This document provides information about sleep medicine and sleep disorders. It discusses topics such as insomnia, restless leg syndrome, narcolepsy, obstructive sleep apnea, and other common sleep disorders. It notes that obstructive sleep apnea is a common and dangerous sleep disorder characterized by recurrent collapse of the pharyngeal airway during sleep, and lists risk factors such as obesity, age, sex, and craniofacial anatomy.
3. SLEEP MEDICINESLEEP MEDICINE
Inter-disciplinary subspecialty; ABMS first board exam inInter-disciplinary subspecialty; ABMS first board exam in
20072007
The International Classification of Sleep Disorders, Second
Edition documents 81 official sleep disorders.
Healthful Sleep is more influential in predictingHealthful Sleep is more influential in predicting
longevity than diet, exercise or hereditylongevity than diet, exercise or heredity
William Dement, M.D., Ph.D. – Promise of SleepWilliam Dement, M.D., Ph.D. – Promise of Sleep
5. Common Sleep ComplaintsCommon Sleep Complaints
By PatientBy Patient
Difficulty falling asleep
Difficulty staying asleep
Feeling headache, tired on
waking up
Day time sleepiness
Concentration/ memory
trouble
By Patient’s FamilyBy Patient’s Family
Snoring
Gasping/ stopping to
breathe
Repeated Leg Jerking
Sleep Walking
Violent Movements -
grabbing, punching,grabbing, punching,
kicking, jumping, runningkicking, jumping, running
out of the bed orout of the bed or yelling,yelling,
swearing,swearing,
8. Insomnia RxInsomnia Rx
Pharmacological management:
Benzodiazepines (BDZ) and benzodiazepine receptor agonists (BZRA)
GABAGABAAA receptors arereceptors are
comprised of a centralcomprised of a central
chloride channel surroundedchloride channel surrounded
by five protein subunits.by five protein subunits.
Nineteen subunits from 7Nineteen subunits from 7
gene familiesgene families
9. ZolpidemZolpidem
AmbienAmbien
ZaleplonZaleplon
SonataSonata
EszopicloneEszopiclone
LunestaLunesta
Zolpidem CRZolpidem CR
Half lifeHalf life 2.5 hours2.5 hours 1 hour1 hour 5-9 hrs5-9 hrs
dependingdepending
on ageon age
2.8-2.9 hrs2.8-2.9 hrs
TmaxTmax 1.5 hours1.5 hours 1 hour1 hour 1 hour1 hour 1.5-2 hours1.5-2 hours
IndicationIndication SleepSleep
onset.onset.
Short termShort term
useuse
SleepSleep
onset.onset.
short termshort term
useuse
Sleep onsetSleep onset
maintenancemaintenance
Long termLong term
useuse
Sleep onsetSleep onset
maintenancemaintenance
Long termLong term
useuse
9
BZRA
10. RLSRLS –– Restless Leg SyndromeRestless Leg Syndrome
A neurological movement disorderA neurological movement disorder
characterized by an irresistible urgecharacterized by an irresistible urge
to move the legs accompaniedto move the legs accompanied
by uncomfortable sensationsby uncomfortable sensations
that often occurthat often occur
in the evening/ at rest or nightin the evening/ at rest or night
11. RLSRLS
Key diagnostic criteriaKey diagnostic criteria Supportive featuresSupportive features
Urge to move the legs – usuallyUrge to move the legs – usually
accompanied or caused byaccompanied or caused by
uncomfortable leg sensationsuncomfortable leg sensations
Sleep disturbancesSleep disturbances
Involuntary leg movementsInvoluntary leg movements
Positive family history forPositive family history for
RLSRLS
Temporary relief with movementTemporary relief with movement
Onset or worsening of symptomsOnset or worsening of symptoms
at rest or inactivity - in theat rest or inactivity - in the
evening or at nightevening or at night
13. SomnambulismSomnambulism
Sleepwalking – common in childrenSleepwalking – common in children
Complex purposeless tasks and wandering episodes of variableComplex purposeless tasks and wandering episodes of variable
duration, with memory impairment for the eventduration, with memory impairment for the event
Starts in the deep stages of N-REM sleep in first third of nightStarts in the deep stages of N-REM sleep in first third of night
Runs in family and often associated with Sleep TerrorsRuns in family and often associated with Sleep Terrors
If starts in an adultIf starts in an adult
• OSAOSA
• DementiaDementia
14. Night TerrorsNight Terrors
• Sleep disorder characterized by high arousal
and appearance of being terrified
• Happens during stage 4 sleep; mostly children
• The children seldom remember the event.
15. Narcolepsy
• A sleep disorder characterized by uncontrollable
sleep attacks
• REM sleep occurs earlier than normal
• Narcolepsy with and without Cataplexy
• Cataplexy – momentary loss of muscle tone
triggered by emotional excitement
16. NarcolepsyNarcolepsy
Neuropeptide hypocretin II,Neuropeptide hypocretin II,
(orexin B) producing cells(orexin B) producing cells
reduced by 85%reduced by 85%––95% in the95% in the
posterior and lateralposterior and lateral
hypothalamushypothalamus
Reduced CSF hypocretinReduced CSF hypocretin
HypothalamusHypothalamus
16
17. RBDRBD –– REM Sleep Behavior D/OREM Sleep Behavior D/O
RBD is a REM sleep parasomnia with emergenceRBD is a REM sleep parasomnia with emergence
of complex and vigorous behaviors.of complex and vigorous behaviors.
More common in >50 years of age, but can occurMore common in >50 years of age, but can occur
at any ageat any age
More prevalent in men and often a precursor ofMore prevalent in men and often a precursor of
ParkinsonParkinson’’s Diseases Disease
18. RBD: Diagnostic CriteriaRBD: Diagnostic Criteria
History of problematic sleep behavior (orHistory of problematic sleep behavior (or
videotaped documentation of such behaviors)videotaped documentation of such behaviors)
PSG evidence of excessive augmentation ofPSG evidence of excessive augmentation of
chin EMG tone or of excessive limb twitchingchin EMG tone or of excessive limb twitching
in REM sleepin REM sleep
19. RBD RiskRBD Risk
RBD is associated with neurological
disorders in 38%–75% of cases –
Neurodegenerative conditions.
Particularly common are:
Parkinson disease
Multiple System Atrophy and
Lewy body dementia
20. RBD D/DRBD D/D
Severe OSASevere OSA
Drug InducedDrug Induced –– Sedatives, TCA, AnticholinergicsSedatives, TCA, Anticholinergics
AlcoholismAlcoholism
Structural Brain Stem LesionsStructural Brain Stem Lesions
23. OSA IS :
CommonCommon
DangerousDangerous
Easily recognizedEasily recognized
TreatableTreatable
24. What is OSA?What is OSA?
Sleep disorder characterized by recurrent episodes ofSleep disorder characterized by recurrent episodes of
narrowing or collapse of pharyngeal airway during sleepnarrowing or collapse of pharyngeal airway during sleep
despite ongoing breathing efforts.despite ongoing breathing efforts.
These often lead toThese often lead to
• Acute derangements in blood gas disturbancesAcute derangements in blood gas disturbances
• Surges of sympathetic activationSurges of sympathetic activation
• Periodic arousal from sleep (fragmented sleep)Periodic arousal from sleep (fragmented sleep)
26. WHAT IS OSA?WHAT IS OSA?
Episodes of complete or partial collapse of airwayEpisodes of complete or partial collapse of airway
are translated to # of apnea and hypopneaare translated to # of apnea and hypopnea
events (AHI).events (AHI).
• Apnea = cessation of airflowApnea = cessation of airflow >> 10 seconds10 seconds
• Hypopnea = Decreased airflowHypopnea = Decreased airflow >> 10 seconds10 seconds
associated with:associated with:
ArousalArousal
Oxyhemoglobin desaturationOxyhemoglobin desaturation
27. WHY DOES THIS MATTER?WHY DOES THIS MATTER?
Excessive daytime somnolenceExcessive daytime somnolence
Impaired cognitive performanceImpaired cognitive performance
DM/metabolic syndromeDM/metabolic syndrome
Poor quality of lifePoor quality of life
Increased risk of MVAIncreased risk of MVA
Adverse cardiovascular outcomesAdverse cardiovascular outcomes
Pulmonary hypertensionPulmonary hypertension
28. Prevalence of OSAPrevalence of OSA
3-7 % in general US adult population3-7 % in general US adult population
Higher in population subsetsHigher in population subsets
Ancoli-Israel and colleagues reported that 70% of men and 56%Ancoli-Israel and colleagues reported that 70% of men and 56%
of women between 65 and 99 years of age had obstructiveof women between 65 and 99 years of age had obstructive
sleep apnea defined as an AHI of at least 10 events per hoursleep apnea defined as an AHI of at least 10 events per hour..
Ancoli-Israel S, Kripke DF, Klauber MR, Mason WJ, Fell R, Kaplan O. Sleep-disordered breathing inAncoli-Israel S, Kripke DF, Klauber MR, Mason WJ, Fell R, Kaplan O. Sleep-disordered breathing in
community-dwelling elderly. Sleep 1991;14:486–495community-dwelling elderly. Sleep 1991;14:486–495
29. ObesityObesity
Alters upper airway mechanics duringAlters upper airway mechanics during
sleepsleep
1.1. Increased parapharyngeal fatIncreased parapharyngeal fat
deposition:deposition:
neck circumference:neck circumference: >> 17” males17” males
>> 16” females16” females
With subsequent:With subsequent:
smaller upper airwaysmaller upper airway
increase the collapsibility of theincrease the collapsibility of the
pharyngeal airwaypharyngeal airway
30. Majority of OSA still undiagnosed
RISK FACTORSRISK FACTORS
ObesityObesity
AgeAge
SexSex
RaceRace
Craniofacial anatomyCraniofacial anatomy
Smoking and Alcohol consumptionSmoking and Alcohol consumption
31. OBESITYOBESITY
Strongest risk factor for OSAStrongest risk factor for OSA
• Present in > 60% of patients referred forPresent in > 60% of patients referred for
a diagnostic sleep evaluationa diagnostic sleep evaluation
• Wisconsin Sleep Cohort StudyWisconsin Sleep Cohort Study
A one standard deviation difference in BMIA one standard deviation difference in BMI
was associated with a 4-fold increase inwas associated with a 4-fold increase in
disease prevalencedisease prevalence
32. OBESITYOBESITY
Alters upper airway mechanics during sleepAlters upper airway mechanics during sleep
1.1.Increased Para pharyngeal fat deposition:Increased Para pharyngeal fat deposition:
neck circumference:neck circumference: >> 17” males17” males
>> 16” females16” females
With subsequent:With subsequent:
smaller upper airwaysmaller upper airway
increase the collapsibility of theincrease the collapsibility of the
pharyngeal airwaypharyngeal airway
33. OBESITYOBESITY
2. Changes in neural compensatory mechanisms that2. Changes in neural compensatory mechanisms that
maintain airway patency:maintain airway patency:
diminished protective reflexes whichdiminished protective reflexes which
otherwiseotherwise
would increase upper airway dilator musclewould increase upper airway dilator muscle
activity to maintain airway patencyactivity to maintain airway patency
34. OBESITYOBESITY
3. waist circumference3. waist circumference
Fat deposition around the abdomen producesFat deposition around the abdomen produces
reduced lung volumes (functional residualreduced lung volumes (functional residual
capacity) which can lead to loss of caudalcapacity) which can lead to loss of caudal
traction on the upper airwaytraction on the upper airway
low lung volumes are associated withlow lung volumes are associated with
diminished oxygen storesdiminished oxygen stores
35. AGEAGE
Mechanisms proposed:Mechanisms proposed:
• Anatomic susceptibilityAnatomic susceptibility
• Preferential deposition of fat in thePreferential deposition of fat in the
Para pharyngeal areaPara pharyngeal area
• Changes in the body structures around theChanges in the body structures around the
pharynxpharynx
• Deterioration of protective reflex mechanismsDeterioration of protective reflex mechanisms
36. Risk Factor: AgeRisk Factor: Age
0
5
10
15
20
25
30
35
30-39 Yrs 40-49 Yrs 50-60 Yrs
Female
Male
% with
AHI > 5
Adapted from Young T et al.
N Engl J Med 1993;328. 2006 American Academy of Sleep medicine
37. CRANIOFACIAL ANATOMYCRANIOFACIAL ANATOMY
Mandibular body lengthMandibular body length
RetrognathiaRetrognathia
Tonsilar hypertrophyTonsilar hypertrophy
Enlarged tongue or soft palateEnlarged tongue or soft palate
Inferiorly positioned hyoid boneInferiorly positioned hyoid bone
Maxillary and mandibular retro positionMaxillary and mandibular retro position
Decreased posterior airway spaceDecreased posterior airway space
39. Other OSA risk factorsOther OSA risk factors
Alcohol consumptionAlcohol consumption
Sedatives (benzodiazepines)Sedatives (benzodiazepines)
reduce nerve output to compensatoryreduce nerve output to compensatory
dilator musclesdilator muscles
increase OSA severity in patients withincrease OSA severity in patients with
preexisting syndrome.preexisting syndrome.
40. DIAGNOSISDIAGNOSIS
Combined assessment of clinical features andCombined assessment of clinical features and
objective sleep study dataobjective sleep study data..
The gold standard:The gold standard: overnightovernight
polysomnogrampolysomnogram
The Polysomnogram (PSG):The Polysomnogram (PSG):
• Provides detailed information on sleepProvides detailed information on sleep
state andstate and
respiratory and gas exchangerespiratory and gas exchange
abnormalities.abnormalities.
45. PSGPSG
Duration of the diagnostic studyDuration of the diagnostic study
should be at leastshould be at least
six hours.six hours.
split-night studiessplit-night studies
• First half = diagnosisFirst half = diagnosis
• Second half = initiation of CPAP therapySecond half = initiation of CPAP therapy
((when obvious OSAS is present)when obvious OSAS is present)
46.
47.
48. OSA Clinical featuresOSA Clinical features
1. Excessive daytime sleepiness1. Excessive daytime sleepiness
2. fatigue2. fatigue
3. memory impairment3. memory impairment
4. personality changes4. personality changes
5. morning headaches or nausea5. morning headaches or nausea
6. depression6. depression
51. Comorbidities of OSA: MVAComorbidities of OSA: MVA
0
0.05
0.1
0.15
0.2
0.25
0.3
0.35
0.4
0.45
No Apnea Sleep Apnea All Drivers
Accident / driver / 5 yrs
Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.
2006 American Academy of Sleep Medicine
56. Other DevicesOther Devices
Single use deviceSingle use device
contains a mechanicalcontains a mechanical
valve with very lowvalve with very low
inspiratory but highinspiratory but high
expiratory resistanceexpiratory resistance
The high expiratoryThe high expiratory
resistance results in +veresistance results in +ve
pressure throughoutpressure throughout
exhalation, which splintsexhalation, which splints
open the upper airway,open the upper airway,
making it more resistantmaking it more resistant
to collapse onto collapse on
subsequent inspirationsubsequent inspiration
Berry RB et al. SLEEP 2011;34(4):479-485.
59. Circadian Rhythms OverviewCircadian Rhythms Overview
SuprachiasmaticSuprachiasmatic
nucleus (SCN), anucleus (SCN), a
paired structure locatedpaired structure located
in the anteriorin the anterior
hypothalamus containshypothalamus contains
a circadian pacemakera circadian pacemaker
The biological clocksThe biological clocks
work on a 24.3 hourwork on a 24.3 hour
cycle rather than a 24cycle rather than a 24
hour onehour one
6060
Complete lesionsComplete lesions
of the SCN abolishof the SCN abolish
circadian rhythmscircadian rhythms
SCN transplantsSCN transplants
into the thirdinto the third
ventricle andventricle and
hypothalamushypothalamus
restoresrestores
rhythmicityrhythmicity
60. Circadian Rhythms DefinitionCircadian Rhythms Definition
The mechanism throughThe mechanism through
which light inhibitswhich light inhibits
melatonin secretion bymelatonin secretion by
the pineal gland involvingthe pineal gland involving
the neural pathwaythe neural pathway
originating in the retinaoriginating in the retina
and passing through theand passing through the
suprachiasmatic nucleussuprachiasmatic nucleus
in the brain, to reachin the brain, to reach
pinealocytes viapinealocytes via
adrenergic nerves andadrenergic nerves and
adrenergic receptors, andadrenergic receptors, and
subsequently to thesubsequently to the
peripheryperiphery
61. Circadian RhythmsCircadian Rhythms
Delayed Sleep PhaseDelayed Sleep Phase
The most common circadian rhythm sleepThe most common circadian rhythm sleep
disorder; it usually begins in adolescence anddisorder; it usually begins in adolescence and
is manifested as habitually delayed sleep andis manifested as habitually delayed sleep and
waking timeswaking times
May significantly impede scholastic andMay significantly impede scholastic and
occupational achievementsoccupational achievements
Treatment with melatonin or bright lightTreatment with melatonin or bright light
augmented with behavior and lifestyleaugmented with behavior and lifestyle
modification may be effectivemodification may be effective
62. Shift WorkTreatmentShift WorkTreatment
Sleep hygieneSleep hygiene
Bright light exposure (continuous orBright light exposure (continuous or
intermittent) beginning early during the nightintermittent) beginning early during the night
shift and terminating 2 h before the end of theshift and terminating 2 h before the end of the
shiftshift
Avoiding bright light by wearing dark glassesAvoiding bright light by wearing dark glasses
during the morningduring the morning
Melatonin, hypnotics, caffeine and modafinilMelatonin, hypnotics, caffeine and modafinil
also have their usesalso have their uses
63. Other Sleep DisordersOther Sleep Disorders
• Bruxism – teeth grinding
• Enuresis – bed wetting
• Myoclonus – sudden jerk of a body part
occurring during stage 1 sleep
–Everyone has occasional episodes of
myoclonus
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The risk of developing sleep apnea increases with increasing age. This slide shows the results of a study which evaluated the prevalence of sleep-disordered breathing in a general middle aged adult population.6 The percentage of subjects with 5 or more apneas and hypopneas per hour of sleep increases with increasing age in both men and women.
Cigarette smoking is also a risk factor for the development of sleep apnea. A longitudinal epidemiologic study showed that smokers are at an increased risk for developing sleep apnea when compared to nonsmokers. This slide shows that current smokers are at a greater risk than former smokers, and both are at greater risk than never-smokers for developing moderate-severity sleep apnea.27 This risk increases in a dose related manner, such that heavy smokers have a greater risk than light smokers. This risk from smoking is independent of sex, age and Body Mass Index (BMI).
This slide depicts an obstructive apnea. The top channel shows the electroencephalogram (EEG) pattern of sleep. The next channel represents airflow. The next three channels show ventilatory effort by movements of the rib cage and abdomen and changes in esophageal pressure, all of which reflect contraction of respiratory muscles. The last channel indicates oxyhemoglobin saturation.
During an apnea, the upper airway collapses resulting in cessation of airflow. Ventilatory effort continues and increases in an attempt to overcome the obstruction, shown by the increase in esophageal pressure change. Rib cage and abdominal movements are in the opposite direction as a result of the diaphragm contracting against an occluded airway, forcing the abdominal wall to distend out and the chest wall to move inward.
The increasing efforts to breathe lead to an arousal from sleep, shown on the EEG, and results in opening of the airway and a resumption of normal breathing. The lack of airflow during the apnea also causes hypoxia, shown by the drop in oxyhemoglobin saturation.
This slide shows an obstructive hypopnea. During sleep, there is a partial obstruction of the upper airway which increases airway resistance and results in a reduction in airflow. This decrease in airflow occurs despite increased ventilatory effort, shown by the change in esophageal pressure. The rib cage and abdomen are moving in opposite or paradoxical movements, reflecting increased difficulty breathing against a partially closed airway.
The hypopnea may or may not cause a decrease in oxyhemoglobin saturation depending on the length of the hypopnea, the degree of reduction in airflow, and the baseline saturation level.
The increased ventilatory effort causes an arousal from sleep, which is associated with relief of the partial upper airway obstruction and resumption of normal airflow.
Shown here is data comparing the automobile accident rate in sleep apnea patients with matched controls and with all Virginia drivers. The accident incidence was seven-fold greater in patients with sleep apnea than in matched controls without the disorder. The percentage of individuals with one or more crashes was also greater in the patients with apnea (13%) than in the controls (6%). The automobile crash rate for sleep apnea patients was 2.6 times the crash rate of all licensed drivers in Virginia.9 The risk of automobile accidents is related to severity of disease, with the highest rates seen in patients with severe apnea.12
This slide depicts the therapeutic effect of continuous positive airway pressure (CPAP). In the panel on the left, you can see upper airway closure in an untreated sleep apnea patient. Note that the airway closure is diffuse, involving both the palate and the base of the tongue. In the second panel, CPAP is applied and the airway is splinted open by the positive pressure.
This slide depicts the uvulopalatopharyngoplasty (UPPP) surgical technique.
The panel on the left depicts the preoperative upper airway, demonstrating a long soft palate and the presence of palatine tonsils. The incision site is marked with the dotted line.
The panel on the right depicts the postoperative oropharynx, with amputation of the uvula, bilateral palatine tonsillectomy, and trimming and suturing together of the anterior and posterior tonsillar pillars.