NREM sleep accounts for 75-80% of sleep time in adults and is divided into 3 stages - N1, N2, and N3. REM sleep makes up the remaining 20-25% and is characterized by low muscle tone and rapid eye movements. Common sleep disorders include insomnia, sleep apnea, restless leg syndrome, and narcolepsy. Obstructive sleep apnea is the most common sleep disorder and involves repetitive pauses in breathing during sleep due to upper airway collapse. Narcolepsy involves irresistible daytime sleep attacks and loss of muscle tone in response to emotions.

1. SLEEP ORDER AND DISORDERS
DR. PIYUSH OJHA
DM RESIDENT
DEPARTMENT OF NEUROLOGY
GOVT MEDICAL COLLEGE, KOTA

2. 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.”

3. 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.

4. • 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.

5. 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

6. • 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

7. • 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

8. • 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

9. • 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.

10. • 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.

11. • 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)

12. 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

13. 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)

14. • 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)

15. • 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)

16. 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

17. 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.”

18. • 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.

19. • 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.

20. • 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.

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

22. 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.

23. • 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%).

24. • 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.

25. • 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.

26. • 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.

27. 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

28. 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.

29. • 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.

30. • 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.
•

31. 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.

32. • 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

33. 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.

34. 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)

35. – 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.

36. • 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

38. 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.

39. 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.

40. • 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)

41. • 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)

42. 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.

43. 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

44. 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

45. 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

46. 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.

47. PSG STUDY SUGGESTIVE OF PLMD

48. 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

49. 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.

50. 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

51. 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

52. 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

53. 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)

54. • 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

55. • 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

56. • 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)

57. • 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

59. STANFORD SLEEPINESS SCALE

60. Score > 10 – excessive sleepiness

61. LABORATORY ASSESSMENT OF SLEEP
DISORDERS

62. • 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)

63. • 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

64. 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

65. • 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

66. 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 OSAS
16-29 – Moderate OSAS
>30 – Severe OSAS
•

67. • 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

68. 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.

69. 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.

70. 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.

71. Actigraph / Actometer

72. NORMAL ACTIGRAPH REPORT

73. PRINCIPLES OF MANAGEMENT OF
SLEEP DISORDERS

74. • 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.

75. 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.

76. • 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

77. 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

78. 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

79. 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

80. 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

81. 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.

82. TREATMENT OF RLS-PLMS
MAJOR DRUGS MINOR DRUGS
•Dopaminergic agents :
Pramipexole, Ropinirole
•BZDs : clonazepam,
Temazepam
•Antiepileptic medication :
Gabapentin, Pregabalin
•Opiates : codeine,
oxycodone, methadone,
propoxyphene
•Tramadol
•Baclofen
•Carbamazepine
•Clonidine
•propranolol

83. THANK YOU

84. 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

85. 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