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CLINICAL PRACTICE GUIDELINES

Clinical Practice Guidelines for Sleep Disorders

Ravi Gupta, Sourav Das1, Kishore Gujar2, K K Mishra3, Navendu Gaur4, Abdul Majid5
Dept. of Psychiatry and Sleep Medicine, Himalayan Institute of Medical Sciences, Doiwala, Dehradun, 1Consultant
Psychiatrist and Sleep Specialist, Medica Superspeciality Hospital, Kolkata; Somnos Sleep Clinic, Kolkata. 2Dy. Medical
Superintendent, YCM Hospital, PCMC, Pimpri, 3HOD, Dept. of Psychiatry, JNMC, Wardha, 4Director, Gaur Mental-Health
Clinic, Ajmer-305001, 5Department of Psychiatry, SKIMS Medical College, Srinagar

Participants of expert group on CPG for Sleep Disorders is a common complaint with a number of Psychiatric
Ravi Gupta, Kishore Gujar, K K Mishra, Navendu Gaur, disorders e.g., depression, anxiety, and withdrawal from the
Abdul Majid, Gautam Saha, Amrit Pattojoshi, RK Solanki substances that depress cerebral functioning. In addition,
we now have evidence that link the depression, bipolar
disorder and schizophrenia with the disordered circadian
INTRODUCTION rhythms and many of these patients show delayed sleep
wake phase cycle.Similarly, antidepressants are known
Sleep disorders are common, still we have limited data to induce a number of sleep disorders including NREM
regarding the prevalence and management of sleep parasomnias (sleep talking, sleep walking) as well as REM
disorders from India. Although the systematic research parasomnias (REM sleep behavior disorder) and restless
is limited from our country, still case reports from Indian legs syndrome.Antipsychotics may cause weight gain and
thus they may lead to obstructive sleep apnea in a number
population suggest that we see all kinds of sleep disorders.
of patients.Similarly, opioid users suffer from central sleep
apnea and during withdrawal many of them develop RLS.
Prevalence of various sleep disorders is shown in Table 1.
Both these conditions may worsen the quality of the sleep.
Among all, we have population data for two disorders from
Secondly, daytime manifestations of a number of sleep
Indian adult population- one is Obstructive Sleep Apnea
disorders e.g., insomnia, hypersomnia, restless legs
(OSA) and second is Restless Legs Syndrome (RLS). Sleep syndrome, sleep apnea mimic that of Psychiatric disorders
problems have been investigated among Indian children e.g., depression, fibromyalgia, chronic fatigue syndrome
more frequently through variety of approaches, most and somatoform disorders.
common through the questionnaire based screening in
school-based cohorts. Considering the recent evidences and changes in the
management of sleep disorders,, Indian Psychiatric Society
Knowledge of sleep disorders is essential for psychiatrists has decided to update the existing guidelines. However,
for two reasons.First, some of the sleep disorders are few points must be kept in mind while you consider these
common in Psychiatric patients. They may be related directly guidelines for your practice:
to the pathophysiology of psychiatric illness, or may be the 1. These are consensus statements
consequence of the treatment modalities offered. Insomnia 2. Original research in this area from India is limited. Most
of the literature reviewed has been generated from the
Address for correspondence: studies involving Caucasian and European population.
Dr. Ravi Gupta,
Department of Psychiatry and Sleep Medicine, Himalayan
They are culturally, phenotypically and genetically
Institute of Medical Sciences, Doiwala, Dehradun. different from Indian population. All three factors-
E-mail: sleepdoc.ravi@gmail.com
This is an open access article distributed under the terms of the Creative
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DOI:
How to cite this article: Gupta R, Das S, Gujar K, Mishra
KK, Gaur N, Majid A. Clinical Practice Guidelines for Sleep
10.4103/0019-5545.196978
Disorders. Indian J Psychiatry 2017;59:116-38.

S116 © 2017 Indian Journal of Psychiatry | Published by Wolters Kluwer ‑ Medknow

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Gupta, et al.: CPGs for sleep disorders

culture, phenotype and genotype influence the sleep Table 1: Prevalence of various sleep disorders in general
patterns, pathophysiology of sleep disorders and their population
management- both pharmacological as well as non- Disorder Prevalence
pharmacological. Insomnia 10‑15%
Hypersomnia Not known
With this background, we will discuss the guidelines Obstructive Sleep Apnea# 14%
regarding management of individual sleep disorders. Restless legs syndrome# 2%
Delayed Sleep wake phase disorder 10%
Advanced Sleep Wake phase disorder 1%
INSOMNIA Shift worker disorder 2%
# Data from Indian population
ICD-10 defines insomnia as a condition where there is a
problem in initiating the sleep, staying asleep or waking up Table 2: Sleep Disorders that may mimic insomnia
early in the morning at least for 3 nights/week for at least Sleep related breathing disorders
1 month. It should be associated with significant distress • Obstructive sleep apnea
and persistent preoccupation with the deficiency of sleep. • Central sleep apnea
Central disorders of hypersomnolence
Narcolepsy
DSM-5 defines insomnia as a condition where a problem has Sleep related movement disorders
been reported in initiating , maintaining the sleep or there • Restless Legs Syndrome
is an early morning awakening. This problem should occur • Nocturnal Myoclonus (sleep starts)
despite adequate opportunities to fall asleep and must • Sleep Related leg cramps
• Sleep related bruxism
occur at least 3 nights a week. It should be associated with
• Sleep related rhythmic movement disorder
significant distress in the personal, social or occupational Parasomnias
life. If it persists for at least 1 month but less than 3 months, • Sleep‑walking
it is considered as episodic; if it persists for at least 3 months, • Sleep terrors
it is considered as persistent insomnia. • Nightmare disorder
Circadian Rhythm Sleep Disorders
• Advanced Sleep Wake Phase disorder
Our understanding regarding insomnia has changed over • Delayed Sleep Wake phase disorder
the years. Earlier we used to differentiate between primary • Shift worker disorder
and secondary insomnia, however, the recent research • Irregular Sleep wake rhythm disorder
Others:
has challenged this belief. Current literature suggests
• Sleep related asystole
that insomnia cannot be considered merely as a symptom • Sleep related epilepsy
of psychiatric disorders. It is rather co-morbid with the • Sleep related laryngospasm
psychiatric and other medical conditions, and if not treated
early, through the process of kindling it becomes chronic Through a careful history and clinical examination, these
which has multiple health and economic implications. conditions can be ruled out (Table 2).

For this reason, in the third edition of International While taking the history of a patient with insomnia, special
Classification of Sleep Disorder (ICSD-3), which appeared in focus should be provided to the initiation of symptoms,
2014, insomnia has been divided into two categories: short its course and progression. Information from the
term insomnia disorder and chronic insomnia disorder. In bed-partner/ room-partner who had seen the patient while
addition, subtyping of the primary insomnia into adjustment, asleep should be sought and incorporated.(Table 3).
psychophysiological, paradoxical and idiopathic that
prevailed till ICSD-2 has been omitted. This has happened He should be asked for the daytime symptoms of insomnia,
for multiple reasons.First, all the insomnia sufferers have in as in their absence, insomnia can’t be diagnosed. Frequency
common one issue i.e., hyperarousal and second, change in of symptoms must be asked along with the duration and
the sleep related behavior and compensatory mechanisms frequency of symptoms per week. It must be ensured
were found similar across different insomnia subtypes. that the patient has adequate opportunities to fall asleep.
Hence, all the modalities that are used for the treatment of Excessive daytime sleepiness must be ruled out. Clues
insomnia are directed towards reducing the hyperarousal. regarding the predisposing, precipitating and perpetuating
factors of insomnia should be assessed in detail.
Assessment and evaluation
Management of the insomnia case starts with the history It is essential to ask for the sleep pattern while the patient was
taking and general physical examination. It is of paramount asymptomatic and compare it with the sleep schedule during
importance as a number of sleep disorders may mimic symptomatic period. Sleep related behavior and rituals must
insomnia. Hence, having knowledge regarding these mimics be asked before and after the symptoms onset as they may
will help the clinician to reach to an accurate diagnosis. provide a good idea about the possible interventions.
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Table 3: Information regarding a typical night Table 4: Other medical disorders that may induce sleep
Information regarding Description disturbance
Sleep Schedule • Time to bed Cardiovascular
• Time to fall asleep • Arrthythmias
• Wake time • Congestive heart failure
• Time taken to get up from bed • Myocardial infarction
• Quality of nocturnal sleep • Varicose veins
• Daytime Napping Pulmonary
• Timing • Chronic obstructive pulmonary disease
• Duration • Interstitial lung disorder
• Quality of sleep during naps • Scoliosis
• Number of naps GIT
• Regularity of this schedule • Peptic ulcer disease
Nocturnal Awakenings, if any • Number of awakenings • GERD
• Reasons for awakenings • Chronic constipation
• Time taken to fall asleep again CNS
Pre‑bedtime behavior • What does he do since evening • Intracranial space occupying lesions
• Mental state before going to bed • Dementia
Compensatory strategies • Behavior and thoughts during • Seizures
nocturnal awakenings • Stroke
Addictive substances • Nature of substance consumed • Parkinson’s disease
• Usual timing Neuromuscular disorder
• Usual effect: Stimulant/ Genitourinary
Somnolent • Chronic kidney disease
• Frequency of consumption • Benign Prostatic hypertrophy
• Withdrawal/Intoxication Musculoskeletal:
interfering with sleep • Rhumatoid arthritis
Drugs • If person is taking any drug, • Connective tissue diseases
then effect of drug on sleep
Environment of the bedroom • Look for possible factors that
Severity of insomnia may be assessed using a brief
can interfere with sleep
Time spent in bed in awake state questionnaire- Insomnia severity index, available in English
in a whole day as well as Hindi.

This should be followed by a thorough general physical

Many of the patients with insomnia start worrying while examination and if any system appears dysfunctional, that
they are not able to fall asleep in the bed. Dysfunctional should be examined in detail.
thoughts before the bedtime or while in bed lead to
hyperarousal and they may be assessed using Dysfunctional Sleep diary provides a good opportunity to assess the sleep-
Beliefs and Attitudes about Sleep, which is available in pattern and helps in differentiating insomnia from circadian
English as well as Hindi Language. rhythm sleep disorders. (Figure 2).

Many of the medical conditions may induce symptoms that At times, objective data is necessary to reach to a diagnosis
may mimic insomnia. Hence, the disorders provided in and in those cases actigraphy may be performed. In cases of
Table 4 must be ruled out. chronic insomnia that is not responding to treatment, video-
synchronized 24-channel polysomnography is desirable.
Algorithm for the diagnosis of insomnia is depicted in Fig 1.
Formulating a treatment plan
Effect of the insomnia on the daytime functioning must Treatment of insomnia is individualized and tailor-made.
be assessed. Special care should be taken to differentiate For the short term insomnia, pharmacotherapy is indicated,
between fatigue and sleepiness. Mood during the day must while for the chronic insomnia, cognitive behavior therapy
be assessed. Depression and other psychiatric disorders for insomnia (CBT-I) is preferred.
that may mimic daytime symptoms of insomnia may be
differentiated by asking “how do you feel during the day Various hypnotic agents are described below. Importance
which is followed by a good night sleep?”. If the patient of behavioral intervention should not be underestimated
reports a remarkable improvement, diagnosis of psychiatric and it is better that they should be started even in cases
disorder shall be deferred till the insomnia resolves. with short term insomnia. For example, a person might
be having genetic predisposition to insomnia and a recent
If the patient is undergoing any treatment for other medical stress might have precipitated the insomnia, which could
disorders (pharmacological as well as non-pharmacological), be perpetuated by the dysfunctional beliefs about sleep or
its’ effect on the sleep should be examined. maladalptive strategies to control it. Common maladaptive

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Gupta, et al.: CPGs for sleep disorders

Paent presenng with complaints suggesve of insomnia

No
Adequate opportunies for sleep No Insomnia
Yes
No
Dayme Symptoms of Insomnia No Insomnia
Yes

Difficulty Iniang Sleep Early morning awakening

Difficulty maintaining Sleep
> 30 min for > 3 Nights/wk > 30 min for > 3 Nights/wk
> 30 min for > 3 Nights/wk

No Total Sleep Time normal

Symptoms of RLS Total Sleep Time Total Sleep
Abnormal acvity at night Snoring present if le to sleep
normal if le to sleep me
Yes Yes decreased
Yes
Yes Screen for NO

OSA
RLS Delayed Sleep Wake Phase Disorder
Seizures
Advanced sleep
Parasomnia wake phase
disorder
High Risk

Nocturnal EEG
REMBD Level 1
NREM
Polysomnography
Normal

NREM
No
Parasomnia
OSA or
Normal
RBD
Confirmed

Terminal Insomnia
Inial Insomnia Middle Insomnia

Duraon

<3 >3
months months

Short term Chronic

Insomnia Insomnia

Figure 1: Algorithm for the diagnosis of Insomnia

strategies that we see include, but not limited to- spending Goals of the therapy
excessive time in bed, start smoking or start drinking 1. Improve the sleep onset latency, total sleep time and
caffeine while awake, spending time on screen while awake reduce awakenings, thus improving sleep efficiency
or spending majority of the time during the day in bed. 2. Improving quality of sleep
3. Ameliorate or significantly reduce the daytime
Wherever indicated, opinion from a relevant specialist symptoms of insomnia
may be sought. If there is evidence of sleep disorders 4. Sustain the effect of treatment and reduce the chances
that mimic insomnia, management should be directed to of the relapse
those disorders, rather than the insomnia. In some cases,
insomnia is co-morbid with these sleep disorders, and in Choice of treatment settings
these cases, both should be treated. Treatment of insomnia is usually offered on an outpatient

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Figure 2: Sleep diary depicting long sleep onset latency with normal total sleep time when the patient is following natural pattern
of sleep. However, the patient gets the sleep late in the night and wakes up late in the morning. This data suggests delayed
sleep wake phase disorder

basis. Hospitalization may rather worsen the condition by agents may have residual daytime effects and may produce
enhancing hyperarousal. However, in some patients it may the somnolence during the day (Table 6).
improve sleep by removing environmental factors and may
provide a clue to the underlying pathophysiology. Melatonin and its agonists include the melatonin itself
and the molecules that act on MT1 and MT2 receptors.
Pharmacological treatment Melationin is available as 3 mg tablet formulation.
Pharmacological treatment for the insomnia is limited to short- This may be used to induce sleep, however, data do not
term insomnia and they are not routinely recommended for support its efficacy as a hypnotic agent. It is rather used
the management of chronic insomnia. A wide variety of drugs as a chronobiotic. Melatonin receptor agonists- ramelteon
is available that may induce sleep e.g., benzodiazepines, (8-24 mg/day) and agomelatine (25-50 mg/day) are available
Benzodiazepine receptor agonists, sedating antidepressants, in India. Remelteon is a short-acting-drug with half-life of
second generation antipsychotics, antihistaminics, melatonin around 3-4 hours. It shows an improvement in the time to fall
and its agonists and orexin receptor antagonists. Table 5 shows asleep with minimal adverse effects.Agomelatine is another
the factors that influence the choice of a particular drug. molecule that in addition to having an agonist action on
melatonin receptors, also has antagonist action on 5-HT2C
Benzodiazepinesand benzodiazepine receptor agonists receptors. It has been found effective in improving both
(BzRA) are usually divided into short, intermediate and sleep and mood in clinical trials, and because of it’s short
long acting and one of them may be chosen based upon half life (1-2 h) is free from daytime somnolence.
the case. In general, short acting are preferred when the
patient is having difficulty in sleep initiation, intermediate Orexin-receptors antagonists have recently been discovered
acting when the patient has difficulty in maintaining the for the management of insomnia. Controlled trial data is
sleep and long acting when the patients complain of early available for one of the molecule i.e., Survorexant. It has
morning awakening. However, intermediate and long acting been found to improve total sleep time with variable findings

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on the nocturnal arousals and time spent awake after sleep is available for treatement with Z drugs for as long as 6
onset. Usual prescribing dose varies between 10-40 mg/day. months without any major adverse effects. Considering the
Common adverse effects include nausea abnormal dreams. limited availability of trained CBT-I therapist, consensus
was reached that in certain circunstances where CBT-I
Sedating antidepressants e.g., tricyclics, trazodone and is not possible for any reason, pharmacothepray may be
mirtazapine may be used if there is comorbid psychiatric institutedfor long term.
disorder that warrants their use. In addition, they may also
be preferred when adverse effects of the benzodiazepines Non-Pharmaclogical therapies
and BzRAs are not tolerable. However, there are insufficient Cognitive behaviour therapy for Insomnia (CBT-I) is
evidences for their efficacy in insomnia. the mainstay of therapy for chronic insomnia. It is a
multicomponent therapy that includes education regarding
Antihistaminicdrugs are available as over-the-counter drugs, sleep physiology, sleep hygiene, addressing dysfunctional
and they are commonly used for self medication.However, beliefs, stimulus control therapy, sleep restriction and
data regarding their efficacy in insomnia is limited. However, relaxation training.Each of these components may be used
a tricyclic drug Doxeipin has been approved for the treatment as a primary focus in a given patient which makes this
of insomnia in low doses (10 mg). At this dose, it primarily therapy highly individualized. In general, goal of the therapy
acts on the H1receptors and work as an antihistaminic. is to reduce the hyperarousal, hence, educating the patient,
cognitive restructuring (to address dysfunctional belief) and
Antipsychotics are used off-label for the treatment of relaxation are necessary in almost all patients. CBT-I has been
insomnia, particularly chlorpromazine, clozapine, olanzapine found effective for long term management of insomnia in
and qutiapine. However, we do not have data regarding their the randomized controlled trials comparing it with hypnotic
efficacy as hypnotic agents. In addition, while prescribing agents. It has been repeatedly shown that though, it takes
them, it is essential to consider potential adverse effects some time to show its effects, once they appear, they are
e.g., metabolic syndrome and extrapyramidal symptoms. longer lasting as compared to pharmacotherapy and also
reduce the chances of relapse.One of the major advantages of
Long term pharmacotherapy the CBT-I is the fact that it has also been found useful in cases
Although the pharmacotherapy is not routinely of insomnia co-occurring in context of medical disorders.
recommended for the long term treatment in view of
availablibility of non-pharmacological therapies, still, data Since the CBT-I is time consuming and requires the expertise,
it has been tried to be delivered through internet, computer
Table 5: How to choose a drug from the available and in groups.Though the computerized CBT-I has been
molecules? found superior to the placebo and pharmacotherapy, still it’s
Age of the patient and risks associated with sedation efficacy has been found low when compared to the face to
Comorbid psychiatric and other medical disorders face CBT-I. Administration of CBT-I in a group has also been
Pharmacokinetic properties of the molecule in question
Drug interactions with other medication that the patient is taking
tried, with the results similar to the computerized CBT-I.
Adverse effects of the drug in question: short term as well as long term
Availability of the molecule Results of sleep education and sleep hygiene alone have
Cost of the drug been found to have limited value unless they are associated
Allergy to the molecule in question
with some other component of the CBT-I.

Table 6: Benzodiazepines and Benzodiazepine Receptor Agonists

Molecule Half Life (hr) Dose (mg/d) Formulations Common Adverse effects
Benzodiazepines
Oxazepam 3‑20 10‑30 mg Tablet Memory lapses, daytime sleepiness,
ataxia, fall, automatism, slurred speech
Trialzolam 1.5‑5.5 0.5‑1 mg Tablet
Lorazepam 10‑20 1‑4 mg Tablet/Injection
Alprazolam 6‑20 0.25‑1 mg Tablet/Sustained released
Diazepam 20‑50 5‑20 mg Tablet/Injection
Clonazepam 18‑40 0.5‑2 mg Tablet/Mouth dissolving
Nitrazepam 30‑40 5‑10 mg Tablet
Benzodiazepine
Receptor Agonists
Zaleplon 1 5‑10 Tablet Memory lapses, hallucinations,
Eszopiclone 5 1‑2 Tablet paradoxical excitement
Zolpidem 2‑4 5‑10 Tablet/Extended release/Sublingual low
dose/Sublingual high dose/Oral spray

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Exercise, especially the aerobic exercise along with the Special population
sleep hygeine has been found to be beneficial for the Pharmacotherapy should be cautiously advised to the
sleep and daytime activity. It has been found to reduce the elderly because of the drug interactions and adverse
time taken to fall asleep and improve the sleep efficiency effect profile. This should also be cautiously used in
in randomized control trials.Thus, patients should not be children and patients with other medical disorders for
advised not to engage into any exercise before bed-time, as the same reasons. CBT-I is not possible in patients with
conventionally thought. Rather they should be allowed to neurocognitive deficits and non-compliant patients,
analyse their sleep reactivity towards the exercise and if is hence they should not be started it without assessing
found to interfere with sleep, then they should be advised their motivation.
not to get engaged into it before bedtime.
Pregnancy: Duing first trimester it is best to avoid all
One of the focus of the therapy is to reduce the total time medications. In disabling cases, sedating antihistaminitcsmay
spent in bed in an effort to fall asleep by sleep restriction. be used for the shortest possible period.
Evidence is less robust regarding the utility of the sleep
restriction therapy.However, a recent review suggested Lactation: Amount of psychotropicdrugs that is excreted in
that sleep restriction therapy is one of the most effective milk varies from molecule to molecule. Reader is advised
components of the CBT-I.This must not be used in cases to consult the pharmacology book for details regarding
of bipolar disorders and epilepsy as it may worsen the individual molecule.
comorbid medical condition.
HYPEROSMNIA
In Indian context, since patients have been found focussing
on the daytime worries, rather than on the sleep, problem Alertness is an integral necessity for learning, performance
solving technique may be added.Recently, mindfulness and safety. Excessive daytime sleepiness impairs productivity
based relaxation therapy has been found to improve the and exponentially increases the risk of accidents, particularly
sleep.Mindfulness based stress relaxation (MBSR) has in occupations like transportation, military, healthcare,
been found equally efficacious to the face to face CBT-I, factory workers etc. excessive sleepiness is reported by
pharmacotherapy and better than sleep hygiene alone.This 10-25% of the general population in different parts of the
has been found more efficacious when it has been included world. However, as of now there are no prevalence studies
as a component of CBT-I. from India on hypersomnia/ excessive sleepiness.

Management as per the different phases of illness International Classification of Sleep Disorder, 3rd edition
On of the major issues with the patients with chronic (ICSD 3) defines daytime sleepiness as: “the inability to
insomnia is that they desperately want to sleep soon after stay awake and alert during the major waking episodes of
the initiation of treatment. However, CBT-I takes longer time the day, resulting in periods of irrepressible need for sleep
to improve the situation because it is delivered in sessions. or unintended lapses into drowsiness or sleep”. Sleepiness
And each session has a focus which is guided by prevailing varies in severity and is more common during sedentary,
sleep problems since last session. During CBT-I patient is boring, and monotonous situations that require little
expected to maintain a sleep diary and change his cognition active participation. Some patients are aware of increasing
and behavior. Many of the patients are not able to do that. In sleepiness before falling asleep, whereas others can fall asleep
those cases, the treatment is started with pharmacotherapy with little or no prodromal symptoms (“sleep attacks”).
along with the CBT-I. Gradually, the pharmacotherpay is
tapered and patient remains only on the CBT-I. Thus, patient The most common cause of excessive daytime sleepiness
benefits from the immediate response of hypnotics that (EDS) in modern day world is the combination of suboptimal
reduces the burden and hyperarousal in addition to long duration of sleep, poor sleep hygiene, and changing
term benefits of CBT-I. Though many sleep specialists are work schedules. In addition, various sleep disorders like
practicing it, still it has not been thoroughly investigated. obstructive sleep apnea, circadian rhythm sleep disorders
and periodic limb movement disorder may be associated
When to stop treatment with excessive daytime sleepiness.
Though we do not have any literature on this issue, still,
for the short term insomnia, patient should be requested Primary causes of hypersomnolence have been classified
to give drug holidays intermittently and to restart the under the heading of “Central disorders of hypersomnolence”
treatment when the symptoms appear again. CBT-I may in ICSD 3. The various central causes of hypersomnolence
be discontinued once the sleep of the patient is stabilized according to different classification systems is given in
for at least 4 weeks, though this number has been chosen the table 7 below and Algorithm to approach a case of
arbitrarily. hypersomnia is given in Fig 3.

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Table 7: Comparative terminologies of causes of hypersomnolence between ICD‑10 and ICSD‑3

ICSD 3 ICD 10 ICD 10 code:
Narcolepsy Type 1 Narcolepsy With Cataplexy G47.411
Narcolepsy Type 2 Narcolepsy Without Cataplexy G47.419
Idiopathic Hypersomnia Idiopathic Hypersomnia With Long Sleep Time G47.11
Idiopathic Hypersomnia Without Long Sleep Time G47.12
Kleine‑Levin Syndrome Recurrent Hypersomnia G47.13
Hypersomnia Due to a Medical Disorder Hypersomnia Due to Medical Condition G47.14
Hypersomnia Due to a Medication or Substance F11‑F19
Hypersomnia Associated with a Psychiatric Disorder Hypersomnia due to other mental disorder F51.13
Insufficient Sleep Syndrome Insufficient sleep syndrome F51.12
Primary Hypersomnia F51.11
Other hypersomnia not due to a substance or F51.19
known physiological condition

Symptoms of Excessive insufficient sleep, inadequate Psychoeducation/ Sleep

Daytime Sleepiness sleep hygiene, job or familial Hygiene/ Behavior Therapy/
Yes
stressors and work schedules CBTi
from history

Recurrent hypersomnia, e.g. No

Klein Levin syndrome (usually
associated with behavioral Episodic/ recurrent
change, hyperphagia, Suggestive history for hypersomnia:
irritability) Yes No
Irresistable urge for sleep in daytime (or
in middle of activities)/ sleep attacks/
cataplexy/ hypnagogic or hypnapompic
Yes
Rating scales: hallucinations/ sleep paralysis/ REM
Polysomnography Within Epworth Sleepiness Scale behavioral disorders/ prolonged sleep
Normal limits Sleep diary Yes time/ confusional arousals

Full night attended Level I

Polysomnography preferably Objective evidence of OSA/ Treat accordingly
with video recording CSA/ PLMD/ Parasomnias
Yes
Followed by Multiple Sleep
Latency Test next day With cataplexy or CSF
MSLT findings: Hypocretin 1 conc. either <=
MSLT: SL<=8 min, >= 2 SOREMPs Yes 110pg/mL or <1/3 of mean
reference values
MSLT findings:
MSLT: SL<=8 min, < 2 SOREMPs
Yes No
Narcolepsy Narcolepsy
Total 24 hr sleep time >=660 Type 1 Type 2
Idiopathic
mins by 24 hour PSG/ wrist Hypersomnia
actigraphy +sleep log Yes

Underlying medical
Yes Underlying medical condition Hypersomnia due to condition diagnosed by MRI/
judged to be directly causing a medical disorder SPECT/ Immunology etc.
the excessive sleepiness Yes
Yes
No
Attributable to sedative Hypersomnia due to a
Primary Narcolepsy
medications, alcohol or drugs medication or
Narcolepsy secondary to
of abuse Yes substance
(Type 1 or 2) medical
condition
(Type 1 or 2)
Attributable to underlying Hypersomnia
psychiatric conditions like associated with a
moods disorders, somatic Yes psychiatric disorder
symptom disorder etc.

Figure 3: Algorithm for the diagnosis of Hypersomnia

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Hypersomnias of central origin associated with anti-Ma-2 or anti-aquaporin-4 antibodies,

Narcolepsy type 1: caused by a deficiency of hypothalamic multiple sclerosis, myotonic dystrophy, Prader-Willi syndrome,
hypocretin (orexin) signaling. Excessive daytime sleepiness Parkinson disease, and head trauma.
and signs of REM-sleep dissociation are the characteristic
features of narcolepsy, however, the most specific feature Idiopathic hypersomnia: is characterized by excessive
is cataplexy (defined as more than one episode of generally daytime sleepiness that occurs in the absence of cataplexy,
brief (< 2 minutes), usually bilaterally symmetrical sudden is accompanied by no more than one SOREMP on MSLT and
loss of muscle tone with retained consciousness). There preceding polysomnogram combined, and is not adequately
are repeated daily episodes of an irrepressible need to explained by another disorder. Sleep drunkenness,
sleep or lapses into sleep (sleep attacks). Most patients consisting of prolonged difficulty waking up with repeated
awaken refreshed after a sleep episode but begin to feel returns to sleep, irritability, automatic behavior, and
sleepy again after variable times. Many narcolepsy patients confusion may be present. Subjects typically do not easily
have lapses in vigilance, sometimes in combination awaken to alarm clocks and frequently use special devices
with automatic behavior, such as writing gibberish or or procedures to wake up. Naps are generally long, often
interrupting a conversation with a completely different more than 60 minutes, and described as unrefreshing by
topic. Apart from cataplexy and sleep attacks, 33% to 80% 46% to 78% of patients. Associated symptoms which suggest
of narcolepsy patients have hypnagogic hallucinations and/ a dysfunction of the autonomic nervous system may be
or sleep paralysis. Hypnagogic hallucinations are defined present. These symptoms include headache, orthostatic
as vivid dreamlike experiences occurring at the transition disturbance, perception of temperature dysregulation, and
from wake to sleep. Typically, hypnagogic hallucinations peripheral vascular complaints (Raynaud-type phenomena
have a multimodal or “holistic” character, often combining with cold hands and feet).
visual, auditory, and tactile phenomena. Hypnopompic
hallucinations are similar but occur at sleep to wake Recurrent Hypersomnia: Kleine-Levin syndrome is
transitions. Sleep paralysis describes the disturbing characterized by recurrent episodes of excessive
temporary inability to move voluntary muscles at sleep- sleepiness,however, associated cognitiveand behavioral
wake transitions. Despite being awake and conscious of disturbances are not uncommon. A typical episode
the sleeping environment, it is impossible for subjects to lasts a median 10 days (range, 2.5–80 days), with rare
move their limbs or even open their eyes. The experience episodes lasting several weeks to months. Usual reported
may last for several minutes and can be very distressing. triggering factors for the first episodes are infection or
Other symptoms may include ptosis, blurred vision, and alcohol intake, with further episodes recurring every
diplopia, presumably as a result of sleepiness. Obesity is 1–12 months (median three months) for years. During
another common symptom of narcolepsy. episodes, patients may spend as long as 16 to 20 hours
per day in sleep, and they usually wake-up only for the
Narcolepsy type 1 due to a medical condition: This condition natural calls (incontinence is not observed). They remain
is primarily associated with central nervous system (CNS) arousable, but are irritable if prevented from sleeping.
disorders, including autoimmune or paraneoplastic When they are awake during episodes, most patients
disorders associated with anti-Ma2 or antiaquaporin4 appear exhausted, indifferent, confused with psychomotor
antibodies, and tumors or other lesions of the hypothalamus retardation. Anterograde amnesia is typical and most of the
or severe head trauma. patients report derealization. A larger chunk of patients eat
ravenously (66%, although one third eat less), nearly half of
Narcolepsy type 2: is characterized by excessive daytime them turn hypersexual (53%, principally men), may show
sleepiness and abnormal manifestations of REM sleep on childish behavior and nearly half appear depressed (53%,
polysomnography/MSLT [mean sleep latency less than or predominantly women). They often become anxious when
equal to eight minutes and two or more sleep onset REM left alone and after seeing strangers, and nearly third of them
periods (SOREMPs) on an MSLT (or one SOREMP on an MSLT experience hallucinations and delusions (30%). Importantly,
and one on the preceding nocturnal polysomnogram)]. patients are completely asymptomatic in between episodes.
Cataplexy is absent, although some atypical sensations of
weakness triggered by unusual emotions such as stress Hypersomnia Due to a Medical Disorder:Patients with
and anger may be reported. Refreshing daytime naps are this disorder have excessive nocturnal sleep, daytime
characteristic. Sleep paralysis, hypnagogic hallucinations, sleepiness, or excessive napping that is attributable to
or automatic behavior, memory lapses, automatic behavior, a coexisting medical or neurological disorder. Daytime
ptosis, blurred vision, and diplopia may be present. sleepiness may be of variable severity and may resemble
that of narcolepsy (i.e., refreshing naps) or idiopathic
Narcolepsy type 2 due to a medical condition: Neurologic disorders hypersomnia (i.e., long periods of unrefreshing sleep).
associated with narcolepsy type 2 include tumors or sarcoidosis Other symptoms of narcolepsy e.g., sleep paralysis,
of the hypothalamus, autoimmune or paraneoplastic disorders hypnagogic hallucinations and automatic behavior may

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be present. Hypersomnia due to a medical disorder is only Management

diagnosed if the medical condition is judged to be directly A. Pharmacotherapy: Pharmacotherapeutic options for the
causing the excessive sleepiness. Hypersomnolence has management of hypersomnia are depicted in Table 8.
been described in association with a number of conditions
e.g., metabolic encephalopathy, head trauma, stroke, B. Behavioral Treatment:
brain tumors, encephalitis, systemic inflammation (e.g.,
chronic infections, rheumatologic disorders, cancer), • Education about type of hypersomnia, course, prognosis
genetic disorders, and neurodegenerative diseases. and management principles
• Regular frequent nap times of 10-20 mins at 2-4 hour
Hypersomnia due to a medication or substance:Patients intervals during the day
with this disorder have excessive nocturnal sleep, daytime • Emphasize need for a regular nocturnal sleep schedule
sleepiness, or excessive napping that is attributable to • Try to obtain 9 hours of nocturnal sleep
sedating medications, alcohol, or drugs of abuse. This
diagnosis also includes hypersomnolence associated CIRCADIAN RHYTHM SLEEP DISORDERS
with withdrawal from amphetamines and other stimulant
drugs. The circadian rhythm sleep disorders comprise of following
disorders having major feature is a misalignment between
Subtypes the patient’s sleep pattern and the sleep pattern that is
Hypersomnia due to sedating medications: desired or regarded as the societal norm ie. share a common
Hypersomnia due to substance abuse: underlying chronophysiologic basis.
Hypersomnia due to stimulant withdrawal: 1. Time Zone Change (Jet Lag) Syndrome
2. Shift Work Sleep Disorder
Hypersomnia associated with a psychiatric disorder: 3. Irregular Sleep-Wake Pattern
Patient may report increased duration of nocturnal sleep 4. Delayed Sleep-Phase Syndrome
associated with daytime sleepiness or excessive napping. 5. Advanced Sleep-Phase Syndrome
In addition, they often complain of poor quality and 6. Non-24-Hour Sleep-Wake Disorder
nonrestorative sleep. Patients are often intensely focused 7. Circadian Rhythm Sleep Disorder Not Otherwise
on their hypersomnolence, and psychiatric symptoms Specified
may become apparent only after prolonged interviews or
psychometric testing. Associated psychiatric conditions Diagnostic subtypes can be specified with the diagnosis of
include mood disorders, conversion or undifferentiated intrinsic type (due to neurologic disease) or extrinsic type
somatoform disorder, and less frequently other mental (due to environmental or social circumstances) Severity
disorders such as schizoaffective disorder, adjustment Criteria: Mild: Moderate: Severe:
disorder, or personality disorders.
Duration Criteria: Acute: Subacute: Chronic:
Subtypes:
Hypersomnia associated with mood disorder Major problem among all CRSDs is the inability to fall asleep or
Hypersomnia associated with a conversion disorder or somatic staying awake when desired or expected. Since sleep episodes
symptom disorder occurring at inappropriate times, the corresponding wake periods
also seen at undesired times. Therefore, the patient complains
Insufficient sleep syndrome:Many people curtail a small of insomnia or sleepiness but importantly both of them are
portion from their normal sleep duration for prolonged occurring at inappropriate times. For most of the CRSDs, once
periods owing to societal or professional demands. Since sleep is initiated, the major sleep episode is of normal duration
sleep deprivation has cumulative effect, they remain in a with normal architecture. However, if any other sleep disorder
state of chronic partial sleep deprivation that is insufficient to appears to influence the sleep timing, diagnosis of CRSD should
maintain normal levels of alertness and wakefulness. Physical be deferred.For example patients with inadequate sleep hygiene
examination reveals no medical explanation for the patient’s may show some degree of shift in sleep and wake timing. Hence,
sleepiness. A detailed history of the sleep pattern reveals that CRSD should be diagnosed only when the symptoms can be
patient is not spending adequate time in sleep and that he ascribed to the major shift in timing of sleep.
has curtailed his sleep in past few days/months. Sleep time
that is markedly extended on weekend nights or during 1. Time Zone Change (Jet Lag) Syndrome: Synonyms and
holidays compared to weekday nights is also suggestive Key Words: Jet lag, transmeridian flight desynchronosis, air
of this disorder. Individuals with this condition may show travel, transmeridiandyschronism.
cognitive and behavioral symptoms e.g., irritability, attention
deficits, distractibility, reduced drive, anergia, dysphoria, Essential Features: Time zone change (jet lag) syndrome
fatigue, impatience, incoordination, and tiredness. consists of varying degrees of difficulties in initiating or

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Table 8: Pharmacotherapy for Hypersomnia

Used for: Drug Mechanism of action Dose range (mg/day) Pediatric use
Hypersomnia Amphetamine stimulants 5‑60 mg Not recommended in pts<3 years
in Narcolepsy, Methyphenidate stimulants 20‑40 mg in adults; Not recommended in pts<6 years.
Idiopathic 5‑20 mg in children Parameters of growth are should be
hypersomnia, etc. regularly monitored in children
Modafinil non‑amphetamine 100‑400 mg SECNE
wakefulness‑promoting
medication
Armodafinil (R)‑ enantiomer of modafinil with 50‑250 mg SECNE
a longer half‑life.
Sodium oxybate rapidly acting sedative/hypnotic/ 4.5‑9 g per night SECNE
(also used for Cataplexy, anesthetic medication.
sleep paralysis, hypnagogic
hallucinations)
Selegiline MAO‑B inhibitor that is 5‑10 mg SECNE
metabolized to amphetamine and
methylamphetamine
Atomoxetine selective noradrenaline reuptake 10‑25 mg generally well tolerated in children and
inhibitor (NARI) adolescents
Reboxetine selective noradrenaline reuptake 10 mg SECNE
inhibitor (NARI)
Ritanserin 5‑HT2 antagonist 5‑10 mg SECNE
Cataplexy Fluoxetine Selective serotonin reuptake 10‑40 mg Safety and effectiveness assessed in
inhibitor (SSRI) children aged 8‑18 yrs with major
depressive disorder and 7‑18 yrs with
OCD
Venlafaxine# serotonin‑norepinephrine reuptake 75‑375 mg SECNE
inhibitor (SNRI)
Protriptyline Tricyclic antidepressant (TCA) 10 mg SECNE
Viloxazine selective norepinephrine reuptake 50‑200 mg SECNE
inhibitor (NRI)
Imipramine Tricyclic antidepressant (TCA) 25‑200 mg SECNE
Clomipramine Tricyclic antidepressant (TCA) 25‑200 mg Can be used in children aged 10 years
and above
Desipramine Tricyclic antidepressant (TCA) 25‑200 mg Not approved for use in children
Recurrent Lithium* Mood Stabiliser 300‑900mg Special caution advised
hypersomnia (Klein
Levin Syndrome)
SECNE – Safety and effectiveness in children not established; NE – Not established *Carbamazepine and valproate can also be used for KLS, some benefit noted
in behavioral symptoms, but no consistent benefit observed in hypersomnia #Duloxetine and desvenlafaxine can also be used to treat cataplexy, though there is
lack of formal research data at present.

maintaining sleep, excessive sleepiness, decrements in time and wake time both are delayed in relation to the
subjective daytime alertness and performance, and somatic environmental timing, however, total sleep time remains
symptoms (largely related to gastrointestinal function) adequate (Fig 1). These patients can’t fall asleep till late in the
following rapid travel across multiple time zones. night and wake up late in the morning having optimal duration
of sleep. If they go to bed early in the evening, they have a long
2. Shift Work Sleep Disorder: Symptoms of insomnia or sleep onset latency and if they are made to wake up early in
excessive sleepiness are seen in association of work shifts. morning, they have reduced awareness and feel sleep.
These patients are often having work shifts that defy the
natural sleep-wake cycle and thus they feel sleepy or unable 5. Advanced Sleep-Phase Syndrome: This is opposite of the
to fall asleep at inappropriate time, e.g., while on work or delayed sleep phase disorder. These patients starts feeling
after reaching home, respectively. sleepy early in the evening, spent optimal time in sleep but
wake up early. If they are made to stay awake till late in
3. Irregular Sleep-Wake Pattern: These patients have night, they show reduced vigilance.
inconsistent timings of sleep and wakefuleness, although
the total duration of sleep remains normal in 24 hours. 6. Non-24-Hour Sleep-Wake Syndrome
When their circadian rhythm is examined through sleep
diary or actigraphy, it appears constantly changing. When seen through sleep diary and Actigraphy, these
patients have optimal duration of sleep, although the timing
4. Delayed Sleep-Phase Syndrome: In this condition, sleep of sleep appears delayed by 1-2 hours each day.

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In January of 2014, the FDA approved the melatonin agonist level, Parkinsonism disorder, end stage renal disease is
HetliozTM (tasimelteon) for the treatment of N24SWD among important.
the blind. This is the first FDA-approved drug for any CRSWD.
Management
Diagnosis of CRSD The selection of therapy depends upon a number of
Polysomnography and Morningness-Eveningness factors, including disease severity, patient age, co
Questionnaire is not routinely indicated for any of the morbidities (e.g., pain, depression, anxiety and history of
CRSDs. Actigraphy is recommended for the delayed sleep impulse control behaviours), drug side effects and patient
wake phase disorder and advanced sleep wake phase preferences.
disorder but may also be used to diagnose other CRSDs.
Sleep diary must be maintained to diagnose all CRSDs. 1. Non – pharmacological
Actigraphy is a good tool to measure the progress.
Proper maintenance of sleep hygiene, exercise, restriction
Management of coffee beverages, pneumatic compression stocking help
Planned naps are recommended for Shift worker disorder. in the symptom reduction
Timed bright light therapy is useful for shift worker disorder
and delayed sleep wake phase disorder. Jet lag disorder can Behavioral strategies — Use of the following interventions
be managed by timed melatonin administration. Hypnotics is supported primarily on the basis of clinical experience in
may be used to induce sleep in Shift worker disorder, some cases, and small randomized trials
however, stimulants are usually not recommended for the • Avoidance of aggravating factors, including
management of CRSDs. consideration of withdrawal of possibly predisposing
medications
RESTLESS LEG SYNDROME • Moderate regular exercise
• Reduced caffeine intake
Restless legs syndrome/Willis-Ekbom disease (RLS/ • For symptomatic relief – walking, bicycling, soaking the
WED) is characterized by an urge to move legs that affected limbs, and leg massage, including pneumatic
is often accompanied by dysesthesias in the muscles. compression
The urge improves with the movement of the legs or • Short daily hemodialysis for patients with end-stage
application of a counterirritant. Symptoms are seen only renal disease.
in the evening and rest worsens the symptoms.A number
of conditions like nocturnal leg cramps, habitual leg Avoidance of aggravating factors — Sleep deprivation is
movement, varicose, arthralgia, positional leg discomfort known to aggravate symptoms of restless legs syndrome/
and leg edema must be excluded before making the Willis-Ekbom disease (RLS/WED) in many patients, and
diagnosis of RLS. This condition interferes with the sleep general principles of sleep hygiene should be reviewed.
significantly. In some patients, significant sleep fatigue
or poor concentration is reported in absence of RLS, Psychotropic drugs e.g., antidepressants, antipsychotics
but with polysomnographic evidence of periodic limb and other dopamine-blocking antiemetics such
movements during sleep (PLMS), in all such cases the as metoclopramide, and sedating antihistamines (including
term periodic limb movement disorder (PLMD) is used. those found in nonprescription medications) may lead to
It is an autosomal dominant, sensorimotor disorder in emergence of RLS/WED or worsening of prior symptoms.
which patient complains of a peculiar creepy or crawling Most antidepressant classes have been associated withRLS/
sensation in the extremities Prevalence varies between WED, including tricyclics, selective serotonin reuptake
2-11% across different studies depending upon the inhibitors, and serotonin-norepinephrine reuptake inhibitors.
geographical locations and populations included.
Discontinuation of antidepressantsmay not be possible
Assessment & evaluation in case of RLS among all patients. In all such cases, symptoms of
The diagnosis of restless leg syndrome is primarily secondary RLS/WED should be treated in the same
based on the symptoms reported by the patient or the way as primary RLS/WED. Bupropion is an alternative
observer. Nocturnal polysomnography may help in the antidepressant that may be less likely to induce or
diagnosis by having PLMs in the recording. Serum iron worsenRLS/WED.
level estimation may be helpful as iron is a co-factor
for tyrosine hydroxylase which is essential for synthesis Iron replacement
of dopamine.The Cambridge Hopkins RLS diagnostic Serum ferritin concentration lower than 45 to
questionnaire(CHRLSQ )and its Hindi version can be 50 mcg/L (ng/mL) has been associated with an increased
used during surveys and epidemiological studies. severity of restless legs syndrome. If the serum ferritin
Looking for risk factors viz - elderly population, low iron level is lower than 75 ng/ml, iron replacement is

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suggested. However, care must be taken not to induce • Pramipexole 0.125 mg once daily. The dose may be
iron overlaod. increased by 0.125 mg every two to three days until
relief is obtained. In a clinical trial, all three doses
Both oral iron therapy as well as intravenous iron have been of pramipexole (0.25, 0.50, and 0.75 mg daily) were
found effective in treatment of RLS. equally effective, and some patients responded to the
initial dose of 0.125 mg daily. However, side effects
2. Pharmacological were more common with the 0.50 mg and 0.75 mg
daily doses. Therefore, it is expected that 0.25 mg daily
The major classes of drugs used include dopaminergic has the best therapeutic margin. Most patients require
agents, alpha-2-delta calcium channel ligands, opioids, and 0.5 mg or less, but doses up to 1 mg may be needed.
benzodiazepines • Ropinirole 0.25 mg once daily. The dose may be
increased by 0.25 mg every two to three days until
Chronic persistent symptoms relief is obtained. Most patients require at least 2 mg,
Chronic persistent restless legs syndrome is defined as RLS and doses up to 4 mg may be needed. The maximum
that is frequent and troublesome enough to require daily recommended dose is 3 mg in patients with end-stage
treatment, with symptoms usually occurring at least twice renal disease on hemodialysis.
a week on average and resulting in moderate or severe
distress. Rotigotine — Rotigotine is a non-ergot dopamine
agonist that is formulated as a 24-hour transdermal patch
Choice of therapy — Patients who do not respond to non .Transdermal rotigotine is a once-daily patch that is
pharmacologic therapy and correction of iron deficiency, typically started at 1 mg/24 hours and titrated upwards to a
pharmacologic treatment with a dopamine agonist or an maximum dose of 3 mg/24 hours. Application site reaction
alpha-2-delta calcium channel ligand is recommended. is the most common adverse effect of rotigotine, reported
• For patients with very severe RLS/WED, co morbid by 40 to 50 percent of patients.
depression, or obesity / metabolic syndrome, a dopamine
agonist is preferred over other drugs as initial therapy. Alpha-2-delta calcium channel ligands — Gabapentin
• For patients with comorbid pain, anxiety, or insomnia enacarbil, gabapentin, and pregabalin are alternative
or a history of impulse control disorder or addiction choices for patients with chronic persistent RLS.
associated with use of a dopamine agonist an alpha-2-
delta calcium channel ligand. Is preffered Gabapentin enacarbil — Several randomized, placebo-
• Most other patients, initial trial an alpha-2-delta calcium controlled studies have demonstrated that gabapentin
channel ligand because of the of augmentation with enacarbil is effective in reducing RLS/WEDsymptom severity.
dopamine agonists, but other potential side effects of The recommended dose of gabapentin enacarbil for
the various drugs should also be considered. In general, RLS/WED is 600 mg, taken in the early evening
older patients are more prone to side effects of alpha-
2-delta ligands. If the first drug chosen is ineffective Gabapentin —Limited data suggest gabapentin may be
or poorly tolerated, then a drug of the other class effective in RLS/WED.
should be tried , including levodopa, benzodiazepines,
and opioids, but generally these are reserved for Pregabalin — Pregabalin in the doses of 75-300 mg/day
intermittent use or in patients with more refractory found effective in treatment of RLS.
symptoms.
Duration of therapy
Dopamine agonists — A number of dopamine agonsits are RLS/WED is often a lifelong disease, but the optimal and
available in market e.g., cabergoline, lisuride, pergolide, safe duration of pharmacologic therapy has not been well
pramipexole, ropinirole,rotigotine, and sumanirole. All established. Most of the supporting data are based on
except sumanirolehave been found superior to placebo. In relatively short (≤12-week) randomized trials, with fewer
two trials, cabergoline and pramipexole were superior to long-term extension studies supporting efficacy for 6
levodopa for improvement in disease severity as measured to 12 months of therapy with either a dopamine agonist
by the International Restless Legs Syndrome Study Group or gabapentin enacarbil.
(IRLS) rating scale.
Special populations
Pramipexole and Ropinirole — Action of pramipexole and Pregnancy and lactation — Management of restless
ropinirole usually starts 90 to 120 minutes after intake. legs syndrome during pregnancy should be individualized
Therefore, these medications should be started two hours based on symptom severity, comorbidities such as
before RLS/WED symptoms start. The recommended doses depression or anxiety, and patient preferences. Many
are as follows: patients can be managed successfully with education,

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reassurance, iron supplementation if indicated, and self-defence. The reported prevalence rates are 0.38%-0.5% in
nonpharmacologic strategies. Pharmacologic therapies such general population and, probably higher (≥6%) in 70-90 year
as clonazepam or carbidopa-levodopa may be considered olds. Even more interesting is the equally higher prevalence
for severe symptoms. of RBD in psychiatric population (5.8%). The early-onset
(<50y) variety (EORBD) has more atypical clinical presentation
End-stage renal disease — The management of RLS/WED in showing female preponderance, less violent behaviour, may
patients with end-stage renal disease is similar to that in occur early during the night, and may get out of bed more
patients with normal renal function. However, medication frequently. There is preponderance of idiopathic cases and
doses may need to be adjusted, especially if the patient is more association is seen with narcolepsy, depression, anti-
not yet receiving dialysis, as dopamine agonists and alpha- depressants and parasomnia overlap disorder (POD).
2-delta ligands are all excreted by the kidneys. Careful
attention to iron status is especially important in this group.. Indian demographics regarding this illness are largely
unknown and the published evidence is limited to half a
REM-SLEEP BEHAVIOUR DISORDER dozen case reports, retrospective chart reviews, prospective
questionnaire-based study and a case control study. All
Most parasomnias are benign unwelcome phenomenon discuss RBD as part of PD except one (table 9).
observed in and around sleep that seldom present alarmingly.
It is a common observation that more often than not, they are The aetiology of RBD is still speculative. RBD may be either
a cause of least concern both to patient and clinician. One such primary idiopathic type (iRBD) or secondary (table 10) to
sleep-related phenomenon is REM-sleep behaviour disorder other disorders. It is unclear whether the idiopathic variety
(RBD) that was first systematically defined 30 years back. It is an independent entity or it is merely a precursor
is a kind of parasomnia characterized by dream enactment ‘cryptogenic’ prodromal syndrome anti-dating degenerative
behaviour (DEB) that emerges during rapid eye movement brain disorders predominantly of α-synucleinopathy type
sleep and may lead to injury or disturbance of sleep. Behaviours ((Parkinson’s disease (PD), dementia of Lewybody(DLB),
include excessive abnormal and/or purposeful motor activities Multiple system atrophy (MSA)). RBD patients are at higher
such as vocalization and simple limb twitching to flailing risk of having cognitive, motor and autonomic impairments
and punching of arms, sitting up, and kicking. Occasionally, at baseline. It may be that spontaneous iRBD precede a
patients climb out of bed, something akin to sleep walking. parkinsonian neurodegenerative illness by several decades
More complex and violent behaviours may occur rarely or and thus have a prognostic and therapeutic relevance. The
many a times during the same night, most action occurring risk of iRBD converting to parkinsonian disorder varies
in bed. Not keeping with their waking personality, the between 40-80% over 5-15 years. There is now a growing
vocalizations may be loud and full of abuse and obscenities. body of evidence that suggests that depression may also be
The routine REM-sleep atonia is typically absent. It manifests a preclinical marker of PD in iRBD cases and anti-depressants
as sustained muscle activity or transient phasic muscle simply unmask the underlying pathology. Following are the
twitches in either the chin or limb electromyography (EMG) on environmental and behavioural risk factors associated with
polysomnography (PSG). Most cases arise after the age of 50. RBD (in common with PD):
Its usual presentation in a speciality clinic is like a 65-year old, 1. traumatic brain injury,
male whose partner expresses concern about some unusual 2. farming,
sleep behaviour or who had injured himself or assaulted his 3. pesticide exposure, and
partner during sleep while having vivid, action-filled dreams of 4. low education.

Table 9: Evidence base on RBD‑ Indian studies

Authors Year Title Type of study Journal
Vibha D et al. 2011 RBD in Parkinson’s disease: a clinical case control study from India Case control Clinical Neurology
&Neurosurgerry
Gupta R et al. 2013 REM sleep behavior disorder in Parkinson’s disease: A case from India Case report Journal of Neurosciences
confirmed with polysomnographic data in Rural Practice
Mahale R et al. 2014 Rapid eye movement sleep behaviour disorder in young ‑ and older ‑ onset Cross‑sectional Sleep Medicine
Parkinson disease ‑ a questionnaire‑based study
Yadav R et al. 2015 Is palmomental reflex an important clinical marker of REM sleep behaviour Cross‑sectional Movement Disorders
disorder in patients with Parkinson’s disease?
Gupta S et al. 2015 Idiopathic REM Sleep Behavior Disorder: A Report on Two Cases with Case report Indian journal of
Contrasting Features Psychological Medicine
Siddiqui M M et al. 2015 Detection of rapid eye movement behaviour disorder using short time frequency Experimental Biomedical Research
analysis of PSD approach applied on EEG signal (ROC‑LOC)
Prashanth R et al. 2014 Parkinson’s disease detection using olfactory loss and REM sleep disorder Experimental Engineering in Medicine
features and Biology Society

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Table 10: Secondary causes of RBD physician is unaware of RBD or the case may be misdiagnosed
Multiple System Atrophy Brain tumours a more common ailment such as epilepsy or sleep-walking.
Dementia of Lewy Body Multiple sclerosis Thus, an elaborate history with direct questions to
Parkinson’s disease (PD) Guillain‑Barre syndrome confirm the presence or absence of the symptoms of some
Mild Cognitive Impairment Stroke
Spinocerebellar Ataxia 3 Narcolepsy
parasomnia is a must [Figure 4].
Guadeloupean parkinsonism Obstructive sleep apnoea (Pseudo‑RBD)
Alzheimer’s disease Medications (anti‑depressants, beta‑blockers) In RBD, a careful interviewing of bed-/room-partner will help
Progressive supranuclear Substance withdrawal (alcohol, barbiturate) in eliciting of a history of brief recurrent DEB that occur
palsy
chiefly in the latter half of the night with patient confined
Huntington’s disease Limbic Encephalitis
Frontotemporal dementia to bed distinguishing it from non-REM sleep parasomnias
that predominantly occur during first half without any dream
mentation. Two major classificatory systems define the
Studies on animal model suggest involvement of brainstem criteria for RBD diagnosis- International classification of sleep
REM-sleep regulating nuclei, namely dorsal pontinesublateral disorders- third edition (ICSD-3) criteria and DSM-5 (Table
dorsal nucleus and/or magnocellular reticular formation. 11 & 12). The DSM-5 now classifies RBD as an independent
The role of several genetic links is under study at present. disorder. ICD-10 is yet to come up with its own criteria of RBD
though ICD-10 CM does include RBD (G47.52) as a billable
The risk of sleep-related injury (SRI) is markedly increased in code for the purpose of reimbursement claims in America.
RBD cases and their bed partners (33%-95%). DEB vary from
harmless actions like knitting, singing, etc., to injurious ones There are several disorders that can present in a fashion similar
and common injuries include bruises, abrasions, lacerations, to RBDs that one needs to rule out. It should be also kept in
fractures and dislocations, attempt at strangulation of partner mind that these conditions may co-exist with RBD (Table 13).
and occasionally, subdural hematomas. Lifetime incidence of On such example is POD, a younger-onset variant of RBD.
head injury is around 20%. Risk factors for SRI are:
• Idiopathic RBD A baseline neurological examination (NE) that involves
• Severe limb movements during DEB specific evaluation of cognition and screening for
• Dream recall extrapyramidal symptoms should be done once a diagnosis
• Falling out of bed during DEB of RBD is established (Table 14). RBD precedes parkinsonian
neurodegenerative disorders and is fairly prevalent (50-90%) in
It is to be noted that as against the common wisdom, α-synuclein disorders, while in rest of the neurodegenerative
DEB frequency has not been found to be associated disorders RBD follows (except spinocerebellar ataxia 3) other
with the frequency and severity of SRI. Cases of PD- neurological deficits and is uncommon.
RBD are less likely to injure themselves compared to
idiopathic RBD and injuries and falls are more common Following investigations will aid to the diagnosis of RBD:
in PD-RBD than PD alone. RBD is a progressive disorder
and spontaneous remissions are witnessed very seldom. Specific
There can be a gradual reduction of RBD symptoms over • PSG with time-synchronized video (vPSG) is the single
the years in approximately 30% of the patients and they most important investigation.
may remit spontaneously in 14-30% of RBD-PD patients • Electro-oculogram (EOG) monitoring
per year. These data are probably reflective of progressive • EMG with multiple channels for chin, bilateral extensor
neurodegeneration. DEB is absent in up to 30% of reported digitorum, and tibialis anterior muscles.
cases of RBD. • Electrocardiogram (ECG)
• Nasal air flow
Assessment and evaluation • Arterial blood oxygen saturation.
Despite the presence of RBD in a higher number of patients
with PD, less than 1% complain about it at the time of The revised scoring of PSG features of RBD has been detailed
presentation. The reasons can be in AASM Manual for the Scoring of Sleep and Associated
• RBD being considered not severe enough or infrequent Events: Rules, Terminology and Technical Specifications,
to consult a physician Version 2.2. RBD is the only parasomnia that requires vPSG
• Symptoms being perceived not worthy of discussion for confirmation of diagnosis.
• Unaware of their presence
• Waiting for them to resolve with time Others
• Feel shy to discuss. To aid in diagnosis or monitor:
• Routine lab investigations
Even if the above hiccups get surmounted, the required • Neuroimaging – currently used as research tools to
support may still elude the patient either because the identify pre-clinical disease markers

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• Transcranialsonography (TCS)- substantianigra (SN) Scales/Questionnaires/Inventories

echogenicity, a disease marker Since access to vPSG is limited, clinical interview and
• Positron-emission tomography (PET)- to assess questionnaires may come in handy in early screening of RBD
severity and extent of neurodegeneration cases and related morbidities. Number of tools are available
• Single photon emission computed tomography for this purpose and to choose the right tool will depend on
(SPECT)- to study the SN dopaminergic neuronal whether it is required for rapid screening of RBD in general
status population, or in specific specialized population such as
• Post-mortem brain autopsy psychiatric cases and patients suspected of neurodegenerative
illness, or to monitor progress of illness or effects of some
Table 11: ICSD‑3 criteria intervention, and who is the source of information. It is to be
Criteria A‑D must be met noted that despite their ease of availability and applicability,
Repeated episodes of sleep related vocalization and/or complex motor screening tools are not a replacement for vPSG. RBD scales
behaviours* help us point out probable RBD cases and thus to plan out
These behaviours are documented by PSG to occur during REM sleep
RBD specific assessment and targeted intervention services
or, based on clinical history of dream enactment, are presumed to occur
during REM sleep without causing a resource crunch.
PSG recording demonstrates REM sleep without atonia (RWA)**
The disturbance is not explained more clearly by another sleep disorder, For RBD screening
mental disorder, medication, or substance use
1. RBD Questionnaire-Hong Kong (RBDQ-HK)
On occasion, there may be patients with a typical clinical history of RBD
with DEB, who also exhibit typical RBD behaviours during vPSG, but do 2. RBD screening questionnaire (RBDSQ),
not demonstrate sufficient RWA, based on the current evidence‑based data, 3. Mayo sleep questionnaire (MSQ),
to satisfy the PSG criteria for diagnosing RBD. In such patients, RBD may 4. RBD1 questionnaire,
be provisionally diagnosed, based on clinical judgement. The same rule
applies when vPSG is not readily available.
5. Innsbruk RBD inventory,
*Dream enactment is not exclusive to RBD **In ‘Subclinical’ RBD, criteria C is
present in absence of dream enactment For RBD severity
1. RBD severity index (in Japanese),
Table 12: DSM‑5 criteria of RBD (327.42) 2. Minnesota parasomnia injury scale,
Recurrent episodes of arousal during sleep associated with vocalization
and/or complex motor behaviours For sleep
These behaviours arise during rapid eye movement (REM) sleep and 1. Epsworth sleepiness scale,
therefor usually occur more than 90 minutes after sleep onset, are more 2. Pittsburgh sleep quality index
frequent during the later portions of the sleep period, and uncommonly
occur during daytime naps.
Upon awakening from these episodes, the individual is completely awake, For baseline cognitive screening
alert, and not confused or disoriented. 1. Modified mini-mental state examination
Either of the following: 2. Montreal cognitive assessment
RWA on PSG
A history suggestive of RBD and an established synucleinopathy
diagnosis (e.g., parkinson’s disease, multisystem atrophy) For parkinsonian features
The behaviours that cause clinically significant distress or impairment in 1. Unified Parkinson disease rating scale
social, occupational, or other important areas of functioning (which may
include injury to self or bed partner)
The disturbance is not attributable to the physiological effects of a Formulation of a treatment plan & Choice of treatment
substance (e.g., a drug of abuse, a medication) or another medical setting [Figure 4]
condition Any treatment plan concerning RBD will involve reduction of
Coexisting mental and medical disorders do not explain the episodes
DEB and prevention of injury, irrespective of frequency and

Table 13: Differential diagnosis of RBD

Disorders of arousal Others
Primary Secondary
Sleep terror Periodic limb movement disorder Physiologic hallucinations of sleep
Sleep walking Nocturnal seizures (e.g., frontal lobe epilepsy) Dissociative/conversion disorder
Sleep talking Gastroesophageal reflux disease Malingering
Confusional arousals Obstructive sleep apnoea Domestic violence
Post‑traumatic stress disorder
Vertigo
Absence seizures
Epilepsy in mentally retarded
Other seizure disorders (e.g., juvenile myoclonic
epilepsy, benign epilepsy of childhood)
Hereditary quivering chin syndrome

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Table 14: Neurological history and examination‑salient severity of DEB. The choice of treatment setting will be largely
features determined by the presenting complaints. Hospitalization
Triad of impending Explore for Early bradykinesia Subtle signs on NE: may be required for assessment of RBD, treatment of SRI
neurodegeneration: • Difficulty in turning over • Affect and/or current medical condition. SRIs in RBD can be life-
• RBD with chronic in bed • Voice volume
threatening and may have medico-legal consequences.
unexplained • Slowing of eating or dressing • Speed of articulation
• Hyposmia • Above difficulties • Blink rate
• Constipation unilateral (u/l)/bilateral • Motor tone While formulating a treatment plan of RBD following should
• If, Impaired colour (u/l significant of • Cogwheel rigidity be included:
identification, rapid parkinson’s disease) • Gait testing: stride
conversion to PD • Change of hand‑writing length, arm swing,
• Non-pharmacological measures
•*psychiatric disorders • Lowering of speech volume number of steps to • Safety measures
(depression) may also • Whether ever felt feet stuck turn, freezing • Removal or minimization of aggravating factors
be a predating factor to the floor • Postural instability
• Counselling of patient and care-givers

No
Adequate opportunity for sleep Rules out insomnia

No
Difficulty in maintaining sleep Evaluate for other sleep disorders

No
Evaluate for OSA &/or other sleep
Abnormal behavioural activity during night sleep
disorders

Clinical features of a parasomnia

No
Assess for NREM parasomnias/ other
Suggestive of RBD
causes of insomnia

vPSG fulfilling diagnostic criteria

Assess for type of RBD

No
Assess & manage causes of secondary
iRBD RBD

Environmental & life style modifications

No
Try different drug &/or non-
Response
pharmacological measures

Yes
Continue indefinitely Response

No

Regular follow-up and monitoring for

appearance of any neurodegenerative disorder Review diagnosis

Figure 4: Diagnosis and management of REM-sleep behaviour disorder

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Table 15: Drugs used in treatment of RBD

Molecule t1/2 (hr) Dose (mg/d) Formulations Adverse effects
Benzodiazepines
Alprazolam 12‑15 1‑3 Tablet/extended Sedation, fatigue, dizziness, ataxia, confusion,
release/solution forgetfulness (B)
Clonazepam 30‑40 0.5‑2 Tablet (B) + blood dyscrasias, grand-mal seizures
Temazepam 8‑15 7.5‑30 Capsules (B) + hallucinations, mania, hypotension, hypersalivation
Triazolam 1.5‑5.5 0.125‑0.5 Tablet (B) + Anterograde amnesia, mania, dry mouth, hypersalivation
Non‑benzodiazepine
receptor agonist
Zopiclone 3.5‑6.5 7.5 Tablet Sedation, dizziness, ataxia, dose‑dependent amnesia,
hyperexcitability
Melatonin and
melatonin‑receptor
agonists
Melatonin 0.33‑0.83 (dose 3‑12 Tablet, capsule, Vivid dreams, nightmares, drowsiness, abdominal cramps,
& route cream, lozenges, headache, irritability, ↑depression, ↑risk of seizures in
dependent) intranasal spray children with severe neurological problems. RARE‑ ↓libido,
gynaecomastia, psychosis
Agomelatine 1‑2 25‑50 Tablet Nausea, dizziness, somnolence, hyperhidrosis. RARE‑ mania,
hepatitis
Ramelteon 2‑5 8 Tablet Sedation, dizziness, fatigue, headache
Anti‑depressants
Desipramine 24 50‑300 Tablet Blurred vision, constipation, urinary retention, increased
appetite, dry mouth, weight gain, sedation, sexual dysfunction.
RARE‑↑intraocular pressure, paralytic ileus, ↑QTc
Paroxetine 24 10‑40 Tablet‑IR & CR Sexual dysfunction, diarrhoea, constipation, insomnia,
sweating, tremors. RARE‑ hyponatremia, suicidality, mania,
bleeding
Pramipexole 8‑12 0.5‑1.5 Tablet Dizziness, Sleep attacks, somnolence, insomnia, nausea,
constipation, asthenia, peripheral oedema, impulse control
disorders, gambling, sexual urges, hallucinations & psychosis,
RARE‑ dyskinesias, rhabdomyolysis, peritoneal/pleural/
pulmonary fibrosis
Dopaminergic
L‑dopa 0.83‑1.5 250‑1250 Tablet, Agitation, delusions, hallucinations, confusion, tremors,
extended‑release, fainting; depression, blurring of vision, blepharospasm.
capsule RARE‑ hypertension, priapism, seizures, gastrointestinal
bleeding
Herbal
Yoku‑kan‑san/Yi‑Gan 1.72‑12.3 2.5‑7.5 Freeze‑dried granules Hypokalaemia (in old), drowsiness, tiredness, gastrointestinal
San (component upset. RARE‑ interstitial pneumonitis, dermatitis,
dependent) hepatotoxicity
Acetyl cholinesterase
inhibitors
Donepezil 70 5‑10 Tablet Nausea, diarrhoea, vomiting, ↓appetite, weight loss,
insomnia, abnormal dreams, muscle cramps. RARE‑ seizures,
syncope (B)
Rivastigmine 1‑2 6‑12 Capsule, liquid, (B) + headache, asthenia, sweating
transdermal
GABA agonist
Sodium Oxybate 0.5‑1 2500‑9000 Oral solution Swelling over face or extremities, weight gain, paraesthesias.
Anxiety, rash, perspiration, palpitation, tightness in chest,
seizures, coma.
Anti‑epileptic
Carbamazepine 12‑17 (repeated 400‑1200 Tablet, capsule, Sedation, dizziness, confusion, unsteadiness, headache,
doses) suspension nausea, vomiting, diarrhoea, rash. RARE‑ aplastic anaemia,
Anti‑psychotic
Clozapine 5‑16 N.A. Tablet ↑risk for diabetes/dyslipidaemias, ↑salivation, sweating,
sedation, constipation, weight gain. RARE‑ tardive dyskinesia,
agranulocytosis, seizures (dose‑dependent), neuroleptic
malignant syndrome, deep vein thrombosis and pulmonary
embolism, ↑risk of death and cerebrovascular events in elderly
patients with dementia‑related psychosis

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• Others Pharmacological treatment

• Pharmacotherapy The only REM-sleep parasomnia where pharmacotherapy is
clearly indicated is RBD. Many pharmacological agents have
Non-pharmacological meassures been tried for this purpose, but there is marked variation
The primary goal of RBD treatment is SRI prevention. in their efficacy and there is lack of standardization of the
Among the non-pharmacologic measures, modification of dose of medication and the duration of its continuation
sleep environment should be initiated as the first step. (Table 15). Among all the medications utilized till date,
the most robust support is for clonazepam and melatonin.
A. Environmental modification may include: A medication that improves sleep quality with minimum
Patient safety. e.g., day time effects and results in improvement of objective
lowering of bed measures of RBD such as RWA on PSG should be chosen.
putting a mattress on the floor alongside bed
sleeping on the floor mattress itself Clonazepam
shift bed/ bedroom to the lowest floor of the house Recommended as first-line medication. The evidence
barricading with pillows around the bed base is almost exclusively in terms of retrospective
using a bed with padded rails case reports and case series in over 300 patients. Initial
minimize furniture around the bed response to low dose clonazepam (0.5-2mg) is seen in
maximize the distance from ungrilled windows upto 90% of patients but later tolerance and treatment
soft-pad the sharp edges of furniture around the house failures are reported. Because of its long half-life, it may
remove fire-arms or knives from within reach become a cause of concern if causing impaired alertness,
(preferably lock away) morning sedation and gait impairment in parkinsonian
safety locking of windows and doors disorders and elderly patients and can worsen concomitant
physical restraint. e.g., sleeping bags, padded belts, obstructive sleep apnoea (OSA). It vanquishes DEB but do
padded waterbeds not re-establish REM sleep atonia. It helps markedly in
Partner safety reduction of SRI, one study reporting a reduction from
Bed partner should sleep separate from the patient 80.8% pre-treatment events to 5.6% post-treatment levels.
till the problem symptoms of RBD are brought Patients on clonazepam should be regularly monitored
under control with treatment. for development of newer symptoms of dementia or gait
It is a matter of investigation whether environmental disorders. Clonazepam is metabolized by cytochrome p450
manipulation is enough in itself for the management of RBD enzyme system (cyp2C19 & cyp3A4). Thus, the possibility
or it has only an adjunct role to pharmacotherapy. of drug-drug interactions should be kept in mind especially
in elderly population where polypharmacy is a rule rather
B. Patient or caregiver should be asked to maintain a sleep diary than exception.
C. Avoid sleep deprivation- maintain adequate total sleep
time with a fixed waking time. Melatonin
D. Avoid alcohol and/or other recreational drugs. The pineal gland secretion, melatonin when used
E. Treat co-morbid sleep disorders, if any. exogenously is said to be effective in RBD in few case reports,
F. Reassure and counsel patient and family about need case series and a small randomized controlled trial of eight
of treatment, regular follow-ups, and the possibility of patients. Recent studies find melatonin as efficacious as
onset of a neurodegenerative disorder. clonazepam in RBD with a better adverse effect profile
G. Review ongoing medication charts. Remove or reduce and re-establishment of REM atonia especially in those
the dose of aggravating agent wherever possible. with dementia or sleep apnoea. Efficacy is not known in
Antidepressants can trigger RBD or expose RBD in up cases where RBD co-exists with both PD/dementia and
to 6% cases of depression. Tapering off might result depression that requires treatment with anti-depressants.
in symptom reduction but not complete remission Most patients respond to 3mg dose with minimal or no side
in such cases. Bupropion is the only anti-depressant effects. The mechanism of action of melatonin in RBD is not
not reported to be associated with RBD till date. known, though calmodulin antagonism is suggested as a
Thus, it might be considered for use in those where potential mechanism and the effects probably go beyond
pharmacotherapy is indicated for depression. simple hypnosis.

Along with these measures, pharmacological treatment Others

should be instituted. As no large randomized double-blind In cases where clonazepam and melatonin are not
or head-to-head controlled trials are available till date indicated or are refractory to these medications, other
to assess efficacy of medications, the current treatment medications may be tried. But so far, the evidence in
guidelines are largely expert consensus, based on evidence their favour is inadequate or at times, contradictory.
of large case series or small clinical trials. e.g., there are just two case reports of successful RBD

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treatment with sodium oxybate. Acetylcholinesterase It should be noted that most patients who ultimately
inhibitors may be instituted in patients with dementia or developed neurodegenerative illness were on clonazepam
synuleinopathies. indicating clonazepam’s ineffectiveness as a preventive
agent. It is recommended that an annual neurological
Among all the tried medications, the only preparation that examination should be done for the earliest detection and
is claimed to have some neuroprotective effects in in-vitro management of PD.
and in-vivo animal studies is Yi-Gan San/Yoku-kan san. It
is a Chinese/ Japanese traditional kampo preparation that Special populations
consists of seven different herbs- Japanese Angelica root The basic tenets of diagnosis, assessment and management
(3g), Atractylodeslancea rhizome (4g), Bupleurum root (2g), of medicine are equally applicable to the special populations
Poriasclerotium (4g), Glycyrrhiza root (1.5g), Cnidium rhizome of RBD. The following few things should be kept in mind
(3g), and Uncaria hook (3g). Its neuropharmacodynamic while dealing with them:
actions include serotonergic, glutamatergic, cholinergic,
dopaminergic, adrenergic, GABAergic along with Children
anti-inflammatory, anti-stress, neuroplasticity, and Assessment of children will require a careful approach
neuroprotective effects. It is through these mechanisms depending on their ability to communicate which can be
it is supposed to exert its effects in its primary indication limited given their age or co-morbidity. Idiopathic RBD in
for behavioural and psychological symptoms of dementia this population is rare and is usually seen in context with
including alzheimer’s disease, dementia of Lewy body, and narcolepsy, epilepsy, brain tumours, or, medication effects.
PD. There is one case report of successful management of
three RBD patients with Yi-Gan San. Elderly
After the onset of idiopathic RBD almost half of the patients will
Other Pharmacological Treatment Modalities develop a parkinsonian disorder within a decade, and nearly
It is very ironic that currently there are no cognitive or 80-90% will develop some neurodegenerative disorder in their
cognitive-behaviour therapies available for REM-sleep lifetimes. Therefore, middle-aged or elderly people presenting
“behaviour” disorder probably highlighting the with RBD symptoms should be counselled and monitored
‘non-functional’ organic nature of the disorder. Two about these future possibilities. An opportunity to enrol them
therapies- one behaviour and one somatic- does require a in any ongoing research clinical drug trials for developing and
mention though. testing disease-modifying drugs can also be explored.

Bed Alarm Relying on the brain’s ability to process complex Women

auditory stimuli during REM sleep similar to wake state and RBD is infrequently reported in females. This may be
low arousal threshold for external stimulus Howell et al. at because firstly, they might be having less injurious and
university of Minnesota developed a pressurized bed alarm less dramatic behaviours during dream enactment; and
customized with a pacifying pre-recorded message in a secondly, they may outlive their partner (gender difference
familiar person’s reassuring voice to calm down the patient at in life expectancy) thus having less likelihood of coming
the onset of dream enactment behaviour. This prevents bed- to the notice of family members and receive the required
exiting and averts potential injuries. It can be used in patients medical attention. All medications require caution for use
who are refractory to pharmacotherapy or do not tolerate it. during pregnancy and lactation and should be taken only
under expert guidance.
Deep brain stimulation of subthalamic nucleus is
ineffective in RBD though it does improve the subjective The paramount importance of recognizing RBD as a
sleep quality. treatable parasomnia lies in the fact that it can prevent
serious life-threatening injuries. Psychiatrists should
Management as per different phases of illness & when to actively screen for the presence of RBD as patients usually
stop do not come forward to report these symptoms for a
RBD is a progressive neurological disorder. Though variety of reasons. The population of India grew at 17.7%
clonazepam is highly effective and works in almost 70-90% between 2001-11. During the same period there was a
of the cases, relapse rates are high on discontinuation so quantum jump in the population of those above 60 years- a
pharmacologic treatment should be continued indefinitely. staggering 35.5%. With an all-time high elderly population
Regular monitoring to assess risk for neurodegenerative of 8.6%, it is high time we brace-up for the identification of
disorders should be taken up keeping in mind the strong RBD and appreciate its importance as a pre-clinical marker
relationship of RBD as a prodrome of such illnesses. of neurodegenerative illnesses. The success of any future
neuroprotective and preventive interventions will, thus,
At present, there are no treatment strategies available to rely on early and reliable identification of illness in its
prevent or delay the development of PD in iRBD cases. nascent stage.

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Table 16: Symptoms of Obstructive sleep apnoea (OSA) cerebrovascular disorders, diabetes mellitus, pulmonary
Somatic symptoms Cognitive and Behavioural symptoms hypertension, arrhythmias, systemic hypertension,
Daytime sleepiness Decreased concentration memory disturbances, cognitive dysfunction and sexual
Fatigue Memory loss problems.
Irritability Decreased libido
Snoring Learning difficulties In addition, psychiatric disorders and OSA are also
Gasping/choking at night Impaired cognitive functioning
Morning headaches Personality changes
frequently comorbid, especially depression.Mood
Non-refreshing sleep Depression disturbance may represent a consequence of sleep apnoea.
Nocturia Anxiety Psychiatric disorders associated with weight gain may
also contribute to and promote the development of sleep
apneas. Medications with depressent effect on CNS can
Table 17: Medical history to be taken in patients
worsen or exacerbate the symptoms of OSA.Patients with
with OSA
sleep apnea often have fregmatned sleep and thus they may
Depression
Sedatives
have daytime symptoms of poor quality sleep e.g., fatigue,
Parkinsonism lethary, poor appetite, poor concentration, memory lapses,
Narcolepsy headache, distressed mood that may be mistaken for
Restless leg syndrome/periodic limb movement disorder depression. Fregmented sleep often presents as multiple
Hypothyroidism
somatic symptoms during the daytime suggesting the
β‑blockers
Idiopathic hypersomnolence diagnosis of somatoform disorder.
Excess alcohol
Previous head injury The symptoms are the direct consequences of OSA and
DystrophicaMyotonica occur due to the repetitive collapse of upper air ways.
Stimulants (caffeine, theophyllines, amphetamines)
Thin and lean individuals with significant apnoea are likely
OBSTRUCTIVE SLEEP APNOEA (OSA) to show upper airway abnormalities. These include, e.g.,
hypertrophic tonsils and adenoids, a low-set palate or
Sleep apnoea is charcaterized by recurrent pauses (at least palatal webbing, a large uvula, a large tongue or a small
5/hour) in breath, each lasting at least 10 seconds and is mandible.
important for the Psychiatric practice as it can mimic or
exacerbate symptoms of psychiatric disorders such as Risk factors, Screening, Examination and Diagnosis of OSA
depression, anxiety and panic disorder. The prevalence of OSA is higher in patients who have a
combination of the following risk factors: obesity, neck
Three types of apnoeas have been described in literature. larger than 17 inches for men or 16 inches for women,
In obstructive sleep apnoea (OSA), cessation of breathing male gender, middle age, large tonsils, or recessed chin.
occurs despite persistent respiratory efforts. In central Besides anatomical factors, physiological factors that
apnoea, there is no respiratory effort. Mixed apnoea has influence the tone of the upper airway muslces play
initial part similar to central apnea but in the later part, equally important role in generation of OSA. It is prudent
effort to breath is seen with absence of airflow throughout to screen all patents who are at risk since untreated OSA
the period. Excessive daytime sleepiness, one of the major is an independent risk factor for mortality. In addition,
symptoms of OSA is seen in one-third of the patients and information regrading conditions as described in Table 17
many report mid-nocturnal awakenings due to chocking must be gathered.
which may be mistaken for panic. On the other hand, central
sleep apnea has subtle clinical manifestations and often Physical Examination
these patients present with chronic non-restorative sleep. Examination is very important to exclude other causes for
the patient’s symptoms mentioned below:
Obstructive sleep apnoea (OSA) is a common disorder
with an estimated prevalence in the general population of Following points should be kept in mind during physical
2–5% (Table 16). Apnoea during sleep leads to decrease in examination
blood oxygen level which leads to disturbance in sleep and
frequent arousals. Sleep apnoea severity is assessed with • Weight and height should be documented.
apnoea-hypopnoea index (AHI), which is the number of
apnoeas and hypopnoeas per hour of sleep. • Mandibular and tongue abnormality.
• Assessment of Nasopharyngeal abnormality.
Obesity is a major risk factor for OSA. Untreated OSA leads
to significant clinical problems including cardiovascular and • Measurement of Blood Pressure.

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• Perform routine respiratory, cardiovascular and I. Mandibular Advancement Splints (MAS). This works
neurological examination to detect any coexisting disease. by moving the mandible forward along with the
tongue and increasing the caliber of upper airway.
Diagnosis
Certain questionnaires e.g., STOP-Bang, Berlin Questionnaire Surgical Options
have been developed to screen the OSA. However, the gold The treatment of choice for moderate to severe OSAS is
standard for the diagnosis of OSA is polysomnography. continuous positive airway pressure (CPAP) devices , but
Ideally, in-lab attended video-synchronized full patient adherence to these devices has been a limiting factor.
polysomnography (level 1) is indicated for the diagnosis of In ‘selected cases’, surgical treatment on the upper airway
OSA, however, among high risk cases, limited channel level (UA) or on the facial skeleton may be beneficial in alleviating
3 polysomnography may also be used. This is also known as this disease or improving the use of CPAP. Following surgical
Home Sleep testing. procedures can be beneficial to patients with OSA.

Treatment Any of the single staged procedure has not been found
Depending upon the severity the various treatment options effective in management of OSA in large controlled trials.
is most appropriate for the management of OSA. Patient should be educated regarding possible recurrence
of OSA after 1-2 years of surgery, especially when it is done
Treatment options can be broadly divided into: on the soft tissues.
1. Patient education
2. Behavioural interventions Treatment for comorbidities
3. Non-surgical options Hypothyroidism, depression, etc, are more prevalent
4. Surgical options. .Obstructive sleep apnea (OSA) and hypothyroidism are
5. Treatment for comorbidities. relatively common disorders that have similar clinical
features and are thought to be causally linked. The
Patient Education mechanisms proposed to explain how hypothyroidism
Patients and their attendants should be educated about the might cause OSA include mucoprotein deposition in the
pathophysiology, risk factors, clinical consequences and the upper airway, decreased neural output to the upper airway
treatment of OSA. musculature, obesity, and abnormalities in ventilatory
control.
Education should include behavioural modification like
weight loss, sleep position, alcohol avoidance, risk factor Treatment of hypothyroidism in the presence of sleep apnea
modification, and medication effects. is potentially hazardous and may lead to cardiovascular
complications. Management by a combination of Nasal
Behavioural Interventions continuous positive airways pressure(CPAP) and low-dose
Lifestyle changes can be very effective in mitigating the thyroxine is helpful in this situation.
symptoms of sleep apnoea. However, large control trials are
not available in this regard. OSA patients may have comorbid depression or any other
1. Weight loss is most important in all those who are psychiatric illness. In such cases bothe the disorders must
overweight. Weight reduction improves symptoms in be adequately and optimally treated.
OSA
2. Exercise Obstructive sleep apnea (OSA) leads to frequent arousals,
3. Avoidance/Reduction of smoking and alcohol is which are characterized by fragmented sleep. Persistent
beneficial. sleep loss can lead to depressive symptoms. Patients may
4. Sedatives or sleeping tablets should be avoided. be treated for depression, but if the underlying symptoms
5. Snorers should be discouraged from sleeping on their are caused by OSA and the apnoea is not treated, depressive
backs. symptoms can remain. We may be treating someone with
antidepressants when what we really should be doing is
Non-Surgical Options
treating their sleep disorder, which could in turn restore
1. Positive Air Pressure (CPAP). This is the “gold standard”
their normal mood.
treatment for OSA. Optimal pressure of the PAP should
be titrated as per the standard guidelines so as to
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