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SLEEP DISORDERS
DR.SHUCHI PANDE
INTRODUCTION
• Sleep is a state of decreased awareness of environmental stimuli that is
distinguished from states such as coma or hibernation by its relatively rapid
reversibility.
• Sleep is an universal behavior.
• Sleep is also an essential component for good health and optimal cognitive
function.
• For peak performance, human
need 8 hrs sleep a day.
FUNCTIONS OF SLEEP
1. Restoration and recovery
2. Energy conservation
3. Memory consolidation
4. Discharge of emotion
5. Thermoregulation
6. Homeostasis
7. Maintenance of immune system
MONITORING HUMAN SLEEP
• Sleep is generally defined by combining BEHAVIORAL OBSERVATION
with ELECTROPHYSIOLOGICAL RECORDING.
• WHAT ARE THE TOOLS OF SLEEP MEDICINE ?
Clinical interview
Polysomnography
Multiple sleep latency test (MSLT)
Actigraphy
POLYSOMNOGRAPHY
• Study to asses pattern of sleep disturbances
• Parameters Monitored
1. Electroencephalography (EEG) : EEG channel used to monitor sleep stage. most
laboratories use 2 central channels and 2 occipital channels, with ear references as an
adjunct to help identify sleep latency and arousals.
2. Electrooculography (EOG): Two channels are used to monitor both horizontal and
vertical eye movements. Electrodes are placed at the right and left outer canthi.
Evaluation of the eye movements is necessary for 2 reasons.
 documentation of the onset of REM sleep
 to note the onset of sleep(the presence of slow-rolling eye movements )
3. Electromyography (EMG): One(usually chin or mentalis and/or submentalis) used to
record atonia during REM sleep or lack of atonia in patients with REM-related parasomnias.
COMMON POLYSOMNOGRAPHIC MEASURES
1. Sleep latency: Period of time from turning out the lights until the
appearance of stage II sleep
2. Early morning awakening: Time of being continuously awake from the last
stage of the sleep until the end of the sleep record (usually at 7 AM)
3. Sleep efficiency: Total sleep time / total time of the sleep record × 100%
4. Apnea index: Number of apneas longer than 10 seconds per hour of sleep
5. Nocturnal myoclonus index: Number of periodic leg movements per hour
6. Rapid eye movement (REM) latency: Period of time from the onset of
sleep until the first REM period of the night
7. Sleep-onset REM period: REM sleep within the first 10 minutes of sleep.
ARCHITECTURE OF SLEEP
• Rapid eye movement (REM) sleep
Frequent bursts of eye movement activity
Paradoxical sleep
In infant  Active sleep
• Non-rapid eye movement (NREM) sleep
Orthodox sleep
In infant  Quiet sleep
STAGES OF SLEEP
• NREM sleep, which usually precedes REM sleep, is subdivided into
three (N1 to N3) stages.
• N1 (formerly stage 1 sleep), characterized by :
1. Loss of alpha activity
2. Appearance of a low-voltage, mixed-frequency EEG pattern with
prominent theta activity (4 to 7 Hz)
3. Occasional vertex sharp waves (V waves) over the central regions
may also appear
4. Eye movements become slow and rolling
5. Skeletal muscle tone relaxes.
STAGES OF SLEEP
• Stage N2 (formerly stage 2) is heralded by the appearance of sleep
spindles and K complex (high amplitude negative sharp wave followed
by positive slow waves) in the EEG.
• N3 (formerly stage 3 and 4) is also defined as slow wave sleep (SWS),
delta sleep, or deep sleep, because the arousal threshold increases
incrementally from stage N1 to N3.
• REM sleep or Stage R is characterised by Saw Tooth Wave, rapid eye
movement and atonia with phasic twitches.
ORGANIZATION OF SLEEP :
NREM (75 percent)
• Stage 1: 5 percent
• Stage 2: 45 percent
• Stage 3: 12 percent
• Stage 4: 13 percent
REM (25 percent)
REM period occurs about every 90 to 100 minutes during the night. The first REM period
tends to be the shortest, usually lasting less than 10 minutes; later REM periods may last
15 to 40 minutes each. Most REM periods occur in the last third of the night, whereas most
stage 4 sleep occurs in the first third of the night.
EFFECT OF AGE
• Total sleep time decreases with age. Average daily values are as follows:
newborns, 16 to 18h; young children, 10h; adolescents, 8h; adults, 7.5h
and possibly less than this in elderly people.
• NREM sleep shows an overall decrease across the lifespan.
• NREM–REM sleep cycles occur at intervals of 50 to 60 min in infants who
often enter REM at the start of their sleep period. This interval between
sleep cycles remains until adolescence when the periodicity changes to 90
to 100 min, which persists into adult life.
• Continuity of sleep is greatest in early childhood and least at the extremes
of age.
• Circadian sleep–wake rhythms : Full-term neonates show 3- to 4-h sleep–
wake cycles. Sleep periods have largely shifted to the night and
wakefulness to daytime by 12 months.
PHYSIOLOGY IN SLEEP
• Autonomic Nervous System : The autonomic nervous system reaches its most
stable state during SWS in comparison to wakefulness; e.g., blood pressure, heart
rate, and respiratory rate are at their lowest mean values and least variable
during SWS.
• Cardiovascular System : Blood pressure, heart rate, and cardiac output decrease
during NREM sleep.
• Pulmonary System : Respiratory rate and minute ventilation decrease during
sleep, and upper airway resistance increases as a result of muscle relaxation,
most significantly during REM sleep.
• Thermoregulation : Brain and body temperature are down regulated during
NREM sleep, particularly SWS, as a result of both a decreased hypothalamic
temperature set point as well as active heat loss.
• Sexual Function : Characteristic of REM, In men  penile erection
In women  increased vaginal blood flow & clitorial erection.
• NEUROENDOCRINE SYSTEM -
GH : Released primarily in night , enhanced during SWS.
GH again enhances SWS by feedback.
Prolactin : peaks after GH. It enhances REM sleep.
TSH : Peaks just before sleep. Sleep reduces TSH secretion.
ACTH & Cortisol : HPA axis is most inactive during onset of
sleep and rises shortly before awakening.
NEUROBILOGY OF SLEEP
1. Histamine
2. Dopamine
3. Norepinephrine
4. Serotonin
5. Acetylcholine
These neurotransmitter circuits as a group are called Ascending
Reticular Activating System , because they are known to work together
to regulate arousal.
GABA
• The part of the brain most important in regulating sleep duration is
the hypothalamus. Certain groups of hypothalamic neurons and
adjacent groups of basal forebrain neurons produce the
neurotransmitter γ-aminobutyric acid (GABA). Projections of these
GABA neurons inhibit the firing of cells involved in wakefulness.
Several groups of neurons have been shown to be inhibited by this
action—including neurons containing histamine, norepinephrine,
serotonin, hypocretin, and glutamate—and this inhibition promotes
sleep.
CLASSIFICATION OF SLEEP DISORDER
1. DSM-V
2. ICSD-2
3. ICD-10
The subjects of sleep disorder covers only NON-ORGANIC type in ICD-
10. Sleep disorders of organic origin, non-psychogenic disorders such as
narcolepsy, cataplexy, sleep apnoea and episodic movement disorders
are discussed under other categories (G).
DSM 5 CLASSIFICATION
1. Insomnia disorder
2.Hypersomnolence disorder
3 Narcolepsy
4.Breathing-related sleep disorders,
including:
• Obstructive sleep apnea hypopnea
• Central sleep apnea-
i.idiopathic central sleep apnoea,
ii.Cheyne stokes breathing,
iii.central sleep apnoea comorbid with
opioid use
• Sleep-related hypoventilation
5.Circadian rhythm sleep disorders,
including:
i. Delayed sleep phase type
ii.Advanced sleep phase type
iii.Irregular sleep-wake type
iv.Non-24-hour sleep-wake type
v.shift work type
vi.unspecified type
•
INSOMNIA
DSM-V defines insomnia disorder as dissatisfaction with sleep quantity
or quality associated with one or more of the following symptoms :
1. Difficulty in initiation of sleep
2. Difficulty in maintaining sleep with frequent awakenings
3. Early morning awakening with inability to return to sleep
TYPES OF INSOMNIA
ADJUSTMENT INSOMNIA : Associated with anxiety, anticipation of
anxiety provoking event (exam). Transient in nature.
SLEEP STATE MISPERCEPTION or PSEUDOSOMNIA : patient
complaining of difficulty in sleep but no objective evidence of sleep
disruption is found.
PSYCHOPHYSIOLOGICAL INSOMNIA : problem in going to sleep,
stress, object related to sleep becomes conditioned to insomnia.
IDIOPATHIC INSOMNIA : Starts in early life. Neurochemical imbalance
of brainstem reticular formation, impaired regulation of raphe
nucleus, locus ceruleus or basal forebrain dysfunction.
INSOMNIA & PSYCHIATRIC ILLNESSES
• MAJOR DEPRESSIVE DISORDER :
Insomnia is an independent risk for suicide in MDD
 sleep latency, nocturnal awakening, early awakening
 SWS in first NREM-REM cycle
Shortened REM latency
More REM sleep earlier in night
Increased REM density
• Bipolar ,mania: severe insomnia may precede relapse
• Schizophrenia : stage N3 as negative symptoms increased
• PTSD: nightmares , stage N3, hyperarousal
TREATMENT OF INSOMNIA
• Treatment of insomnia should be directed at identifiable causes, or
those factors that perpetuate the disorders such as temperament and
life style, ineffective coping and defense mechanism, inappropriate
use of alcohol or other substances maladaptive sleep wake schedules,
and excessive worry about poor sleep.
1. NONPHARMACOLOGICAL
2. PHARMACOLOGICAL
SLEEP HYGIENE EDUCATION
• Maintain regular hours of bedtime and arising
• Avoid heavy meals near bedtime
• Avoid daytime napping
• Exercise daily, but not later in the evening
• Minimize caffeine intake and smoking within 8 hr of bedtime
• Do not look at clock in night
• Make bedroom comfortable, preferably slightly cool
• Do not use alcohol while going to sleep
• Go to bed only when sleepy
• Minimize light, noise and excessive temperature during sleep
• Avoid evening stimulation: substituted radio or relaxed reading for television. Practice
evening relaxation routines
RELAXATION THERAPY
• Insomnia patients tend to have high levels of cognitive, physiologic,
and/or emotional arousal both day and night.
• Imagery training, meditation are used to lower presleep cognitive
arousal.
• Yoga may be an effective method for relaxation when done properly
(e.g. Shavasana).
SLEEP RESTRICTION THERAPY
• Goal is to decrease the amount of time in bed to increase the
percentage of time spent in bed asleep.
• Patients should stay in bed only as long as their average sleep time:
but no less than 5 hr.
• Get up at the same time each day.
• Do not nap during the day.
• When sleep efficiency is 85% (i.e., sleeping for 85% of the time in
bed), go to bed 15 min earlier.
• Repeat this process until you are sleeping for 8 hours or the desired
amount of time.
STIMULUS CONTROL THERAPY
• Based upon the theory that insomnia is conditioned response to
temporal (bedtime) and environmental (bedroom/bed) cues that are
associated with sleep.
• Bed and bedroom should be associated with rapid onset of sleep
• Go to bed only when sleepy
• Use bed only for sleep
• Get out of bed and go to another room when unable to fall asleep
and return only when sleepy
• Keep regular morning arising regardless of duration of sleep the night
before
PHARMACOLOGOCAL MANAGEMENT
Principles:
• Start with the lowest effective dose
• Use intermittent dosing
• Prescribe medications for short-term use
• Discontinue the medications gradually
• Be alert for rebound insomnia
28
• Benzodiazepines
• Lorazepam (1-6mg)
• Clonazepam (0.5-5mg)
• Temazepam (10-20mg)
• Flurazepam (15-30mg)
• Alprazolam (0.25-1mg)
• Triazolam(0.125-0.25mg)
• Non Benzodiazepines
• Zolpidem (10-20mg HS)
Other classes of Medications
__________________________
29
• Melatonin Receptor Agonists
• Melatonin (2-10mg)
• Antidepressants Prescribed for insomnia
symptoms, typically at low doses
• Trazadone (500-200mg)
• Mirtazapine (15-45mg)
• Doxepin (50-150mg)
• Amitryptyline (50-200mg)
• Antipsychotics
• Olanzapine (2.5-10mg)
BENZODIAZEPINES
• Most commonly prescribed agents for treatment of insomnia
• May be used as adjunctive therapy with behavioral therapy
• Have been proven effective for short-term insomnia treatment
• Use usually limited to a maximum 4 weeks duration
• Long term use increase chances of habituation and withdrawal symptoms
• Tolerance to hypnotic effects develops on repeated administration
• Rebound Insomnia occurs
• Alter sleep patterns least
• Are safer than other drugs in overdose
BENZODIAZEPINE LIKE HYPNOTICS (Z DRUGS)/
NONBENZODIAZEPINE
• Similar hypnotic effects to benzodiazepines but side effects tend to be
less
• Does not alter normal sleep patterns and is not associated with
tolerance or rebound insomnia
• Patients fail to respond to one should not offered another
• More expensive than BDZ
• Only to be used if adverse effects to BDZ
ANTIHISTAMINES
• DIPHENHYDRAMINE
• Most widely available OTC preparation for insomnia
• Inhibition of H1 receptor
• Research does not support efficacy
• Anticholinergic side effects
• Sedation and hangover for long half life
MELATONIN RECEPTOR AGONIST
• RAMELTEON is indicated for the treatment of insomnia characterized
by difficulty with sleep onset
• Dose: 8 mg
• High-affinity binding to melatonin MT1 and MT2 receptors
• No evidence of abuse potential or rebound insomnia
• AGOMELATINE : not only hypnotic but also action on GAD & MDD
HYPERSOMNIA• Hypersomnolence is a serious, debilitating, potentially life threatening
noncommunicable condition.
1. Insufficient sleep
2. Neurologic dysfunction in brain regulating sleep
3. Disrupted sleep
• What does excessive sleepiness cause :
Traffic accident
Errors/accident at work
Decreased work productivity
Deficit in cognitive function, learning & memory
Alcohol interaction
Stimulant seeking
Insulin resistance
Increased sympathetic activity
Obesity
KLEINE-LEVIN SYNDROME
• Also known as sleeping beauty syndrome.
• This is a rare syndrome characterized by -
1) Hypersomnia (always present)
2) Hyperphagia (usually present)
3) Hypersexuality (associated at times)
• Predominantly afflicts male in adolescence
• Recurrent episodes of sleepiness, episode lasting for few days to
several weeks
TREATMENT OF HYPERSOMNIA
• Most widely used and successful t/t : Stimulant
• First choice : Modafinil
• Amphetamines (if Modafinil fails)
• Patients intolerant or insensitive to stimulant, stimulant
antidepressant, MAOI or SSRI may be used.
• METHYSERGIDE may be effective in resistant cases.
NARCOLEPSY
• Excessive day time sleepiness, often disturbed night time sleep and
disturbance of REM sleep.
• Recurrent intrusion of REM sleep into transition between sleep and
wakefulness
• Hallmark of Narcolepsy- Decreased REM latency
(about <10 mins)
• Age of onset- 15-25 yrs, with a stable course throughout life.
NARCOLEPSY
• Classical Tetrad of symptom-
1) Sleep Attacks
2) Cataplexy
3) Hypnogogic Hallucination
4) Sleep Paralysis
• Decreased CSF 'Orexin' protein level / hypocretin -1 immunoreactivity
value.
CATAPLEXY
• Cataplexy is a sudden loss of muscle tone that causes feelings of
weakness and loss of voluntary muscle control. Usually cataplexy is
the second symptom to present after EDS. By itself, cataplexy could
be wrongfully diagnosed as a seizure disorder. Cataplectic attacks vary
in severity from slight momentary drooping of the eyelids, to quite
severe with the inability to stand. Most commonly, persons with
narcolepsy experience mild cataplectic attacks, where arm or leg
muscles become weak, speech is slurred or their head droops. Even
in the most severe attacks, sufferers remain fully conscious, entirely
aware of what is occurring, and what is happening around them.
These attacks can occur randomly, but most often are brought on by
any strong emotions. Laughter is reported as the most common
stimulus.
HIPNOGOGIC and HYPNOPOMPIC
HALLUCINATION
• There are two different types of hallucinations associated with
narcolepsy. Hypnogogic hallucinations occur at the onset of sleep,
while hypnopompic hallucinations occur while waking. These
hallucinations can occur along with sleep paralysis or as one is falling
asleep or waking up. Both of these hallucinations are a portion of the
REM sleep cycle interfering with normal wakefulness. The
hallucinations are very vivid and can incorporate what is occurring
around the person who is hallucinating. People who have experienced
these events report are very frightening and disturbing. Most often,
the hallucinations are visual, but they can incorporate all of the
senses.
Sleep Paralysis
• Most commonly occurring on awakening in the
morning ,during the episode,pt are apparently
awake and conscious but unable to move a
muscle.if the symptoms persists for more than
a few seconds ,as it often does in narcolepsy,it
can become extremely uncomfortable.
NARCOLEPSY TREATMENT
• Non-pharmacological
1. Patients Education
2. Scheduled Naps
3. Other Management Approaches
a. Avoid sleep deprivation
b. Regular sleep/awake cycle
c. Avoidance of shift work
NARCOLEPSY TREATMENT
• Pharmacotherapy
• Effective agents for daytime sleepiness –Amphetamine, Dextromphetamine
, Methamphetamine, Methylphenidate, Modafinil , Pemoline
• Agents for Cataplexy, Sleep Paralysis & Hypnagogic Hallucination –
Tricyclic Antidepressants (TCAs):
Clomipramine, Imipramine
Selective serotonin Reuptake Inhibitor
Fluoxetine
BREATHING RELATED SLEEP DISORDER
• There are three types of sleep apnea
1. Obstructive
2. Central
3. Mixed
• Of these, obstructive sleep apnea (OSA) is the most common.
• RISK FACTORS :
1. Excessive weight gain
2. Anatomic abnormalities, such as a receding chin.
3. enlarged tonsils and adenoids, main cause in children.
4. Family history of OSA
5. Alcohol and sedative drugs
6. Hypothyroidism, acromegaly
OBSTRUCTIVE SLEEP APNOEA
• Clinically speaking, an obstructive apnea is defined as a complete
cessation of airflow for more than 10 seconds with persistent
respiratory effort.
• An obstructive hypopnea is defined as a partial reduction in air flow
of approximately 30 percent to 50 percent with persistent respiratory
effort and a reduction in oxygen saturation by at least 3 percent to 4
percent and/or an arousal from sleep.
OSA : TREATMENT
• Weight reduction
• Positional therapy
• Positive pressure therapy (BIPAP , CPAP) : T/T of choice
• Surgical options
CIRCADIAN RHYTHM SLEEP DISORDER
Persistent sleep disturbance due to DESYNCHRONY BETWEEN AN
INDIVIDUAL’S INTERNAL CIRCADIAN BIOLOGICAL CLOCK &
CONVENTIONAL SLEEP WAKE CYCLE.
Types:
1. Delayed sleep phase type: late onset sleep and late awakening
2. Jet lag type: travel across more than 1 time zone
3. Shift work type: frequent change of shift work, night shift
4. Advanced sleep phase syndrome
5. Disorganized sleep-wake pattern
Treatment: melatonin and light exposure
PARASOMNIAS
• Disorders of “partial arousal”.
NREM Sleep Arousal Disorder
1. Sleepwalking
2. Sleep terror
REM Sleep Arousal Disorder
1. REM Behavior Disorder (RBD)
2. Sleep Paralysis
3. Nightmare disorder
SLEEPWALKING
• Repeated episodes of rising from bed during sleep and walking about.
While sleeping the individual has a blank staring face, is relatively
unresponsive and can be awakened with great difficulty.
• Individual can engage in a complex behavior of semi purposeful
actions.
• Sleepwalker may interact with the environment inappropriately,
resulting in injury.
• Disorders of arousal, particularly from deepest stage of sleep (N3).
• Amnesia of the episode is present.
SLEEPWALKING
• Very common in children, peak prevalence
between 4 to 8 yrs.
• Rare in adults  familial pattern.
• D/D : Psychomotor epileptic seizure
Dissociative fugue
• “Specialized forms” : Sleep related eating
Sexsomnia
• T/T : often unnecessary
psychoeducation & assurance
safety issue
medication : benzodiazepines
SLEEP TERRORS
• Recurrent episodes of abrupt terror arousals from sleep, beginning
with a panicky scream. There is intense fear and signs of autonomic
hyperactivity – mydriasis, tachycardia, rapid breathing and sweating.
• Relative unresponsiveness to efforts of others to comfort the
individual during the episode.
• Recall of event, if any, is minimal.
• Risk of injury during episode.
• Occurs during first third of nocturnal sleep, deep sleep (N3).
• Sleep terror and sleep walking – part of same nosologic continuum.
RAPID EYE MOVEMENT BEHAVIOR DISORDER
• Patients with rapid eye movement behavior disorder (RBD) act out
dramatic and/or violent dreams during rapid eye movement (REM)
stage sleep.
• Another feature of RBD is shouting and grunting. RBD seems similar
to other sleep disorders that involve motor activity, like Sleep Walking
or Periodic limb movement disorder.
• RBD movements occur during REM sleep.
• Patients with RBD usually respond to treatment with clonazepam
when taken nightly.
NIGHTMARE DISORDER
• Nightmares are dream experiences loaded with anxiety or fear, of which
the individual has very detailed recall.
• The dream experiences are extremely vivid and usually include themes
involving threats to survival, security or self esteem.
• Often, there is recurrence of similar nightmare theme.
• During a typical episode there is a degree of autonomic discharge but no
appreciable vocalization or body motility.
• Medications known to provoke nightmares : l-DOPA, reserpine,
thioridazine, TCA, B-blocker, benzodiazepine and alcohol abuse
• “Fear of sleeping” type insomnia.
• T/T : Nefazodone, Benzodiazepine, Prazocin.
RESTLESS LEG SYNDROME
(EKBOM SYNDROME)
• Uncomfortable subjective sensation(creepy crawly) in legs
• Worse at night
• Relieved by walking or moving legs
• Sleep initiation insomnia
• Linked to deficiency of DA, iron, B12, and pregnancy and renal disease
• T/T : DA agonist (ropinirole, pramipexole), iron replacement,
levodopa, anti-epileptic (gabapentin)
PERIODIC LIMB MOVEMENT SYNDROME
• Previously known as nocturnal myoclonus .
• Brief, stereotypic, repetitive, non-epileptiform contraction of muscle
during sleep.
• Patient is unaware of the incident
• PLMs are 0.5-5 s in duration and occur every 20-40 s during NREM
• Often accompanied by K complex or brief arousal signal
• Associated with folate deficiency, renal disease, anemia, use of
antidepressant.
• T/T : Benzodiazepine (clonazepam), Opiates.
BRUXISM
• Bruxism, often referred to as “gnashing,” is the act of involuntary teeth
grinding, either while awake or asleep, which results primarily in tooth
damage and jaw pain and which seems to be caused by psychological
effects of everyday stress.
• The sound of teeth grinding can be quite loud and disruptive to bed
partners or roommates.
• These include stress, facial or oral trauma, nervous system malfunction,
poor diet, and allergies.
• Children with bruxism usually stop grinding their teeth before adulthood.
• In adults, alcohol and drug use is suspected to increase the occurrence of
bruxism.
THANK YOU!!!!!

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Sleep disorderS

  • 2. INTRODUCTION • Sleep is a state of decreased awareness of environmental stimuli that is distinguished from states such as coma or hibernation by its relatively rapid reversibility. • Sleep is an universal behavior. • Sleep is also an essential component for good health and optimal cognitive function. • For peak performance, human need 8 hrs sleep a day.
  • 3. FUNCTIONS OF SLEEP 1. Restoration and recovery 2. Energy conservation 3. Memory consolidation 4. Discharge of emotion 5. Thermoregulation 6. Homeostasis 7. Maintenance of immune system
  • 4. MONITORING HUMAN SLEEP • Sleep is generally defined by combining BEHAVIORAL OBSERVATION with ELECTROPHYSIOLOGICAL RECORDING. • WHAT ARE THE TOOLS OF SLEEP MEDICINE ? Clinical interview Polysomnography Multiple sleep latency test (MSLT) Actigraphy
  • 5. POLYSOMNOGRAPHY • Study to asses pattern of sleep disturbances • Parameters Monitored 1. Electroencephalography (EEG) : EEG channel used to monitor sleep stage. most laboratories use 2 central channels and 2 occipital channels, with ear references as an adjunct to help identify sleep latency and arousals. 2. Electrooculography (EOG): Two channels are used to monitor both horizontal and vertical eye movements. Electrodes are placed at the right and left outer canthi. Evaluation of the eye movements is necessary for 2 reasons.  documentation of the onset of REM sleep  to note the onset of sleep(the presence of slow-rolling eye movements ) 3. Electromyography (EMG): One(usually chin or mentalis and/or submentalis) used to record atonia during REM sleep or lack of atonia in patients with REM-related parasomnias.
  • 6. COMMON POLYSOMNOGRAPHIC MEASURES 1. Sleep latency: Period of time from turning out the lights until the appearance of stage II sleep 2. Early morning awakening: Time of being continuously awake from the last stage of the sleep until the end of the sleep record (usually at 7 AM) 3. Sleep efficiency: Total sleep time / total time of the sleep record × 100% 4. Apnea index: Number of apneas longer than 10 seconds per hour of sleep 5. Nocturnal myoclonus index: Number of periodic leg movements per hour 6. Rapid eye movement (REM) latency: Period of time from the onset of sleep until the first REM period of the night 7. Sleep-onset REM period: REM sleep within the first 10 minutes of sleep.
  • 7. ARCHITECTURE OF SLEEP • Rapid eye movement (REM) sleep Frequent bursts of eye movement activity Paradoxical sleep In infant  Active sleep • Non-rapid eye movement (NREM) sleep Orthodox sleep In infant  Quiet sleep
  • 8. STAGES OF SLEEP • NREM sleep, which usually precedes REM sleep, is subdivided into three (N1 to N3) stages. • N1 (formerly stage 1 sleep), characterized by : 1. Loss of alpha activity 2. Appearance of a low-voltage, mixed-frequency EEG pattern with prominent theta activity (4 to 7 Hz) 3. Occasional vertex sharp waves (V waves) over the central regions may also appear 4. Eye movements become slow and rolling 5. Skeletal muscle tone relaxes.
  • 9. STAGES OF SLEEP • Stage N2 (formerly stage 2) is heralded by the appearance of sleep spindles and K complex (high amplitude negative sharp wave followed by positive slow waves) in the EEG. • N3 (formerly stage 3 and 4) is also defined as slow wave sleep (SWS), delta sleep, or deep sleep, because the arousal threshold increases incrementally from stage N1 to N3. • REM sleep or Stage R is characterised by Saw Tooth Wave, rapid eye movement and atonia with phasic twitches.
  • 10.
  • 11. ORGANIZATION OF SLEEP : NREM (75 percent) • Stage 1: 5 percent • Stage 2: 45 percent • Stage 3: 12 percent • Stage 4: 13 percent REM (25 percent) REM period occurs about every 90 to 100 minutes during the night. The first REM period tends to be the shortest, usually lasting less than 10 minutes; later REM periods may last 15 to 40 minutes each. Most REM periods occur in the last third of the night, whereas most stage 4 sleep occurs in the first third of the night.
  • 12. EFFECT OF AGE • Total sleep time decreases with age. Average daily values are as follows: newborns, 16 to 18h; young children, 10h; adolescents, 8h; adults, 7.5h and possibly less than this in elderly people. • NREM sleep shows an overall decrease across the lifespan. • NREM–REM sleep cycles occur at intervals of 50 to 60 min in infants who often enter REM at the start of their sleep period. This interval between sleep cycles remains until adolescence when the periodicity changes to 90 to 100 min, which persists into adult life. • Continuity of sleep is greatest in early childhood and least at the extremes of age. • Circadian sleep–wake rhythms : Full-term neonates show 3- to 4-h sleep– wake cycles. Sleep periods have largely shifted to the night and wakefulness to daytime by 12 months.
  • 13. PHYSIOLOGY IN SLEEP • Autonomic Nervous System : The autonomic nervous system reaches its most stable state during SWS in comparison to wakefulness; e.g., blood pressure, heart rate, and respiratory rate are at their lowest mean values and least variable during SWS. • Cardiovascular System : Blood pressure, heart rate, and cardiac output decrease during NREM sleep. • Pulmonary System : Respiratory rate and minute ventilation decrease during sleep, and upper airway resistance increases as a result of muscle relaxation, most significantly during REM sleep. • Thermoregulation : Brain and body temperature are down regulated during NREM sleep, particularly SWS, as a result of both a decreased hypothalamic temperature set point as well as active heat loss. • Sexual Function : Characteristic of REM, In men  penile erection In women  increased vaginal blood flow & clitorial erection.
  • 14. • NEUROENDOCRINE SYSTEM - GH : Released primarily in night , enhanced during SWS. GH again enhances SWS by feedback. Prolactin : peaks after GH. It enhances REM sleep. TSH : Peaks just before sleep. Sleep reduces TSH secretion. ACTH & Cortisol : HPA axis is most inactive during onset of sleep and rises shortly before awakening.
  • 15. NEUROBILOGY OF SLEEP 1. Histamine 2. Dopamine 3. Norepinephrine 4. Serotonin 5. Acetylcholine These neurotransmitter circuits as a group are called Ascending Reticular Activating System , because they are known to work together to regulate arousal.
  • 16. GABA • The part of the brain most important in regulating sleep duration is the hypothalamus. Certain groups of hypothalamic neurons and adjacent groups of basal forebrain neurons produce the neurotransmitter γ-aminobutyric acid (GABA). Projections of these GABA neurons inhibit the firing of cells involved in wakefulness. Several groups of neurons have been shown to be inhibited by this action—including neurons containing histamine, norepinephrine, serotonin, hypocretin, and glutamate—and this inhibition promotes sleep.
  • 17. CLASSIFICATION OF SLEEP DISORDER 1. DSM-V 2. ICSD-2 3. ICD-10 The subjects of sleep disorder covers only NON-ORGANIC type in ICD- 10. Sleep disorders of organic origin, non-psychogenic disorders such as narcolepsy, cataplexy, sleep apnoea and episodic movement disorders are discussed under other categories (G).
  • 18. DSM 5 CLASSIFICATION 1. Insomnia disorder 2.Hypersomnolence disorder 3 Narcolepsy 4.Breathing-related sleep disorders, including: • Obstructive sleep apnea hypopnea • Central sleep apnea- i.idiopathic central sleep apnoea, ii.Cheyne stokes breathing, iii.central sleep apnoea comorbid with opioid use • Sleep-related hypoventilation 5.Circadian rhythm sleep disorders, including: i. Delayed sleep phase type ii.Advanced sleep phase type iii.Irregular sleep-wake type iv.Non-24-hour sleep-wake type v.shift work type vi.unspecified type •
  • 19. INSOMNIA DSM-V defines insomnia disorder as dissatisfaction with sleep quantity or quality associated with one or more of the following symptoms : 1. Difficulty in initiation of sleep 2. Difficulty in maintaining sleep with frequent awakenings 3. Early morning awakening with inability to return to sleep
  • 20. TYPES OF INSOMNIA ADJUSTMENT INSOMNIA : Associated with anxiety, anticipation of anxiety provoking event (exam). Transient in nature. SLEEP STATE MISPERCEPTION or PSEUDOSOMNIA : patient complaining of difficulty in sleep but no objective evidence of sleep disruption is found. PSYCHOPHYSIOLOGICAL INSOMNIA : problem in going to sleep, stress, object related to sleep becomes conditioned to insomnia. IDIOPATHIC INSOMNIA : Starts in early life. Neurochemical imbalance of brainstem reticular formation, impaired regulation of raphe nucleus, locus ceruleus or basal forebrain dysfunction.
  • 21. INSOMNIA & PSYCHIATRIC ILLNESSES • MAJOR DEPRESSIVE DISORDER : Insomnia is an independent risk for suicide in MDD  sleep latency, nocturnal awakening, early awakening  SWS in first NREM-REM cycle Shortened REM latency More REM sleep earlier in night Increased REM density • Bipolar ,mania: severe insomnia may precede relapse • Schizophrenia : stage N3 as negative symptoms increased • PTSD: nightmares , stage N3, hyperarousal
  • 22. TREATMENT OF INSOMNIA • Treatment of insomnia should be directed at identifiable causes, or those factors that perpetuate the disorders such as temperament and life style, ineffective coping and defense mechanism, inappropriate use of alcohol or other substances maladaptive sleep wake schedules, and excessive worry about poor sleep. 1. NONPHARMACOLOGICAL 2. PHARMACOLOGICAL
  • 23. SLEEP HYGIENE EDUCATION • Maintain regular hours of bedtime and arising • Avoid heavy meals near bedtime • Avoid daytime napping • Exercise daily, but not later in the evening • Minimize caffeine intake and smoking within 8 hr of bedtime • Do not look at clock in night • Make bedroom comfortable, preferably slightly cool • Do not use alcohol while going to sleep • Go to bed only when sleepy • Minimize light, noise and excessive temperature during sleep • Avoid evening stimulation: substituted radio or relaxed reading for television. Practice evening relaxation routines
  • 24. RELAXATION THERAPY • Insomnia patients tend to have high levels of cognitive, physiologic, and/or emotional arousal both day and night. • Imagery training, meditation are used to lower presleep cognitive arousal. • Yoga may be an effective method for relaxation when done properly (e.g. Shavasana).
  • 25. SLEEP RESTRICTION THERAPY • Goal is to decrease the amount of time in bed to increase the percentage of time spent in bed asleep. • Patients should stay in bed only as long as their average sleep time: but no less than 5 hr. • Get up at the same time each day. • Do not nap during the day. • When sleep efficiency is 85% (i.e., sleeping for 85% of the time in bed), go to bed 15 min earlier. • Repeat this process until you are sleeping for 8 hours or the desired amount of time.
  • 26. STIMULUS CONTROL THERAPY • Based upon the theory that insomnia is conditioned response to temporal (bedtime) and environmental (bedroom/bed) cues that are associated with sleep. • Bed and bedroom should be associated with rapid onset of sleep • Go to bed only when sleepy • Use bed only for sleep • Get out of bed and go to another room when unable to fall asleep and return only when sleepy • Keep regular morning arising regardless of duration of sleep the night before
  • 27. PHARMACOLOGOCAL MANAGEMENT Principles: • Start with the lowest effective dose • Use intermittent dosing • Prescribe medications for short-term use • Discontinue the medications gradually • Be alert for rebound insomnia
  • 28. 28 • Benzodiazepines • Lorazepam (1-6mg) • Clonazepam (0.5-5mg) • Temazepam (10-20mg) • Flurazepam (15-30mg) • Alprazolam (0.25-1mg) • Triazolam(0.125-0.25mg) • Non Benzodiazepines • Zolpidem (10-20mg HS)
  • 29. Other classes of Medications __________________________ 29 • Melatonin Receptor Agonists • Melatonin (2-10mg) • Antidepressants Prescribed for insomnia symptoms, typically at low doses • Trazadone (500-200mg) • Mirtazapine (15-45mg) • Doxepin (50-150mg) • Amitryptyline (50-200mg) • Antipsychotics • Olanzapine (2.5-10mg)
  • 30. BENZODIAZEPINES • Most commonly prescribed agents for treatment of insomnia • May be used as adjunctive therapy with behavioral therapy • Have been proven effective for short-term insomnia treatment • Use usually limited to a maximum 4 weeks duration • Long term use increase chances of habituation and withdrawal symptoms • Tolerance to hypnotic effects develops on repeated administration • Rebound Insomnia occurs • Alter sleep patterns least • Are safer than other drugs in overdose
  • 31. BENZODIAZEPINE LIKE HYPNOTICS (Z DRUGS)/ NONBENZODIAZEPINE • Similar hypnotic effects to benzodiazepines but side effects tend to be less • Does not alter normal sleep patterns and is not associated with tolerance or rebound insomnia • Patients fail to respond to one should not offered another • More expensive than BDZ • Only to be used if adverse effects to BDZ
  • 32. ANTIHISTAMINES • DIPHENHYDRAMINE • Most widely available OTC preparation for insomnia • Inhibition of H1 receptor • Research does not support efficacy • Anticholinergic side effects • Sedation and hangover for long half life
  • 33. MELATONIN RECEPTOR AGONIST • RAMELTEON is indicated for the treatment of insomnia characterized by difficulty with sleep onset • Dose: 8 mg • High-affinity binding to melatonin MT1 and MT2 receptors • No evidence of abuse potential or rebound insomnia • AGOMELATINE : not only hypnotic but also action on GAD & MDD
  • 34. HYPERSOMNIA• Hypersomnolence is a serious, debilitating, potentially life threatening noncommunicable condition. 1. Insufficient sleep 2. Neurologic dysfunction in brain regulating sleep 3. Disrupted sleep • What does excessive sleepiness cause : Traffic accident Errors/accident at work Decreased work productivity Deficit in cognitive function, learning & memory Alcohol interaction Stimulant seeking Insulin resistance Increased sympathetic activity Obesity
  • 35. KLEINE-LEVIN SYNDROME • Also known as sleeping beauty syndrome. • This is a rare syndrome characterized by - 1) Hypersomnia (always present) 2) Hyperphagia (usually present) 3) Hypersexuality (associated at times) • Predominantly afflicts male in adolescence • Recurrent episodes of sleepiness, episode lasting for few days to several weeks
  • 36. TREATMENT OF HYPERSOMNIA • Most widely used and successful t/t : Stimulant • First choice : Modafinil • Amphetamines (if Modafinil fails) • Patients intolerant or insensitive to stimulant, stimulant antidepressant, MAOI or SSRI may be used. • METHYSERGIDE may be effective in resistant cases.
  • 37. NARCOLEPSY • Excessive day time sleepiness, often disturbed night time sleep and disturbance of REM sleep. • Recurrent intrusion of REM sleep into transition between sleep and wakefulness • Hallmark of Narcolepsy- Decreased REM latency (about <10 mins) • Age of onset- 15-25 yrs, with a stable course throughout life.
  • 38. NARCOLEPSY • Classical Tetrad of symptom- 1) Sleep Attacks 2) Cataplexy 3) Hypnogogic Hallucination 4) Sleep Paralysis • Decreased CSF 'Orexin' protein level / hypocretin -1 immunoreactivity value.
  • 39. CATAPLEXY • Cataplexy is a sudden loss of muscle tone that causes feelings of weakness and loss of voluntary muscle control. Usually cataplexy is the second symptom to present after EDS. By itself, cataplexy could be wrongfully diagnosed as a seizure disorder. Cataplectic attacks vary in severity from slight momentary drooping of the eyelids, to quite severe with the inability to stand. Most commonly, persons with narcolepsy experience mild cataplectic attacks, where arm or leg muscles become weak, speech is slurred or their head droops. Even in the most severe attacks, sufferers remain fully conscious, entirely aware of what is occurring, and what is happening around them. These attacks can occur randomly, but most often are brought on by any strong emotions. Laughter is reported as the most common stimulus.
  • 40. HIPNOGOGIC and HYPNOPOMPIC HALLUCINATION • There are two different types of hallucinations associated with narcolepsy. Hypnogogic hallucinations occur at the onset of sleep, while hypnopompic hallucinations occur while waking. These hallucinations can occur along with sleep paralysis or as one is falling asleep or waking up. Both of these hallucinations are a portion of the REM sleep cycle interfering with normal wakefulness. The hallucinations are very vivid and can incorporate what is occurring around the person who is hallucinating. People who have experienced these events report are very frightening and disturbing. Most often, the hallucinations are visual, but they can incorporate all of the senses.
  • 41. Sleep Paralysis • Most commonly occurring on awakening in the morning ,during the episode,pt are apparently awake and conscious but unable to move a muscle.if the symptoms persists for more than a few seconds ,as it often does in narcolepsy,it can become extremely uncomfortable.
  • 42. NARCOLEPSY TREATMENT • Non-pharmacological 1. Patients Education 2. Scheduled Naps 3. Other Management Approaches a. Avoid sleep deprivation b. Regular sleep/awake cycle c. Avoidance of shift work
  • 43. NARCOLEPSY TREATMENT • Pharmacotherapy • Effective agents for daytime sleepiness –Amphetamine, Dextromphetamine , Methamphetamine, Methylphenidate, Modafinil , Pemoline • Agents for Cataplexy, Sleep Paralysis & Hypnagogic Hallucination – Tricyclic Antidepressants (TCAs): Clomipramine, Imipramine Selective serotonin Reuptake Inhibitor Fluoxetine
  • 44. BREATHING RELATED SLEEP DISORDER • There are three types of sleep apnea 1. Obstructive 2. Central 3. Mixed • Of these, obstructive sleep apnea (OSA) is the most common. • RISK FACTORS : 1. Excessive weight gain 2. Anatomic abnormalities, such as a receding chin. 3. enlarged tonsils and adenoids, main cause in children. 4. Family history of OSA 5. Alcohol and sedative drugs 6. Hypothyroidism, acromegaly
  • 45. OBSTRUCTIVE SLEEP APNOEA • Clinically speaking, an obstructive apnea is defined as a complete cessation of airflow for more than 10 seconds with persistent respiratory effort. • An obstructive hypopnea is defined as a partial reduction in air flow of approximately 30 percent to 50 percent with persistent respiratory effort and a reduction in oxygen saturation by at least 3 percent to 4 percent and/or an arousal from sleep.
  • 46. OSA : TREATMENT • Weight reduction • Positional therapy • Positive pressure therapy (BIPAP , CPAP) : T/T of choice • Surgical options
  • 47. CIRCADIAN RHYTHM SLEEP DISORDER Persistent sleep disturbance due to DESYNCHRONY BETWEEN AN INDIVIDUAL’S INTERNAL CIRCADIAN BIOLOGICAL CLOCK & CONVENTIONAL SLEEP WAKE CYCLE. Types: 1. Delayed sleep phase type: late onset sleep and late awakening 2. Jet lag type: travel across more than 1 time zone 3. Shift work type: frequent change of shift work, night shift 4. Advanced sleep phase syndrome 5. Disorganized sleep-wake pattern Treatment: melatonin and light exposure
  • 48. PARASOMNIAS • Disorders of “partial arousal”. NREM Sleep Arousal Disorder 1. Sleepwalking 2. Sleep terror REM Sleep Arousal Disorder 1. REM Behavior Disorder (RBD) 2. Sleep Paralysis 3. Nightmare disorder
  • 49. SLEEPWALKING • Repeated episodes of rising from bed during sleep and walking about. While sleeping the individual has a blank staring face, is relatively unresponsive and can be awakened with great difficulty. • Individual can engage in a complex behavior of semi purposeful actions. • Sleepwalker may interact with the environment inappropriately, resulting in injury. • Disorders of arousal, particularly from deepest stage of sleep (N3). • Amnesia of the episode is present.
  • 50. SLEEPWALKING • Very common in children, peak prevalence between 4 to 8 yrs. • Rare in adults  familial pattern. • D/D : Psychomotor epileptic seizure Dissociative fugue • “Specialized forms” : Sleep related eating Sexsomnia • T/T : often unnecessary psychoeducation & assurance safety issue medication : benzodiazepines
  • 51. SLEEP TERRORS • Recurrent episodes of abrupt terror arousals from sleep, beginning with a panicky scream. There is intense fear and signs of autonomic hyperactivity – mydriasis, tachycardia, rapid breathing and sweating. • Relative unresponsiveness to efforts of others to comfort the individual during the episode. • Recall of event, if any, is minimal. • Risk of injury during episode. • Occurs during first third of nocturnal sleep, deep sleep (N3). • Sleep terror and sleep walking – part of same nosologic continuum.
  • 52. RAPID EYE MOVEMENT BEHAVIOR DISORDER • Patients with rapid eye movement behavior disorder (RBD) act out dramatic and/or violent dreams during rapid eye movement (REM) stage sleep. • Another feature of RBD is shouting and grunting. RBD seems similar to other sleep disorders that involve motor activity, like Sleep Walking or Periodic limb movement disorder. • RBD movements occur during REM sleep. • Patients with RBD usually respond to treatment with clonazepam when taken nightly.
  • 53. NIGHTMARE DISORDER • Nightmares are dream experiences loaded with anxiety or fear, of which the individual has very detailed recall. • The dream experiences are extremely vivid and usually include themes involving threats to survival, security or self esteem. • Often, there is recurrence of similar nightmare theme. • During a typical episode there is a degree of autonomic discharge but no appreciable vocalization or body motility. • Medications known to provoke nightmares : l-DOPA, reserpine, thioridazine, TCA, B-blocker, benzodiazepine and alcohol abuse • “Fear of sleeping” type insomnia. • T/T : Nefazodone, Benzodiazepine, Prazocin.
  • 54. RESTLESS LEG SYNDROME (EKBOM SYNDROME) • Uncomfortable subjective sensation(creepy crawly) in legs • Worse at night • Relieved by walking or moving legs • Sleep initiation insomnia • Linked to deficiency of DA, iron, B12, and pregnancy and renal disease • T/T : DA agonist (ropinirole, pramipexole), iron replacement, levodopa, anti-epileptic (gabapentin)
  • 55. PERIODIC LIMB MOVEMENT SYNDROME • Previously known as nocturnal myoclonus . • Brief, stereotypic, repetitive, non-epileptiform contraction of muscle during sleep. • Patient is unaware of the incident • PLMs are 0.5-5 s in duration and occur every 20-40 s during NREM • Often accompanied by K complex or brief arousal signal • Associated with folate deficiency, renal disease, anemia, use of antidepressant. • T/T : Benzodiazepine (clonazepam), Opiates.
  • 56. BRUXISM • Bruxism, often referred to as “gnashing,” is the act of involuntary teeth grinding, either while awake or asleep, which results primarily in tooth damage and jaw pain and which seems to be caused by psychological effects of everyday stress. • The sound of teeth grinding can be quite loud and disruptive to bed partners or roommates. • These include stress, facial or oral trauma, nervous system malfunction, poor diet, and allergies. • Children with bruxism usually stop grinding their teeth before adulthood. • In adults, alcohol and drug use is suspected to increase the occurrence of bruxism.