2.1. Inclusion criteria

2.2. Exclusion criteria

2.3. Explanation for inclusion and exclusion criteria

This review paper aims to understand the different types of sleep disorders and about their treatment, epidemiology, pathophysiology etc. As this paper doesn’t include the severity of each disease in detail or is not related to each disorder’s distribution, it was included in the exclusion criteria and this review paper cites and includes the pathophysiology, epidemiology, diagnosis, symptoms and treatment of 4 different types of sleep disorders i.e. Narcolepsy, Restless leg syndrome and different types of insomnia and sleep apnoea. This information has been reviewed from different types of articles taken within a range of 2002–2025 and is cited in this paper, hence this was all part of the inclusion criteria. This paper didn’t focus on the study designs used in different researches but rather on the lifestyle modification caused by the these diseases and their relation with Covid-19.

2.4. Data extraction

The epidemiology and pathophysiology of each disease was analysed separately from different papers which were carefully analysed using the advanced search using specific keywords on google scholar. Continuous positive airway pressure is dealt in more detail in sleep apnoea for example. In the rest the major studies include regarding how to treat parts of buccal cavity either surgically or naturally in order to reduce pressure and treat the disorders mentioned above gradually. The epidemiology considers different ranges of age and tells how the particular disorders increases or decreases as the age increases. The pathophysiology majorly considers which part of the buccal cavity is affected which causes the disorders and the mechanism in the part of the buccal cavity which ultimately leads to the disorder to be caused such as- Uvulopalatopharyngoplasty (UPPP) for treatment of Obstructive sleep Apnoea.

3.1. Obstructive sleep apnoea

3.2. Central sleep apnoea

4.1. Introduction

The International Classification of Sleep Disorders, whose diagnostic standards are comparable. According to these requirements, symptoms must result in functional distress or impairment that is clinically significant; must exist for a minimum of three nights a week for a minimum of three months, and it must not be connected to any other sleep, health, or mental disorders (Qaseem et al., 2016). Chronic insomnia disorder affects 6% to 10% of people (Mysliwiec et al., 2020) (Figure 4). When there is enough opportunity and conducive conditions for sleep, but difficulties with the onset, maintenance, the beginning, or quality of sleep impairs daytime functioning, it is referred to as insomnia. The majority of research studies use arbitrary definitions, such as a sleep efficiency of less than 85% or a sleep onset delay of more than thirty minutes (Silber, 2005). It is characterised as discontent with the amount or quality of sleep and is linked to problems falling asleep, staying asleep, and waking up early in the morning and not being able to go back to sleep (Qaseem et al., 2016). Its effects on quality of life as well as the psychological, occupational, and economic domains demonstrate how burdensome it is for patients and the healthcare system. Due to obstacles to diagnosis and treatment, insomnia is frequently undiagnosed and untreated (Morin & Benca, 2012).Comorbid insomnia may go untreated even after it is identified because other medical or psychological issues frequently take precedence. Many approaches to treating insomnia have been developed, such as medication, sleep environment modifications, and cognitive behavioural therapy (Bragg et al., 2019).

4.2. Diagnosis

A number of criteria are proposed to diagnose insomnia, despite the lack of defined quantitative definitions. The average reported sleep latency of over thirty minutes, the amount of time spent alert after falling asleep that exceeds thirty minutes, sleep efficiency below 85%, and total sleep time of less than 6.5 hours are some examples of these. The existence of distress, daytime repercussions, or both is essential for the diagnosis of insomnia. People who complain about having trouble falling asleep at night but are not impaired during the day may just be short sleepers (Saddichha, 2010). Based on the traditional signs of insomnia linked to daytime impairment, an official diagnosis of sleeplessness was established. Additionally, a patient received the Patient Health Questionnaire-9 (PHQ-9). Her score of 14 out of 27 on the PHQ-09 indicated that she also had moderate depression (Bragg et al., 2019).

After ruling out a number of other conditions as the primary cause of sleep disturbances, including psychiatric (depression and anxiety), medical (pain), circadian (phase-delay syndrome), or other sleep disorders (restless legs syndrome/periodic limb movements, sleep-breathing disorders), the diagnosis of primary insomnia is essentially made by exclusion. When a sleep disturbance is determined to be directly and temporally linked to another mental, physical, or sleep problem, comorbid insomnia is diagnosed (Morin & Benca, 2011).The DSM-5 and ICSD-3 criteria require a subjective report of a sleep complaint (difficulty falling asleep, staying asleep, or waking up early) occurring at least three times a week for three months, along with at least one related daytime impairment (fatigue, attention impairment, mood disturbance, or impaired performance), in order to diagnose chronic insomnia (Saddichha, 2010).

4.3. Treatment

General patients

Evidence of a moderate calibre demonstrated that CBT-I enhanced treatment response, remission, wakefulness following the general population's sleep onset, efficiency, and quality. In the general population, stimulus control improved sleep onset latency and total sleep time, according to low-quality evidence (Qaseem et al., 2016).

Older patients

Evidence of low-to-moderate quality showed that CBT-I enhanced older people' sleep efficiency, wakefulness following sleep onset, and sleep onset latency. Moderate-quality evidence also demonstrated that CBT-I improved Insomnia Severity Index (ISI) and Pittsburgh Sleep Quality Index (PSQI) scores when compared with controls (Mysliwiec, 2020).

Pharmacologic treatment

Evidence was insufficient to determine the benefits of pharmacologic therapy with Benzodiazepines in the general population or in older adults (Mysliwiec et al., 2020). The behavioural elements of teaching stimuli control and good sleep hygiene (creating a consistent sleep environment and strengthening the link between it and sleep), Relaxation Therapy, Counter arousal techniques, and Sleep Restriction Therapy (restricting the amount of time spent in bed to sleep, then gradually raising the time of bed as sleep efficiency increases) are some examples of behavioural components. Components of cognitive therapy focus on unhelpful ideas and attitudes regarding slumber (Mysliwiec et al., 2020). Benzodiazepines, Benzodiazepine-Receptor agonists, and sedating antidepressants are among the prescription drug classes used to treat insomnia. The FDA has approved the use of long, intermediate, and short half-lived benzodiazepines for treating insomnia, while it has approved the use of intermediate, short, and ultrashort half-lived benzodiazepine-receptor agonists (Silber, 2005).

In patients with primary insomnia, a 14-day trial comparing trazodone, zolpidem, and placebo revealed that trazodone improved sleep latency and duration (measured by a questionnaire) compared to placebo, but zolpidem had a greater effect (Silber, 2005). For patients who are having trouble falling asleep or who wake up during the night and need to take a medication, Zaleplon is an alternative to zolpidem (Bragg et al., 2019).

Doxepin, a tricyclic antidepressant, was used to treat primary insomnia in a four-week study. The results showed significant improvements in sleep efficiency (13 percent increase from baseline), total sleep time (13 percent increase from baseline), and sleep latency (21 percent reduction from baseline) (Silber, 2005). the FDA advises women and elderly or disabled adults to take benzodiazepine and nonbenzodiazepine hypnotics at lower dosages (Qaseem et al., 2016). Since nonbenzodiazepine hypnotics, or “Z-drugs,” the most well-researched, moderately effective, and have fewer side effects than benzodiazepines, they are probably the first class of drugs that doctors typically provide to people who have insomnia. The effects on total sleep time vary, but each medication in this class will reduce sleep latency by about 20 minutes (Bragg et al., 2019).Melatonin and sedating Histamine-1-Receptor Antagonists (Doxylamine and Diphenhydramine) are two over-the-counter medications that are marketed for the treatment of insomnia, but there is insufficient evidence to support the use of these medications (Silber, 2005). According to data from observational studies, hypnotic medications may have major side effects like dementia and fractures. FDA product labels alert patients to potential adverse effects and cognitive and behavioural changes, including impaired driving and auto accidents (Qaseem et al., 2016).

4.4. Cognitive behavioural therapy for insomnia

Changes in behaviour (bad sleep habits, irregular sleep schedules), psychology (unrealistic expectations, worry, unhelpful beliefs), and physiology (mental and somatic tension, hyperarousal) are among the factors that CBT aims to address in order to address insomnia (Morin & Benca, 2012). Treating chronic insomnia with cognitive behavioural therapy for insomnia (CBT-I) is effective. This therapy focuses on thoughts and behaviours related to sleep and consists of multiple sessions and components (Mysliwiec et al., 2020). For patients, mobile applications like the Veterans Affairs' CBT-I coach offer a fresh and user-friendly addition to CBT-I. The CBT-I coach serves as a central location to monitor sleep patterns, offer techniques (like guided imagery and relaxation breathing), and promote positive reinforcement (Bragg et al., 2019). Overall, CBT-I is more cost-effective than pharmaceutical treatment. Pharmacologic treatments for insomnia are meant to be used temporarily, as stated on the FDA label, and patients are advised not to use these medications for prolonged periods of time (Qaseem et al., 2016).

Behavioural components include Counter arousal techniques and Relaxation Therapy, stimulus control (building a stronger link between the environment in which you sleep and your ability to sleep), sleep hygiene education, and Sleep Restriction Therapy (limiting the amount of time you spend in bed to sleep time, followed by a gradual increase in time in bed as sleep efficiency improves) (Mysliwiec et al., 2020).Overall, CBT-I is more cost-effective than pharmaceutical treatment. Pharmacologic treatments for insomnia are meant to be used temporarily, as stated on the FDA label, and patients are advised not to use these medications for prolonged periods of time (Qaseem et al., 2016).

4.5. Acute Insomnia

Three key ideas are important to consider when searching for “caseness,” or whether a person has experienced a condition that qualifies them as a “case,” or if they have not experienced an illness, disease, or disorder. The duration, frequency, and severity of the symptoms are among the concepts that centre on the presenting symptoms and their accompanying features. Furthermore, one must consider the circumstances surrounding the beginning of an illness, such as acute insomnia, when conceptualising the onset of the condition (i.e., triggering factors) (Ellis, Perlis, et al., 2012). Cortisol, the final hormone produced by the HPA axis, is a stress marker that is particularly relevant to the emergence of acute insomnia. The hypothalamus releases Corticotropin-Releasing Hormone (CRH) in reaction to perceived as risks during stressful situations. This, in turn, sets off the Anterior Pituitary Gland's release of Adrenocorticotropin Hormone (ACTH), which in turn sets off the adrenal cortex's release of cortisol. a few studies demonstrate distinct changes to cortisol and the Cortisol Awakening Response (CAR), which may suggest that insomnia disorder is characterised by elevated HPA axis activity. In particular, research has shown that individuals with insomnia have higher levels of cortisol in the morning, more CARs, and higher levels of cortisol in the 24-hour period than those without insomnia disorder. Even though the HPA axis is relevant to insomnia disorder, not much is currently known about how the HPA axis is active during the acute phase of insomnia (Elder et al., 2023).

A recent effort was undertaken to describe and conceptualize Acute Insomnia while taking into account the fundamental components of insomnia disease (as stated in the proposed DSM V nosology). The presence of a trigger and a numerical indicator of the degree of the sleep complaint—such as a Sleep Onset Latency or Wake After Sleep Onset of thirty minutes or more—were added to this definition (Ellis, Gehrman, et al., 2012).

5.1. Pathophysiology

The pathophysiology and aetiology of narcolepsy were clarified by the ground-breaking discovery of the Neuropeptide Hypocretin/orexin, the lack of which is currently thought to be responsible for the majority of Narcolepsy symptoms (Nepovimova et al., 2019). Major pathophysiology appears to be the loss of up to 95% of hypocretin-producing neurons in the lateral hypothalamus, which causes low CSF hcrt-1 levels (Type I narcolepsy) (Abad, 2017). Over 85% of individuals with type 1 narcolepsy are associated with a particular human leukocyte antigen (HLA) allele, HLA DQB1*0602. B cells, dendritic cells, and activated T cells all express HLA class II molecules (Nepovimova et al., 2019). HLA DQB1*06:02 is strongly linked to narcolepsy, and polymorphisms in the T-cell-receptor-α (TCRA) locus on chromosome 14, TNFSF4 (also known as OX40L), Cathepsin H (CTSH), the purinergic receptor P2RY11, the DNA methyltransferase DNMT1, and carnitine palmitoyl transferase (CPT1B) have been found in genome-wide association studies (Abad & Guilleminault, 2017). Sleep paralysis, hypnagogic hallucinations, and cataplexy, among other REM sleep-related abnormalities, are likely caused by a particular combination of pathophysiologic conditions in the brain (Mitler et al., 1987).

It is believed that REM sleep dysregulation symptoms arise from the sporadic activation of REM sleep-promoting neurons during wakefulness, which causes REM sleep manifestations—like cataplexy—to intrude into wakefulness (Thorpy & Bogan, 2020). It has been demonstrated that mice devoid of B and T cells are especially vulnerable to influenza A (H1N1) viral infection, and that autoreactive cytotoxic CD8+ T cells injected into transgenic mice expressing the influenza virus protein hemagglutinin in the hypocretin cells resulted in the destruction of hypocretin neurons (Dauvilliers & Barateau, 2017). This spike in new cases indicates that narcolepsy risk is strongly increased by DQB1*06:02, young age, and specific immune stimuli (Scammell, 2015). Two types of narcolepsies are now recognised by clinicians. People with both disorders exhibit persistent daytime sleepiness and score well on the multiple sleep latency test (Scammell, 2015). Narcolepsy type 1 is typified by cataplexy and very low levels of orexin-A in the cerebrospinal fluid (Scammell, 2015). It is caused by a selective loss of a small population of neurons in the lateral hypothalamus that synthesise hypocretin neuropeptides (Dauvilliers & Barateau, 2017). Cataplexy is absent in type 2 narcolepsy patients, and their orexin-A levels are normal (Scammell, 2015). But have MSLT or PSG + MSLT confirmation of EDS, and the CSF hcrt-1 concentration is not measured, or the CSF hcrt-1 is greater than 110 pg/mL or greater than 1/3 of the mean values obtained in normal subjects (Abad & Guilleminault, 2017) (Figure 6)

Figure 5

Main reasons for Insomnia.

Figure 6

Symptoms of narcolepsy.

5.2. Diagnosis

Narcolepsy can be distinguished from other forms of excessive somnolence by supplementary symptoms. The hypnagogic hallucinations, sleep attacks, cataplexy, and sleep paralysis that comprise the narcoleptic tetrad are among them (Mitler et al., 1987). In order to diagnose each patient and meet the international diagnostic standards of the International Classification of Sleep Disorders (ICSD-32014), overnight PSG and MLT studies were conducted (Abenza-Abildua et al., 2023). In ICSD-3, narcolepsy type 1 is defined as excessive daytime sleepiness lasting longer than three months, accompanied by either cataplexy (a mean sleep latency of eight minutes or less on the multiple sleep latency test.) or a highly specific biological measure called hypocretin-1, with a level in the CSF of 110 pg/mL or less (Dauvilliers & Barateau, 2017). In the US, type 1 is present in 0.02%–0.18% of cases. Although the exact point prevalence of type 2 disease is unknown, 20.5/10,000 has been proposed (Abad & Guilleminault, 2017).

5.3. Treatment

Treatment based on OXR agonists, gene therapy, Orexin Cell Transplantation, or even just substituting Orexin. Orexin delivery methods include intravenous (IV), intracisternal, and intranasal routes (Nepovimova et al., 2019). Orexin replacement therapy should be a successful tactic for re-establishing orexin signalling because narcolepsy type 1 is typified by the loss of orexin neurons. Exogenous orexin peptides, pro-drug precursors, or small-molecule agonists may accomplish this (Nepovimova et al., 2019). Potential therapeutic delivery to the central nervous system (CNS) is typically restricted by the Blood-Brain Barrier's (BBB) permeability. After intravenous injection measured the rate at which 125I-labeled orexin-A and orexin-B entered the brains of albino ICR mice, localising them in the brain parenchyma or binding to BBB endothelial cells. According to their suggestion, orexin-B is a small lipophilic peptide that metabolises quickly in the bloodstream. It was demonstrated that orexin-A is extremely lipophilic and enters mice's brains quickly through simple diffusion (Nepovimova et al., 2019).

Specifically, the inability of orexin peptides to penetrate the blood brain barrier in meaningful amounts has made drug delivery challenging. Even though research on animals revealed that orexin-A administered intravenously raised drug concentrations in brain tissue and lessened the effects of sleep deprivation (Thorpy & Bogan, 2020). All 51 patients had taken the prescribed medications (methylphenidate, modafinil) to treat their drowsiness. Just four (22.22%) of the eighteen anxiety syndrome patients were able to take them on time and at low doses because their symptoms were getting worse (Abenza-Abildua et al., 2023).Sodium Oxybate is the only drug accepted for treating adult cataplexy and sleepiness together. The appropriate course of Anti cataplexic treatment should be determined by the severity of the symptom; mild cataplexy often improves with increased alertness after wake-promoting therapies are started (Dauvilliers & Barateau, 2017).

6.1. Introduction

An overwhelming need to move one's legs and restlessness, frequently accompanied by unpleasant sensations is called as restless leg syndrome (Gossard et al., 2021). It has been stated that restless legs syndrome is either a symptomatic disorder with no known cause or an idiopathic disorder that is frequently linked to end-stage renal disease, pregnancy, and iron deficiency (Trenkwalder et al., 2005). The clinical characteristics of the lower extremities, such as paraesthesia, urticaria, and itching in a family member, were recognised by Mussio-Fournier and Rawak (Tuna Oran et al., 2021) and also by uncomfortable leg sensations that are usually felt during rest before sleep sets in and are eased with movement. RLS usually starts in the thighs or calves and progresses clinically to other lower limb areas, including the foot (Yeh et al., 2016). In addition, persistent sleep loss and trouble falling asleep are frequent and upsetting symptoms of RLS (Maiolino et al., 2021). RLS that is clinically severe affects 2 to 3 percent of people in Europe and America. It severely disrupts sleep, quality of life, and productivity during the day and frequently necessitates years, if not lifetime, of treatment (Allen, 2014).The idea that RLS also carries a higher risk of adverse cardiovascular events has been reinforced by recent research (Maiolino et al., 2021). There is no clear pathogenesis for RLS. Currently, the disorder is divided into two categories: idiopathic (familial or sporadic) and secondary (related to pregnancy, chronic kidney disease, Parkinson's disease, or conditions that cause iron deficiency or changes in iron metabolism) (Lebrato Hernández et al., 2022) (Figure 7).

Figure 7

Symptoms of restless leg syndrome.

6.2. Epidemiology

The prevalence of RLS varies significantly by region; it is highest in populations in Europe (1%–8% in Asian nations, 5%–12% in African nations, and lowest in Asian countries (less than 1%), where the fewest studies have been conducted. RLS affects women more frequently than men, with parity playing a key role (Trotti, 2017).The problems this study raises would be especially significant in epidemiology studies where non-clinicians conduct telephone surveys with members of the public, with the goal of including only patients with primary RLS (Yeh et al., 2016). In fact, the main problem with RLS epidemiological research is that RLS is only identified by the patient's self-reported symptoms. Whether or not objective criteria are eventually useful in diagnosing RLS depends on how well-understood the patient's symptoms are and how forthcoming the patient is with the researcher, as the sensations are subjective to the patient. As previous international studies have noted, the true prevalence rate of restless legs syndrome may actually be underestimated due to a variety of factors, including the belief that restless legs are a minor ailment that doesn't require medical attention, the fear that affected individuals will be shunned in some cultures, and the absence of symptoms when testing a patient while they are awake (Yeh et al., 2016).

6.3. Pathophysiology

RLS may exacerbate mood by interfering with sleep. Mood symptoms can benefit, if only slightly, from RLS treatment. In 9% of patients, antidepressants also induce or exacerbate RLS. With Mirtazapine (28%), this effect is more noticeable than with duloxetine (5%), and it is less noticeable with citalopram (Trotti, 2017). The majority of reports of RLS caused by antidepressants have included serotonergic medications like sertraline, paroxetine, and fluoxetine. Mirtazapine, the first noradrenergic and specific serotonergic antidepressant (NaSSA) with presynaptic antagonistic, 5-HT receptor stimulating, and 5-HT2/5-HT3 receptor-blocking properties, has been linked in a number of case reports to RLS. The most likely second-generation antidepressant to cause RLS is probably mirtazapine. Furthermore, the longest axons of the dopaminergic Diencephalospinal tract project to the dorsal horn of the spinal cord, which has been hypothesised to be a component of the pathological process for RLS. When compared to non-RLS patients, RLS patients also exhibit abnormal activation of the gastrocnemius muscles, which are located in the upper calf, during walking. This finding raises the possibility that patients with RLS may have compromised supraspinal dopaminergic control over the muscle (Yeh et al., 2016).

One possible mechanism through which CNS iron levels influence the pathophysiology of RLS is by means of hypoxic-state pathway activation. The RLS patient's microvasculature showed increased levels of vascular endothelial growth factor (VEGF), hypoxia-inducible factor 2-alpha, and substantia nigra neurons on higher levels (Gossard et al., 2021). They also have been found to have iron deficiency quite frequently, and brain iron deficiency may play a significant role in the pathophysiology of RLS (Earley, 2003) Both Ekbom and Nordlander examined how iron functions in RLS during the initial phases of the illness. Numerous imaging studies have demonstrated a robust correlation between RLS and iron metabolism, especially in the brain (Gossard et al., 2021).

In addition to the spinal component, Lanza et al. state that a number of mechanisms, such as diminished central inhibition and anomalies in peripheral nerve function, may be involved in the pathophysiology of RLS. Dopamine and iron are closely related; a prominent theory suggests that low cellular iron modifies some aspects of the dopaminergic system either directly or indirectly. It is more intricate than just the proportion of these molecules, though. It is reasonable to assume that brain dopamine levels should be low in RLS patients because dopamine agonists alleviate the symptoms of RLS. Studies conducted thus far, however, have not revealed this to be the case (Gossard et al., 2021).

6.4. Diagnosis

The desire to extend one's limbs, notably one's leg, is the primary indicator of RLS diagnosis. Unpleasant and uncomfortable sensations may or may not accompany this urge (Yeh et al., 2016). Subjective sleep quality was impacted in the current study, and participants with recently diagnosed severe degree RLS experienced more sleep disturbances. The degree of RLS was found to positively and significantly correlate with a delay in the onset of sleep in a study conducted in Bangalore, India (Joseph et al., 2022). The clinical Hopkins telephone diagnostic interview was utilised to confirm the diagnosis. Symptoms occurring at least fifteen times within the month before the screening, symptoms that started at least half a year before to screening, and symptoms that mostly happened at night were all considered eligibility requirements. A one-week trial of placebo was also required, with the participant's score on the IRLS Study Group Rating Scale must be at least 15 at the beginning and end. Higher scores on the IRLS scale indicate more severe symptoms: variations in scores greater than three are considered clinically significant. The scale has a range of 0 to 40 (Allen et al., 2014).

Assessments of peripheral iron stores (ferritin, transferrin saturation) should be made both during the initial diagnosis of RLS and later during long-term care (Gossard et al., 2021). Since iron deficiency is often linked to restless legs syndrome, serum ferritin concentration should be tested in all patients (Trenkwalder et al., 2005). Research has also revealed that children with RLS diagnoses have greater rates of ADHD and are more likely to have RLS-diagnosed parents (Yeh et al., 2012).Compared to the general population, people with poor mental and physical health experience RLS more frequently. The risk of developing RLS is also highest in the elderly (Yeh et al., 2012).Most researchers added to their inclusion criteria a minimal IRLSRS score at baseline, generally including participants with a “moderate to severe” condition (Guay et al., 2020).

Diagnosis tests include (Guay et al., 2020) (Figure 8)

Figure 8

Diagnostic methods for restless leg syndrome.

Most of the time, cramps can be easily differentiated from RLS because they are characterised by a distinct knotting of a muscle, whereas the latter causes excruciating localised muscle pain. After a prolonged period of sitting, a patient may experience paraesthesia's in one or both feet. These can be relieved by shifting positions or crossing and uncrossing the legs 43q (Earley, 2003).

6.5. Treatment

For people who have iron deficiency, iron supplements are advised (Marshall et al., 2019).

It has long been known that iron supplementation is beneficial for RLS patients. It's also important to identify and address the source of the iron deficiency. After three months, ferritin levels should be checked while starting first-line oral supplementation. Intravenous injection is an option to consider if oral iron supplementation proves to be ineffective (Limousin et al., 2018). RLS nonpharmacologic treatment may be beneficial when used as adjunctive or monotherapy. Aerobic exercise and lower body resistance reduce the severity of RLS (Trotti, 2017). Based on the vascular theory of the disease, lifestyle interventions that support improved circulation and cardiovascular health as well as overall health are appropriate for treating RLS (Bega & Malkani, 2016). The fact sheet offers advice on cutting back on alcohol, cigarettes, and caffeine in addition to maintaining regular sleep schedules and engaging in moderate exercise on a regular basis (Bega & Malkani, 2016).Those suffering from restless legs syndrome report augmentation because of dopaminergic treatment. The terms “augmentation,” “increase in severity of symptoms,” and “involvement of other body parts” refer to the early onset of symptoms during the day (Trenkwalder et al., 2005). Table 3 gives a brief idea about the medications used for treating sleep disorders and are explained below.

Levodopa

Levodopa has been shown in numerous placebo-controlled randomised trials to be effective in treating RLS (Limousin et al., 2018) levodopa was found to be useful in treating nocturnal symptoms of restless legs syndrome as well as improving both the subjective and objective quality of sleep-in patients with idiopathic and uraemic disease. For the treatment of the syndrome, Levodopa plus Benserazide has been authorised for a number of years in Germany, Switzerland, and Austria (Trenkwalder et al., 2005).

Dopamine agonists

The ergot-dopamine agonists Bromocriptine, Pergolide, and Cabergoline, and the non-ergot dopamine agonists pramipexole, ropinirole, and rotigotine have all been shown to be effective in double-blind studies. The first double-blind randomised crossover study of a dopamine agonist used 7.5 mg bromocriptine at bedtime with five out of six patients having partial subjective improvement in restlessness and paraesthesia (Trenkwalder et al., 2005). A dopaminergic receptor D1, D2, and D3 agonist, pramipexole has a greater affinity for D3 receptors. Its half-life is 8–12 hours, and it takes 1–2 hours for it to start working. Eight level 1A studies have shown how effective it is on RLS both short- and mid-term (6 months) (Limousin et al., 2018).

Clonidine

Despite not having FDA approval, clonidine is a commonly used paediatric sleep aid due to its quick and easy absorption by kids and good tolerance. Alpha-2-adrenergics have occasionally been administered in conjunction with iron supplements. Adult RLS sensory symptoms have been successfully treated with clonidine in one randomised, double-blind, placebo-controlled trial without any negative side effects (L. DelRosso & Bruni, 2019).

Opioids

Opioids were empirically used for many years as a substitute RLS treatment (Limousin et al., 2018), treats RLS via their action on dopaminergic receptors (L. DelRosso & Bruni, 2019). Opioids are considered a therapy option of last resort. Opioids are first-choice medication for patients who are intolerant to dopaminergic agents (Trenkwalder et al., 2005). First-line use of level I opioids, primarily tramadol (Topalgic1), is permissible. There are two dosage forms of Tramadol: a 250 mg/5 mL oral solution and 50 mg capsules. There are pills with dosages of 100 mg, 150 mg, and 200 mg for extended-release forms (Limousin et al., 2018).

Clonazepam

Research using Polysomnography has revealed that clonazepam helps RLS patients sleep better and experience fewer arousals, but it does not effectively lessen the motor and sensory abnormalities linked to the condition (L. DelRosso & Bruni, 2019). It is not advised to use it as the RLS's first line. It can be applied on an as-needed basis (during an exacerbation of RLS, for example) (Limousin et al., 2018). Some common symptoms of sleep disorders are listed in Table 5.