Drug Name:	Zopiclone / Imovane / Zimovane
Dosage:	7.5-20 mg
Packages:	30 – 360 pills
Payment Method:	VISA, MASTERCARD, Paypal
Shipment:	UK-UK US-US EU-EU int.
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Management of Insomnia

Insomnia is generally managed through two main approaches: cognitive behavioral therapy (CBT) and pharmacological treatment. Incorporating healthy dietary practices, such as consuming smaller meals rich in antioxidants, has been shown to improve sleep quality. This is largely due to the role of oxidative stress—particularly reactive oxygen species—in the development of sleep disturbances. Various classes of medications have demonstrated effectiveness in treating insomnia; however, drugs like benzodiazepines may lead to withdrawal symptoms and unwanted metabolic or psychological side effects when discontinued. Long-term use or misuse of these agents can paradoxically contribute to persistent insomnia. Similar concerns apply to alcohol, which is often misused in an attempt to self-induce sleep but ultimately disrupts sleep architecture. The primary pharmacologic options include antihistamines, melatonin, antidepressants, antipsychotics, benzodiazepines, and cyclopyrrolone derivatives. Among the latter group, zopiclone is widely used, alongside agents like pagoclone, pazinaclone, suproclone, and suriclone. This discussion will focus on the pharmacological profile of zopiclone, its therapeutic applications, and management of overdose.

Investigations

Standard diagnostic workup typically includes blood tests for serum electrolytes, glucose, renal and hepatic function (including C-reactive protein), and blood gas analysis (oxygen saturation and pH). In suspected overdose cases, serum levels of zopiclone should be measured. Therapeutic concentrations are generally below 100 μg/L, while levels in severe intoxication can exceed 250 μg/L. Toxicological screening is essential to rule out co-ingestion with other psychoactive substances such as benzodiazepines, barbiturates, cannabinoids, opioids, methadone, cocaine, buprenorphine, ethanol, LSD, and others. Urinalysis is often included for comprehensive assessment. Electroencephalography (EEG) may provide supportive diagnostic evidence, particularly when showing sustained alpha activity with superimposed beta rhythms—an EEG pattern often associated with zopiclone toxicity. Compared to standard immunoassays, EEG can offer more definitive insights in specialized settings. In select cases, neuroimaging (CT or MRI) and cerebrospinal fluid analysis may be required to rule out neurological pathologies or encephalitis.

Treatment

Treatment of zopiclone toxicity is primarily supportive following cessation of the drug. Patients should be monitored in a calm environment, with regular checks of vital signs and appropriate fluid management. Airway protection and hemodynamic stabilization are critical. Flumazenil (Anexate), a GABA_A receptor antagonist, can be administered intravenously to counteract the effects of zopiclone, much like its use in benzodiazepine overdoses. It acts as a competitive inhibitor, displacing zopiclone from its binding site and reversing its sedative effects. The standard therapeutic dose is approximately 1.5 mg per day, continued for several days depending on the clinical scenario and patient response.

Discussion

Chronic insomnia remains a widespread concern across populations worldwide. While the recommended sleep duration for healthy adults is approximately eight hours per night, this need may vary depending on age, lifestyle, and occupational demands. Effective treatment begins with understanding the underlying cause of the condition, as insomnia may be either a primary disorder or a symptom of a broader medical or psychological issue. Many countries now offer specialized sleep centers that provide non-pharmacological interventions, such as cognitive behavioral therapy, before considering hypnotic medications. However, when medication is necessary, several therapeutic classes are available. Primary insomnia can lead to significant emotional disturbances such as irritability, anxiety, and depression. Conversely, various neuropsychiatric conditions—such as anxiety disorders, major depressive disorder, post-traumatic stress disorder, Parkinson’s disease, and Alzheimer’s disease—frequently present with sleep disturbances. Likewise, chronic somatic illnesses such as persistent pain, cancer, cardiovascular disease, asthma, gastroesophageal reflux disease (GERD), hyperthyroidism, and complications related to diabetes are known contributors to insomnia. Pharmacological options include antihistamines, melatonin, antidepressants, antipsychotics, benzodiazepines, and the so-called “Z-drugs.” While benzodiazepines are commonly used for sleep induction, their long-term use is limited by dependency risk and broad side effect profiles. Non-benzodiazepine agents, particularly zopiclone—a cyclopyrrolone compound—have been explored as alternatives due to their targeted mechanism and similar efficacy. This analysis compares zopiclone with the benzodiazepine diazepam, with a focus on their pharmacological properties and side effect profiles. Diazepam is a highly lipophilic compound that easily crosses the blood-brain barrier and permeates neuronal and somatic cells. Zopiclone, while also lipophilic (logP ≈ 0.8), is less so than diazepam and is practically insoluble in water. Both drugs exert their hypnotic effects by binding to GABA_A receptors and share the same pharmacological antidote—flumazenil—used in overdose cases. Antihistamines, such as alimemazine (Vallergan) and promethazine (Phenergan), originally developed as phenothiazine-based treatments for allergic conditions, have also been used off-label to promote sleep due to their sedative side effects. These drugs mimic the structure of chlorpromazine (a first-generation antipsychotic) and act as H1 receptor antagonists. Though sedation was not their intended effect, first-generation antihistamines like diphenhydramine and doxylamine are now widely used for short-term insomnia relief. Unlike many hypnotic agents, antihistamines do not promote oxidative stress or the release of free radicals, which makes them a potentially safer option for select patients. However, older agents in this class are associated with a wide range of side effects, including anticholinergic burden. Newer-generation antihistamines, while better tolerated, lack the sedative effect and are not used therapeutically for sleep induction.

Conclusion

Despite ongoing advances, our understanding of the neurobiological mechanisms and biochemical changes underlying insomnia remains incomplete. As a result, current pharmacological treatments are far from ideal, often accompanied by a wide range of side effects and lacking specificity. Benzodiazepines and Z-drugs—particularly zopiclone—remain among the most effective short-term options for managing insomnia, with quetiapine, a second-generation antipsychotic, used less frequently and typically reserved for cases involving comorbid psychiatric conditions. Although benzodiazepines and Z-drugs share similar mechanisms of action at the neuronal level and the same pharmacological antidote (flumazenil), their clinical efficacy often outweighs potential risks when prescribed for brief periods—typically not exceeding two weeks. Used within this timeframe, they do not present serious complications such as neuroleptic malignant syndrome, which is more commonly associated with both first- and second-generation antipsychotics. While antidepressants and antipsychotics are not primary agents for treating insomnia, they may indirectly improve sleep quality by addressing underlying psychiatric or neurological disorders. Nevertheless, these medications come with their own distinct side effect profiles. Ultimately, treatment decisions should be guided by a careful assessment of each patient’s individual needs, comorbid conditions, and risk factors. Collaboration between clinician and patient is essential to ensure safe, effective, and personalized management of insomnia.