SLEEP ORDER AND DISORDERS

DR. PIYUSH OJHADM RESIDENT

DEPARTMENT OF NEUROLOGYGOVT MEDICAL COLLEGE, KOTA

HISTORY

• Lucretius approx 2000 years ago postulated that sleep is an absence of wakefulness.

• Macnish in 1830 defined Sleep as “suspension of sensorial power in which the voluntary functions are absent but the involuntary functions such as circulation, respiration and other function controlled by the autonomic nervous system, remain intact.”

SLEEP ARCHITECTURE & SLEEP STAGES

• Sleep is divided into 2 independent states :– NREM– REM

• NREM is further divided into 3 stages on the basis of EEG criteria.

• NREM & REM sleep alternate with each cycle lasting approx 90 to 100 mins.( 4-6 such cycles noted during a normal sleep period)

• The duration of REM sleep increases progressively over the night, longest REM cycle may last as long as 1 hour.

• Rechtschaffen & Kales (1968) divided NREM sleep into 4 stages.

• In 2007, American Academy of Sleep Medicine (AASM) task force divided NREM sleep into 3 stages : N1,N2 and N3.

• NREM sleep accounts for 75-80% of sleep time in adult humans.

SLEEP STAGES• WAKEFULNESS :– EEG : alpha (8-13Hz) in quiet wakefulness with eyes closed– High muscle tone– Rapid eye movements (REMs)– Irregular respiration & heart rate

• NREM 1 (N1) :– Non REM light sleep; defines sleep onset– EEG : low voltage, mixed frequency pattern (4-7 Hz) for

more than 50% of the 30 second epoch; Vertex waves ( sharply contoured waves over central region lasting <0.5 secs)

– Muscle tone intermediate– Slow rolling eye movements– Respiration and heart rate becomes regular

• NREM STAGE 2 (N2) :– Major stage of non-REM sleep in adults.– EEG – K-complexes ( negative sharp waves

followed immediately by a positive component) and/or sleep spindles (11-16 Hz lasting > 0.5 secs)

– Muscle tone inermediate– No or few slow eye movements– Regular repirations and heart rate

• NREM STAGE 3 (N3) :– Deep non-REM sleep, slow wave sleep.– EEG – 20 % or more of a 30 sec epoch consists of

0.5-2 Hz waves of amplitude > 75 microvolts– Muscle tone inermediate– Mostly no or eye movements– Regular repirations and heart rate

• REM STAGE (also known as Paradoxical Sleep)

– EEG – low amplitude, mixed freqency EEG– Muscle tone low– REMs, resembling those observed in wakefulness– Irregular respiration and heart rate– Penile or clitorial tumescence

• Sleep requirements change dramatically from infancy to old age.

• Newborns – polyphasic sleep pattern with approx 16 hours sleep/day

• Sleep requirement – approx 10 hrs/day by 3 to 5 years of age

• Adults exhibit a monophasic pattern with approx 7.5-8 hours sleep/night

• In old age biphasic pattern of sleep.

• Newborn infant spends approx 50% of time in REM sleep, which changes to normal adult pattern of 25% REM sleep by 6 months age.o

• On falling asleep, a newborn baby goes immediately into REM sleep, or active sleep, which is accompanied by restless movements of arms,legs and facial muscles.

• By age of 3 months, the NREM-REM cyclical pattern of adult sleep is established.

• Sleep requirement : defined as the optimal amount of sleep required to remain alert and fully awake and to function adequately throughout the day.

• Average adult – 7.5-8 hours

• The chances of death from CAD,cancer or stroke are greater for adults who sleep <4hrs or >9hrs a night compared to those who sleep an average of 8 hours (Kripke et al,1979; again confirmed the findings in 2002)

FUNCTIONS OF SLEEP

• Body and brain tissue restoration (Restorative Theory)

• Energy conservation• Adaptation• Memory reinforcement and consolidation• Synaptic neuronal network integrity• Gene expression in sleep/wakefulness• thermoregulation

CAUSES OF EXCESSIVE DAYTIME SLEEPINESS(EDS)

• PHYSIOLOGICAL CAUSES :-– Sleep deprivation and sleepiness related to lifestyle and

irregular sleep/wake cycle schedule

• PATHOLOGICAL CAUSES :-– Primary sleep disorders : OSA, central sleep apnea

syndrome, Narcolepsy, Idiopathic Hypersomina, Circadian rhythm sleep disorders(jet lag, shift-work sleep disorder), RLS, PLMS, Recurrent or periodic hypersomnia (Klein Levine syndrome)

• General medical disorders (hepatic,renal ,cardiac or respiratory failure, electrolyte disturbances, hypothyroidism)

• Psychiatric causes : Depression• Neurological causes : brain tumor or vascular lesions affecting

thalamus,hypothalamus or brain stem, Post traumatic Hypersomnolescence , MS, Encephalitis Lethargica, Cerebral Trypanosomiasis, AD etc.

• Medication related Hypersomnia: like BZD, Non BZD Hypnotics like Barbiturates, TCA, Antihistaminics, Narcotic analgesics

• Toxin related Hypersomnolescence : Alcohol

CAUSES OF EXCESSIVE DAYTIME SLEEPINESS(EDS)

• Consequences of Excessive Daytime Sleepiness :– Impaired performance and productivity– Impaired short term memory, attention,response

time, attention and cognition– Impaired quality of life– Psychological stress– Increased morbidity and mortality (ie increased

likelihood of accidents)

PRIMARY SLEEP DISORDERS ASSOCIATED WITH EXCESSIVE DAYTIME SLEEPINESS

• Insufficient sleep syndrome due to sleep deprivation

• Obstructive Sleep Apnea Syndrome (OSAS)• Narcolepsy & Idiopathic hypersomnolence• Circadian rhythm sleep disorders• Periodic limb movement disorders (PLMD)• Inadequate sleep hygiene

INSOMNIA

• Most common sleep disorder affecting population & most common disorder encountered in sleep medicine

• Approx 35% has had insomnia complaints;in 10% it is a persistent problem (Chokroverty, 2006)

• The AASM(2005) defines Insomnia as “ inability to initiate or maintain sleep,early awakening, inadequate sleep time, or poor sleep quality associated with a lack of feeling restored and refreshed in the morning, leading to poor daytime functioning.”

• Nonrestorative sleep occuring 3-4 times a week, persisting for more than a month, and associated with impaired daytime functioning is the typical patient complaint.

• Increased association of insomnia with age, female sex, low socioeconomic status, divorce, widowhood, seperation, recent stressand depression and drug or alcohol abuse.

• ACUTE INSOMNIA:– Causes may a change of sleeping

environment( most common cause), Jet lag, acute medical or surgical illnesses, stimulant medications like theophylline, steroids, beta blockers

– May last for few days to few weeks- 3 months at most.

– Once the stressful event is over and patient adjusts to the event, sleep disturbance resolves.

• CHRONIC INSOMNIA :– Most cases of insomnia are chronic and associated

with comorbid conditions like psychiatric, medical, primary sleep related (OSAS), or neurological disorders, or drug and alcohol abuse.

– Inadequate sleep hygiene is also an reason for chronic insomnia.

– Various surveys have shown that individuals with insomnia are more likely to develop new psychiatric disorders, particularly major depression, within 6-12 months.

• Paradoxical Insomnia : a sleep state misperception characterized by subjective complaints of sleeplessness without objective evidence (PSG recording documents normal sleep patterns).

NARCOLEPSY• Term coined by French physician Galineu in 1880• Most cases are sporadic, but some are dominant.• 10-40 times increase prevalence in families.• HLA-DQB1*0602 is a marker for narcolepsy on chromosome 6

across all ethnic groups.• 12-38% of the general population carries the same HLA allele,

but narcolepsy is present in 0.02-0.18% of the population. So the allele is neither necessary nor sufficient for for susceptibility to catalepsy.

• The postulated theory for pathogenseis of Narcolpesy – depletion of Hypocretin( Orexin) neurons in lateral and perifornical region of the hypothalamus.

• Clinical manifestations of Narcolepsy :-• Peak incidence between ages 15-30.

• AASM (2005) divides Narcolpesy into 3 types :– Narcolepsy with Cataplexy– Narcolpesy without cataplexy– Secondary narcolepsy

• Major clinical manifestations of narcolepsy include : narcoleptic sleep attacks(100%), cataplexy(60-70%), sleep paralysis(25-50%), hypnagogic hallucinations (20-40%), automatic behavior(20-40%) and disturbed night sleep(70-80%).

• The classic Narcoleptic sleep attack is an irresistible desire to fall asleep in inappropriate circumstances and at inappropriate places. The spell lasts for a few mins to as long as 20-30 mins and patient generally feels refreshed on waking.

• Attacks persists throughout lifetime with rare temporary remissions.

• Cataplexy is defined as a sudden loss of tone in all voluntary muscles with exception of respiratory and ocular muscles.

• Attacks are triggered by emotional factors in >95% cases.

• Duration is usually from few seconds to few mins.• Consciousness is completely retained during the

attack.• Usually occurs months to years after onset of sleep

attacks.• EEG recording shows evidence of wakefulness during

brief catapleptic spells, but if the attack lasts longer than 1-2 mins, the EEG shows REM sleep.

• In 30% patients, 3 of the 4 major manifestations of the Narcoleptic tetrad (sleep attack, cataplexy, sleep paralysis and hypnagogic hallucinations) occur together, and in about 10% of cases, all 4 features occur together.

DIFFERENTIAL DIAGNOSIS OF NARCOLEPTIC SLEEP ATTACKS CATAPLEXY

• OSAS• Sleep deprivation• insufficient sleep syndrome• alcohol or drug abuse•Periodic hypersomnolence•Medical, neurological or psychiatric disorders causing hypersomnolence•Circadian rhythm sleep disorders

• partial complex seizures•Absence seizures•Atonic seizure•Drop attack•Syncope

SLEEP APNEA SYNDROMES

• Broadly divided into 2 types:– Upper airway OSAS– Central sleep apnea syndromes (CSAS)

• OSAS is the most common sleep disorder referred to sleep laboratories for PSG recordings.

• In OSAS, the site of obstruction is the upper airway.

• While in CSAS, the defect lies in the ventilatory control mechanism in the CNS.

• Apnea consists of 3 types- Central, obstructive and mixed.

• According to AASM scoring manual, Hypopnea requires a reduction of nasal pressure or the alternative airflow sensor signal by 30% or more of the baseline amplitude for at least 10secs accompanied by oxygen desaturation of 4% or more from the pre-event baseline.

• To be clinically significant, the number of apneas and hypopneas per hour of sleep (Apnea-Hypopnea Index, AHI) must be at least 5.

• An arousal is defined a either a transient return of alpha activities(8-13Hz) or beta rhythms (>13Hz) or a change from delta to theta activities in EEG lasting from 3-14 secs.

• Repeated arousal causing sleep fragmentation are important factors causing EDS.

•

OBSTRUCTIVE SLEEP APNEA SYNDROME

• Based on the definition of at least 5 apneas/hypopneas per hour of sleep accompanied by EDS(excessive daytime somnolence)(Young et al 1997), prevalence of OSAS is approx 4% in men and 2% in women between ages of 30-60.

• Risk factors for Obstructive Sleep Apnea Syndrome :– Male gender– Increasing age– BMI – Increasing neck circumference (>17 inches in men &

16 inches in women)– Alcohol– Smoking– Increasing drug use– Nasal allergies– Endocrine disorders– Disorders with craniofacial abnormalities

SYMPTOMS OF OSAS

• NOCTURNAL SYMPTOMS DURING SLEEP :– Habitual loud snoring– choking during sleep– cessation of breathing (apneas witnessed by bed partner)– Sitting up or fighting for breath or confusional arousal– abnormal motor activities during sleep (jerking and shaking

movements)– severe sleep disruption– GERD causing heart burn– nocturnal enuresis( in children)– Profuse nocturnal sweating.

SYMPTOMS OF OSAS

• DAYTIME SYMPTOMS :– Excessive daytime somnolence– Forgetfulness– Personality changes– Decreased libido and impotence in men– Dryness of mouth on awakening– Morning headache in some patients– Automatic behavior with retrograde amnesia– Hyperactivity in children– Hearing impairment (rare)

– Daytime symptoms include EDS characterized by sleep attacks lasting 0.5-2 hrs and occuring mostly when the patient is relaxing.

– The prolonged duration and nonrefreshing nature of these sleep attacks differentiate from norcoleptic sleep attacks.

• PHYSICAL FINDINGS IN OSAS :– Obesity (70%)– Increased BMI– Increased neck circumference (>17 inches in men

and >16 inches in women)– In some patients

• Large edematous uvula• Low hanging soft palate• Large tonsils and adenoids ( esp in children)• Retrognathia• Micrognathia• HTN (45%)(repeated hypoxemias leading to increased

sympathetic activity)• Cardiac arrhythmias• Evidence of CHF

UPPER AIRWAY RESISTANCE SYNDROME

• Controversy regarding this as a separate entity.• Some consider it as initial stage, later progressing

into full blown OSAS.• However in the only longitudinal study performed

by Guilleminault et al (2006), it was noted that only 5% of the patients had developed OSAS 4.5 years later.

• Patients show subtle airflow limitations due to increased upper airway resistance, followed by repeated arousals during sleep at night.

UPPER AIRWAY RESISTANCE SYNDROME

• Nasal pressure monitoring with a nasal canula is more sensitive than use of a thermistor in detecting airflow limitation and increased upper airway resistance.

• Intraesophageal balloon recording is the standard method for detecting upper airway resistance and reveals increasing efforts with increasing intraesophageal pressure leading to arousal but without any apnea/hypopnea.

• May or may not have snoring, but have EDS and all its consequences as in OSAS.

• CPAP titration is used as 1st line therapy.

• One of the commonest movement disorder• Clinical diagnosis• Diagnosis is based on International Restless Legs

Syndrome Study Group (IRLSSG) criteria first established in 1995 and later modified in 2003.

• Possibly autosomal dominant mode of inheritance• Approx 80% of RLS patients have PLMS, and many

also have periodic limb movements in wakefulness.

RESTLESS LEG SYNDROME (RLS)

• RLS has a profound impact on sleep.• Patients often seek medical help for sleep

disturbances- generally difficulty in intiation.• Exact pathophysiology and the site of CNS

dysfunction in idiopathic cases is unclear.• Suggested hypothesis involves an abnormalities

in body’s use and storage of ironand dopamine dysfunction, which could involve changes in dopamine receptors or dopamine uptake.

RESTLESS LEG SYNDROME (RLS)

CLINICAL DIAGNOSTIC CRITERIA FOR IDIOPATHIC RESTLESS LEG SYNDROME (RLS)• ESSENTIAL CRITERIA :– An urge to move the legs, usually accompanied by or caused

by an uncomfortable sensations in the legs.– The urge to move or unpleasant sensations beginning or

worsening during periods of rest or inactivity, such as lying or sitting.

– The urge to move or unpleasant sensations partially or totally relieved by movements such as walking or stretching, at least as long as the activity continues.

– The urge to move or unpleasant sensations are worse in evening or night than during day or only occur in evening or night.

CLINICAL DIAGNOSTIC CRITERIA FOR IDIOPATHIC RESTLESS LEG SYNDROME (RLS)

• SUPPORTIVE CRITERIA :– Dopaminergic responsiveness– Presence of periodic limb movements in sleep or

wakefulness– Positive family history

• ASSOCIATED FEATURES :– Usually progressive clinical course– Normal neurological examination in idiopathic form– sleep disturbance

CAUSES OF SYMPTOMATIC OR COMORBID RESTLESS LEG SYNDROME (RLS)

NEUROLOGICAL DISORDERS

MEDICAL DISORDERS

DRUGS & CHEMICALS

•Polyneuropathies•Lumbosacral radiculopathies•ALS•MS•PD•Poliomyelitis

•Anemia : iron & folate deficiency•DM•Amyloidosis•Uremia•Gastrectomy•Malignancy•COPD•Peripheral vascular diseases•RA•Hypothyroidism

•Caffeine•Neuroleptics•Withdrawl from sedatives or narcotics•Lithium•CCB like nifedipine

DIFFERENTIAL DIAGNOSIS OF RESTLESS LEG SYNDROME (RLS)

PRESENTING WITH EXCESS RESTLESSNESS

PRESENTING WITH NOCTURNAL LEG DISCOMFORT

•Akathisia•Degenerative disease•Myokymia•Hypnic jerks•Essential myoclonus•Orthostatic tremors•Anxiety/depression•PLMD•ADHD

•Small fiber neuropathies•Claudication•Varicose veins•Myalgias•Arthritis•Radiculopathies•Delusional parasitosis

PERIODIC LIMB MOVEMENT IN SLEEP

• PLMS is a PSG finding characterized by periodically recurring stereotyped limb movements, particularly dorsiflexion of the ankles and sometimes flexion of the knees and hip at an average interval of 20-40 secs, a duration of 0.5-10 seconds during predominantly NREM sleep, and occuring for at least 4 consecutive movements.

• Occurs most commonly in RLS patients(80%).• PLMS index – number of PLMS per hour of sleep.

Normal < 5; > 15 suggestive of PLMS.

PSG STUDY SUGGESTIVE OF PLMD

CIRCADIAN RHYTHM SLEEP DISORDERS

• Result from a mismatch between body’s internal clock and geophysical environment, either as a result of malfunction of the biological clock or a shift in the environment causing this to be out of phase.

• Most common circadian rhythm sleep disorders are – Jet lag ( associated with high speed air travel across several

time zones in east/west direction)– shift work sleep disorder– Advanced sleep phase state(ASPS)– Delayed sleep phase state (DSPS)– Irregular sleep/Wake circadian rhythm disorder

KLEINE-LEVINE SYNDROME

• Affects mostly adolescent boys• Characterized by periodic hypersomnolence and bulimia• Patient sleeps for 16-18 hrs a day or more during sleeping

episodes and upon awakening eats voraciously.• Other behavioral disorders include hypersexuality, memory

impairment, confusion, hallucination and polydipsia.• PSG studies show normal sleep cycling.• MSLT show pathological sleepiness without sleep onset REM.• A limbic – hypothalamic dysfunction has been proposed as

etiology.• Lithium has been found effective; valproate as alternative.

SLEEP RELATED MOVEMENT DISORDERS

• Consists of relatively simple stereotyped movements disturbing sleep.

• Includes :– RLS– PLMS– Rhythmic movement disorders (benign sleep/wake

transition disorder with 3 characteristic movements – head banging, head rolling & body rocking)

– Bruxism– Nocturnal leg cramps

PARASOMNIAS• Abnormal movements or behaviors that occurs in sleep or

during arousals from sleep; may be intermittent or episodic and sleep architecture may not be disturbed.

• INCLUDES :– Confusion arousals– Somnambulism– Sleep terrors– RBD– Sleep paralysis– Sleep enuresis– Sleep related groaning (Catathrenia)– Sleep related hallucinations– Sleep related eating disorder

RAPID EYE MOVEMENT SLEEP BEHAVIORAL DISORDERS (RBD)

• Onset : middle age to elderly• Characteristic feature is intermittent loss of REM sleep related

muscle hypotonia or atonia and appearance of various abnormal motor activities during sleep.

• Presents with violent dream-enacting behavior during sleep, causing injury to self or bed partner

• Often misdiagnosed as psychiatric disorder or nocturnal seizure (partial complex seizure)

• Etiology : 40% idiopathic, 60 % associated with structural CNS lesions or alcohol or drugs

• Polysomnography – s/o rapid eye movement without muscle atonia

• Experimental models – bilateral peri locus ceruleus lesions• 90 % response to Clonazepam

APPROACH TO A PATIENT WITH SLEEP COMPLAINTS

• Common sleep related complaints are :– Trouble falling asleep and staying asleep (insomnia)– Falling asleep during day (Daytime

hypersomnolence)– Inability to sleep at right time ( circadian rhythm

sleep disorders)– Thrashing and moving about in bed, with repeated

leg jerking (Parasomnias)– Restless Leg syndrome (RLS)

• Cardinal symptoms of Insomnia :– Difficulty falling asleep– Frequent awakenings, including early morning

awakenings– Insufficient or total lack of sleep– Daytime fatigue, tiredness or sleepiness– Lack of concentration– Irritability, anxiety, and occasionally depression

and forgetfulness– Preoccupation with somatic symptoms like aches

and pains

• Cardinal symptoms of Hypersomnia :– Excessive daytime sleepiness– Falling asleep in an inappropriate place or under

inappropriate circumstances– No relief of symptoms after additional sleep at

night– Daytime fatigue– Inability to concentrate– Impairment of motor skills and cognition– Additional symptoms depending on underlying

etiology

• Detailed history including information on patient’s entire 24 hours

• Detailed sleep history with a sleep questionnaire as well as with sleep log or sleep diary

• Psychiatric , neurological, medical, drug (alcohol) history

• Family history• Physical examination to cover medical and

neurological cause (eg. OSA)

• It is advisable to interview the bed partner, caregiver or parents of the children as well.

• A sleep log kept over a period of 2 weeks period is also a valuable indicator of sleep hygiene.

• Subjective Measures of sleepiness – Stanford Sleepiness scale– Epsworth Sleepiness scale

STANFORD SLEEPINESS SCALE

Score > 10 – excessive sleepiness

LABORATORY ASSESSMENT OF SLEEP DISORDERS

• Diagnostic workup for the primary or comorbid condition causing sleep disturbance

• Laboratory tests for the diagnosis and monitoring of sleep disorders :

• Overnight polysomnography (PSG)• Multiple sleep latency test (MSLT)• Maintenance of wakefulness test (MWT)• Actigraphy• Video PSG

• Standard EEG or video EEG for suspected seizure disorders• Imaging studies :

• Upper airway imaging for OSAS• Neuroimaging (CT,MRI, PET)

• Miscellaneous tests :– PFT in case of suspected bronchopulmonary and

neuromuscular disorders causing disturbed sleep– HLA testing for suspected Narcolepsy– CSF hypocretin-1 levels in suspected narcolepsy– Serum iron and ferritin levels in patients with RLS– NCV and EMG to exclude comorbid or secondary

RLS

POLYSOMNOGRAPHIC STUDY

• An overnight Polysomnography study is the single most important laboratory test for the diagnosis and treatment of patients with sleep disorder.

• A PSG study includes multichannel EEG, EOG, EMG especially of chin and tibialis anterior muscle, airflow, respiratory effort( by Inductance Plethysmography), oxygen saturation by finger oximetry, ECG, nasal pressure monitoring by transducers

• INDICATIONS OF POLYSOMNOGRAPHY :-– Diagnosis of sleep related breathing disorders– CPAP titration in patients with sleep related

breathing disorders.– Follow up treatment to assess effectiveness in

OSAS patients– Preoperative procedure in patients undergoing

upper airway surgery for OSAS– Evaluation of suspected Narcolepsy– Evaluation of parasomnias– Diagnosis of RBD and PLMD

POLYSOMNOGRAPHY FINDINGS IN

• OSAS : recurrent episodes of apnea and hypopnea, mostly obstructive or mixed, and few episodes of central apnea accompanied by O2 desaturation and followed by arousal with resumptions of breathing. – AHI index : <5-normal

5-15 – Mild OSAS16-29 – Moderate OSAS>30 – Severe OSAS

•

• NARCOLEPSY : short sleep latency, excessive duration of sleep with frequent arousals, reduced total sleep time, excessive body movements and reduced slow wave sleep.

• RBD : absence of muscle atonia and presence of transient EMG bursts in upper and lower limbs and cranially innervated muscles during REM sleep.

POLYSOMNOGRAPHY FINDINGS IN

MULTIPLE SLEEP LATENCY TEST

• Important test to effectively document Excessive daytime somnolence (EDS)

• Narcolepsy is the single most important indication for performing MSLT.

• The presence of 2 sleep onset REMs on 4 to 5 nap studies and sleep onset latency of less than 8 mins strongly suggest a diagnosis of Narcolepsy.

MAINTENANCE OF WAKEFULNESS TEST

• MWT is a variant of MSLT measuring the subjects ability to stay awake.

• Consists of 4-5 trials of remaining awake recurring every 2 hours.

• Each trial is terminated if no sleep occurs after 40 mins or immediately after the first 3 consecutive epochs of stage 1 NREM sleep or first epoch of any other stage of sleep.

• If Mean Sleep Latency <8 mins – abnormal• MWT test is less sensitive than MSLT for diagnosing narcolepsy

but more sensitive in assessing the effect of treatment.• MWT 40 minute protocol test also used to assess individuals

whose job constitutes a public or personal safety issue.

ACTIGRAPHY

• Uses an Actigraph (also known as Actometer) worn on the wrist or ankle to record acceleration or decceleration of body movements which directly indicate stage of sleep/wakefulness.

• The actigraph can be worn for days or weeks, hence this test complements sleep log or sleep diary in circadian rhythm sleep disorders, insomnia or excessive daytime sleepiness.

Actigraph / Actometer

NORMAL ACTIGRAPH REPORT

PRINCIPLES OF MANAGEMENT OF SLEEP DISORDERS

• Correction of the underlying cause• If a satisfactory treatment is not available for the primary

condition or does not resolve the problem, then treatment should be directed at specific sleep disturbance.

• Sleep hygiene measures :• Keep a regular sleep wake schedule, including

weekends• Avoid caffeinated beverages after lunch or smoking

specially in evening• Avoid alcohol near bedtime• Restrict sleep to amount needed to feel rested.• Don’t go to bed hungry• Adjust bedroom environment.• Don’t engage in planning next day’s activity at bedtime.• Exercise regularly for about 20-30 mins, preferably 4-5

hours before bedtime.

TREATMENT OF NARCOLEPSY-CATAPLEXY SYNDROME

• Includes Non-pharmacological and Pharmacological measures.

• Non-pharmacological measures include :– Scheduled short daytime naps– Sleep hygiene measures– Periodic attendance at narcolepsy support groups.

• Drugs to treat Narcoleptic sleep attacks :– Modafinil : 200mg/day, max 400 mg/day– Methylphenidate : 5mg tds, max dose 50mg/day– Dextroamphetamine– Methamphetamine

• Drugs to treat Cataplexy and other auxiliary symptoms :– Imipramine : 75-150mg/day– Clomipramine : 75-125 mg/day– Fluoxetine : 20mg/day, max 80mg/day

TREATMENT OF UPPER AIRWAY OSAS

• General measures :– Avoid alcohol and sedative-hypnotics specially in

the evening– Reduce body weight– Avoid sleep deprivation– Regular exercise– Avoid supine sleeping position

TREATMENT OF UPPER AIRWAY OSAS

• Mechanical Devices :– Continuous positive airway pressure (CPAP)

titration– Bilevel positive airway pressure (BiPAP) titration– Oral appliances like mandibular advancement

devices– Tongue retaining devices

TREATMENT OF UPPER AIRWAY OSAS

• Surgical Techniques :– Uvulopalatopharyngoplasty (UVP)– Laser assisted UVP (LUVP)– Palatal implants– Nasal surgery– Maxillomandibular advancement– Anterior hyoid advancement– Tonsillectomy and adenoidectomy

TREATMENT OF INSOMNIA

• BZD Receptor agonists : Flurazepam, Temazepam, Lorazepam, Clonazepam

• Non- BZD Receptor drugs : Zolpidem, zaleplon, Eszopiclone.

• Melatonin Receptor agonists : Ramelton 8 mg at bedtime

• Antidepressants : Trazodone, Amitryptyline, Doxepin, Mirtazapine

TREATMENT OF RLS-PLMS

• Non-pharmacological measures :– Sleep hygiene measures– Avoidance of sleep deprivations– Avoidance of agents that exacerbate RLS (caffeine,

alcohol, smoking, neuroleptics, TCAs, SSRIs)– Hot bath or leg massage at bedtime and mild to

moderate exercise may also be helpful.

TREATMENT OF RLS-PLMSMAJOR DRUGS MINOR DRUGS•Dopaminergic agents : Pramipexole, Ropinirole•BZDs : clonazepam, Temazepam•Antiepileptic medication : Gabapentin, Pregabalin•Opiates : codeine, oxycodone, methadone, propoxyphene

•Tramadol•Baclofen•Carbamazepine•Clonidine•propranolol

THANK YOU

REFERENCES

• Bradley’s Neurology in clinical practice, 6th edition

• Adam & Victor’s Principles of Neurology 10th edition

• Hankey’s clinical neurology 2nd edition• Harrison’s textbook of Internal Medicine 18th

edition

BEHAVIORAL & PHYSIOLOGICAL CRITERIA OF WAKEFULNESS & SLEEP

CRITERIA AWAKE NREM SLEEP REM SLEEP

POSTURE Erect,sitting or recumbent Recumbent Recumbent

MOBILITY Normal Slightly reduced or immobile; postural shifts

Moderately reduced or immobile; myoclonic jerks

RESPONSE TO STIMULATION

Normal Mildly to moderately reduced

Moderately reduced to no response

LEVEL OF ALERTNESS Alert Unconscious but reversible

Unconscious but reversible

EYELIDS Open Closed Closed

EYE MOVEMENTS Waking eye movements Slow rolling eye movements

Rapid eye movements

EEG Alpha waves; desynchronized Synchronized Theta or sawtooth; desynchronized

EMG (muscle tone) Normal Mildly reduced Moderately to severely reduced or absent

EOG Waking eye movements Slow rolling eye movements

Rapid eye movements