effect of zolpidem, concomitant use is not recommended.

Opioid analgesics, antitussives, barbiturates, antidepressants, sedatives, antihistamines, benzodiazepines, clonidine, and antipsychotics (neuroleptics) increase the risk of developing symptoms of central nervous system depression.

Baclofen, thalidomide, pizotifen - when used together, there is an increase in the inhibitory effect on the central nervous system and the risk of respiratory depression increases.

Enhances the effect of imipramine and chlorpromazine, prolongs the half-life of chlorpromazine (chlorpromazine increases drowsiness and the incidence of anterograde amnesia), reduces the maximum concentration (Cmax) of imipramine in plasma.

In the case of anesthesia with narcotic analgesics, a state of euphoria may also develop, which will lead to the formation of mental dependence.

Buprenorphine - when used together, the risk of respiratory depression increases.

Ketoconazole (a potent inhibitor of CYP3A4) reduces the clearance of zolpidem, and therefore may increase its sedative effect.

Flumazenil weakens or eliminates the hypnotic effect.

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