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Senthil Ramasamy, M.DSenthil Ramasamy, M.D..
Board Certified in Neurology & Sleep MedicineBoard Certified in Neurology & Sleep Medicine
 Clinical ConsultationClinical Consultation
 Sleep Studies – PSGSleep Studies – PSG
 Nerve Conduction/ EMGNerve Conduction/ EMG
 EEGEEG
 ALL INSURANCES ACCEPTEDALL INSURANCES ACCEPTED
 Pres, Lovelace, BCBS, UHC, AETNA, CIGNAPres, Lovelace, BCBS, UHC, AETNA, CIGNA
 MedicareMedicare
 MedicaidMedicaid
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
Sleep Disorders ClassificationsSleep Disorders Classifications
Sleep disorders
Hypersomnias
Circadian
dysrhythmias
InsomniasParasomnias
Sleep breathing
disorders
Sleep movement
disorders
4
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,
Chronic InsomniaChronic Insomnia
Psychiatric conditions – Depression/ AnxietyPsychiatric conditions – Depression/ Anxiety
Drug and Alcohol AbuseDrug and Alcohol Abuse
Neurological Disorders – Headache, Stroke,Neurological Disorders – Headache, Stroke,
Dementia, TBI, Parkinson’s syndromeDementia, TBI, Parkinson’s syndrome
Medical Conditions – CAD, CHF, Asthma, COPD,Medical Conditions – CAD, CHF, Asthma, COPD,
GERD, Fibromyalgia, Rheumatologic disordersGERD, Fibromyalgia, Rheumatologic disorders
Primary or Psychophysiologic InsomniaPrimary or Psychophysiologic Insomnia
Insomnia RxInsomnia Rx
Cognitive Behavioral TherapyCognitive Behavioral Therapy
• Sleep restriction consolidationSleep restriction consolidation
• Stimulus control therapyStimulus control therapy
• Sleep hygiene educationSleep hygiene education
• Relaxation therapyRelaxation therapy
7
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
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
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
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
RLS RXRLS RX
DopamineDopamine
agonistsagonists OpiatesOpiates AnticonvulsantsAnticonvulsants OthersOthers
Ropinorol*Ropinorol* TramadolTramadol Gabapentin Enacarbil*Gabapentin Enacarbil* BaclofenBaclofen
Pramipexol*Pramipexol* MethadoneMethadone TopiramateTopiramate ClonazepamClonazepam
Carbidopa/Carbidopa/
levodopalevodopa
CodeineCodeine PregabalinPregabalin ClonidineClonidine
Replace iron in patients with serum Ferritin levels below 50 mcg/L
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
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.
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
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
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
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
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
RBD D/DRBD D/D
Severe OSASevere OSA
Drug InducedDrug Induced –– Sedatives, TCA, AnticholinergicsSedatives, TCA, Anticholinergics
AlcoholismAlcoholism
Structural Brain Stem LesionsStructural Brain Stem Lesions
OSA – Obstructive Sleep ApneaOSA – Obstructive Sleep Apnea
OSA IS :
 CommonCommon
 DangerousDangerous
 Easily recognizedEasily recognized
 TreatableTreatable
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)
PATENT Vs COLLAPSED AIRWAYPATENT Vs COLLAPSED AIRWAY
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
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
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
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
Majority of OSA still undiagnosed
RISK FACTORSRISK FACTORS
 ObesityObesity
 AgeAge
 SexSex
 RaceRace
 Craniofacial anatomyCraniofacial anatomy
 Smoking and Alcohol consumptionSmoking and Alcohol consumption
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
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
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
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
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
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
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
SMOKINGSMOKING
0
1
2
3
4
5
Adjusted Odds Ratio for Sleep Apnea (AHI > 15)
in Former & Current Smokers vs Nonsmokers
Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association.
Former Current
Smokers Smokers
(Adjusted for age,
race, sex, BMI)
Odds Ratio
2006 American Academy of Sleep Medicine
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.
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.
PSGPSG
 Simultaneous recordings of multipleSimultaneous recordings of multiple
physiological signals during sleep.physiological signals during sleep.
• Electroencephalogram (EEG)Electroencephalogram (EEG)
• Electrooculogram (EOG)Electrooculogram (EOG)
• Electromyogram (EMG)Electromyogram (EMG)
• Electrocardiogram (ECG)Electrocardiogram (ECG)
• Oronasal airflowOronasal airflow
• Chest/ Abdomen effortChest/ Abdomen effort
• Snore microphoneSnore microphone
• Oxyhemoglobin saturationOxyhemoglobin saturation
EEG
10 sec
Arousal
Airflow
Effort
(Pes)
SaO2
Effort
(Abdomen)
Effort
(Rib Cage)
2006 American Academy of Sleep Medicine
OSAOSA
EEG
10 sec
Arousal
Airflow
Effort
(Pes)
SaO2
Effort
(Abdomen)
Effort
(Rib Cage)
2006 American Academy of Sleep Medicine
CSACSA
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)
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
www.dentonsleepdisorderlab.com
SLEEP-
Apnea
Chronic
Intermittent
Hypoxia
Ventilatory
Overshoot
Hyperoxia
Increased
Sympathetic
Nervous System
Activity
Intrathoracic
Pressure Swings
Hypercapnia
Increased Arousals
Reduced Sleep
Duration
Increased
Inflammation
Increased
Oxidative Stress
Metabolic
Dysfunction/
Insulin
Resistance
Hyper-
coaguability
Endothelial
Dysfunction
Autonomic
Dysfunction
Systemic
Hypertension
Atherosclerosis
Diastolic
Dysfunction
Congestive Heart
Failure
Stroke
Increased Mortality
and Sudden Death
Cardiac Arrhythmias
PHYSIOLOGIC
PERTURBATIONS
INTERMEDIATE
MECHANISMS
CLINICAL
OUTCOMES
Mehra R Curr Resp Med Rev 2007
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
MEDICAL RMEDICAL Rxx
 Positive Pressure TherapyPositive Pressure Therapy
* CPAP* CPAP
* Bi-PAP* Bi-PAP
 SurgicalSurgical
CPAP MasksCPAP Masks
•Nasal CPAPNasal CPAP •Full Face MaskFull Face Mask •Nasal PillowsNasal Pillows
2006 American Academy of Sleep Medicine
CPAP EffectCPAP Effect
MADMAD
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.
2006 American Academy of Sleep Medicine
UVPPUVPP
MMA GBTMMA GBT
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
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
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
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
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
Senthil Ramasamy, M.DSenthil Ramasamy, M.D..
Board Certified in Neurology & Sleep MedicineBoard Certified in Neurology & Sleep Medicine
 Clinical ConsultationClinical Consultation
 Sleep Studies – PSGSleep Studies – PSG
 Nerve Conduction/ EMGNerve Conduction/ EMG
 EEGEEG
 ALL INSURANCES ACCEPTEDALL INSURANCES ACCEPTED
 Pres, Lovelace, BCBS, UHC, AETNA, CIGNAPres, Lovelace, BCBS, UHC, AETNA, CIGNA
 MedicareMedicare
 MedicaidMedicaid
AthayaAthaya
MedicalMedical
CenterCenter
New 15,000 sfNew 15,000 sf
out patient facilityout patient facility
IN CLOSE PROXIMITY TO 3 WEST SIDE/IN CLOSE PROXIMITY TO 3 WEST SIDE/
RIO RANCHO HOSPITALSRIO RANCHO HOSPITALS
INVITES PRACTICES/ PROVIDERS TO STARTINVITES PRACTICES/ PROVIDERS TO START
IN THE BOOMING PART OF CITYIN THE BOOMING PART OF CITY

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Commercial Space and Sleep Medicine Services

  • 1. Athaya CommercialAthaya Commercial Space for LeaseSpace for Lease
  • 2. Senthil Ramasamy, M.DSenthil Ramasamy, M.D.. Board Certified in Neurology & Sleep MedicineBoard Certified in Neurology & Sleep Medicine  Clinical ConsultationClinical Consultation  Sleep Studies – PSGSleep Studies – PSG  Nerve Conduction/ EMGNerve Conduction/ EMG  EEGEEG  ALL INSURANCES ACCEPTEDALL INSURANCES ACCEPTED  Pres, Lovelace, BCBS, UHC, AETNA, CIGNAPres, Lovelace, BCBS, UHC, AETNA, CIGNA  MedicareMedicare  MedicaidMedicaid
  • 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
  • 4. Sleep Disorders ClassificationsSleep Disorders Classifications Sleep disorders Hypersomnias Circadian dysrhythmias InsomniasParasomnias Sleep breathing disorders Sleep movement disorders 4
  • 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,
  • 6. Chronic InsomniaChronic Insomnia Psychiatric conditions – Depression/ AnxietyPsychiatric conditions – Depression/ Anxiety Drug and Alcohol AbuseDrug and Alcohol Abuse Neurological Disorders – Headache, Stroke,Neurological Disorders – Headache, Stroke, Dementia, TBI, Parkinson’s syndromeDementia, TBI, Parkinson’s syndrome Medical Conditions – CAD, CHF, Asthma, COPD,Medical Conditions – CAD, CHF, Asthma, COPD, GERD, Fibromyalgia, Rheumatologic disordersGERD, Fibromyalgia, Rheumatologic disorders Primary or Psychophysiologic InsomniaPrimary or Psychophysiologic Insomnia
  • 7. Insomnia RxInsomnia Rx Cognitive Behavioral TherapyCognitive Behavioral Therapy • Sleep restriction consolidationSleep restriction consolidation • Stimulus control therapyStimulus control therapy • Sleep hygiene educationSleep hygiene education • Relaxation therapyRelaxation therapy 7
  • 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
  • 12. RLS RXRLS RX DopamineDopamine agonistsagonists OpiatesOpiates AnticonvulsantsAnticonvulsants OthersOthers Ropinorol*Ropinorol* TramadolTramadol Gabapentin Enacarbil*Gabapentin Enacarbil* BaclofenBaclofen Pramipexol*Pramipexol* MethadoneMethadone TopiramateTopiramate ClonazepamClonazepam Carbidopa/Carbidopa/ levodopalevodopa CodeineCodeine PregabalinPregabalin ClonidineClonidine Replace iron in patients with serum Ferritin levels below 50 mcg/L
  • 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
  • 21.
  • 22. OSA – Obstructive Sleep ApneaOSA – Obstructive Sleep Apnea
  • 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)
  • 25. PATENT Vs COLLAPSED AIRWAYPATENT Vs COLLAPSED AIRWAY
  • 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
  • 38. SMOKINGSMOKING 0 1 2 3 4 5 Adjusted Odds Ratio for Sleep Apnea (AHI > 15) in Former & Current Smokers vs Nonsmokers Adapted from Wetter DW et al. Arch Intern Med 1994:154 ©1994 American Medical Association. Former Current Smokers Smokers (Adjusted for age, race, sex, BMI) Odds Ratio 2006 American Academy of Sleep Medicine
  • 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.
  • 41. PSGPSG  Simultaneous recordings of multipleSimultaneous recordings of multiple physiological signals during sleep.physiological signals during sleep. • Electroencephalogram (EEG)Electroencephalogram (EEG) • Electrooculogram (EOG)Electrooculogram (EOG) • Electromyogram (EMG)Electromyogram (EMG) • Electrocardiogram (ECG)Electrocardiogram (ECG) • Oronasal airflowOronasal airflow • Chest/ Abdomen effortChest/ Abdomen effort • Snore microphoneSnore microphone • Oxyhemoglobin saturationOxyhemoglobin saturation
  • 42.
  • 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
  • 50. SLEEP- Apnea Chronic Intermittent Hypoxia Ventilatory Overshoot Hyperoxia Increased Sympathetic Nervous System Activity Intrathoracic Pressure Swings Hypercapnia Increased Arousals Reduced Sleep Duration Increased Inflammation Increased Oxidative Stress Metabolic Dysfunction/ Insulin Resistance Hyper- coaguability Endothelial Dysfunction Autonomic Dysfunction Systemic Hypertension Atherosclerosis Diastolic Dysfunction Congestive Heart Failure Stroke Increased Mortality and Sudden Death Cardiac Arrhythmias PHYSIOLOGIC PERTURBATIONS INTERMEDIATE MECHANISMS CLINICAL OUTCOMES Mehra R Curr Resp Med Rev 2007
  • 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
  • 52. MEDICAL RMEDICAL Rxx  Positive Pressure TherapyPositive Pressure Therapy * CPAP* CPAP * Bi-PAP* Bi-PAP  SurgicalSurgical
  • 53. CPAP MasksCPAP Masks •Nasal CPAPNasal CPAP •Full Face MaskFull Face Mask •Nasal PillowsNasal Pillows
  • 54. 2006 American Academy of Sleep Medicine CPAP EffectCPAP Effect
  • 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.
  • 57. 2006 American Academy of Sleep Medicine UVPPUVPP
  • 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
  • 64. Senthil Ramasamy, M.DSenthil Ramasamy, M.D.. Board Certified in Neurology & Sleep MedicineBoard Certified in Neurology & Sleep Medicine  Clinical ConsultationClinical Consultation  Sleep Studies – PSGSleep Studies – PSG  Nerve Conduction/ EMGNerve Conduction/ EMG  EEGEEG  ALL INSURANCES ACCEPTEDALL INSURANCES ACCEPTED  Pres, Lovelace, BCBS, UHC, AETNA, CIGNAPres, Lovelace, BCBS, UHC, AETNA, CIGNA  MedicareMedicare  MedicaidMedicaid
  • 65. AthayaAthaya MedicalMedical CenterCenter New 15,000 sfNew 15,000 sf out patient facilityout patient facility IN CLOSE PROXIMITY TO 3 WEST SIDE/IN CLOSE PROXIMITY TO 3 WEST SIDE/ RIO RANCHO HOSPITALSRIO RANCHO HOSPITALS INVITES PRACTICES/ PROVIDERS TO STARTINVITES PRACTICES/ PROVIDERS TO START IN THE BOOMING PART OF CITYIN THE BOOMING PART OF CITY

Editor's Notes

  1. Athaya Commercial Space for Lease
  2. 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.
  3. 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).
  4. 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.
  5. 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.
  6. 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
  7. 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.
  8. 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.