Epidemiology of Sleep RLS Disorders Prevalence of 5-13% 1
↑ prevalence with age. Affects every race, socioeconomic class, and all ages F:M – 2:1 2
Positive FHx of RLS (familial pattern in > 50% of patient 70 million people in the U.S. have a sleep problem (NIH) with primary RLS)
Linked to chromosome 12q,14q and 9p 40-50 million adults suffer from a chronic sleep disorder Up to 50% of pts with RLS have Sx in the arms (NIH) Most episodes occur at midnight
80 % of patients with RLS have evidence of PLMS on PSG 3 Effects of sleep loss on work performance may be costing U.S. employer some $18 billion in lost productivity.
1-Sleep. 27 (3). P. 560-583. 2004 2-Neurology. 54 (5). P. 1064-8. 2000 (NSF 1997 poll on Sleeplessness, Pain and the Workplace) 3 -Mov Disor. 12; p. 61-65. 1997
Diagnostic Criteria for RLS in Etiology of RLS Patients Older than 12 y/o
Uremia - 15-40% of pts in HD complain of RLS
Urge to move with unpleasant sensations in the legs Neuropathies
Anemia - iron and folate deficiency
Begins or worsens during periods of rest or inactivity Fibromyalgia
Rheumatoid arthritis
Relieved by movement Anti histaminic drugs
Dopamine receptor antagonists (Ex. metoclopramide)
Worse in the evening or night SSRIs
TCAs
Caffeine
Diagnosis of RLS Supportive Clinical Features of RLS
Clinical Positive family history
Suggested by Immobilization Test (SIT)
- Evaluates for PLM of wakefulness (PLMW) Positive response to dopmaninergic therapy - Positive SIT for diagnosis of RLS if > 40 PLMWs per hour
- High diagnostic accuracy (sensitivity of 82% and Presence of PLMs (during wakefullness or sleep) specificity of 100%) 1
1 - Eur Neurol. 48 (2). p. 108-113. 2002
Sleep. 27 (3). P. 560-583. 2004 Differential Diagnosis of RLS Treatment of RLS
Positional discomfort Sleep hygiene
Sleep starts (hypnic jerks) No ETOH intake at night
PLMD Dopaminergic agents
Sleep-related leg cramps Opioids
Neuroleptic-induced akathisia Anticonvulsivants
Pain (peripheral neuropathy, spinal cord lesions, BZD arthritis) Iron (ferritin level < 50 µg/L or iron saturation < 16%) 1 Hypotensive akathisia
1- Age Ageing. 23, p. 200-203. 1994
Treatment Augmentation Effect
Gabapentin Earlier onset symptoms
Dopaminergic agonists ↑ severity of symptoms
Pramiprexole Spread of symptoms to arms
Ropinirole Occurs in higher doses of levodopa
Levodopa (morning rebound/augmentation) Is a dose phenomenon
Ergoline derivates (bromocriptine; pergolide; arbegoline Rx: - nausea, orthostatic hypotension) - Reduction or discontinuation of medication - Switch to other class or combine drugs
Rebound Associated Factors with RLS and PLMD
Is an end of dose effect Iron Defficiency Symptoms during the night or in the early morning
Not dopamine specific End Stage Renal dz, Parkinson’s dz, Attention-deficit hyperactivity dz, pregnancy, PTSD, Multiple Sclerosis Rx: ↑ dopamine dose or dopamine with ↑ half life Dopamine receptor Antagonists (metoclopramide, prochloperazine)
Antipsychotics
Most antidepressants (except bupropion)
Sleep. 2003;26:31-5 Narcolepsy Narcolepsy
Debilitating disease
Psychological impact 1880 by Jean Baptiste E. Gelineau Reduced quality of life
Marital difficulties Greek Socioeconomical impact - Narke = numbness -Total annual indirect cost in Germany – US$ 11,860 - Lepsis = attack, seizure -43% unemployment rate related to narcolepsy -Early retirement
SLEEP, Vol. 27, No. 6, 2004
Narcolepsy Cataplexy
Tetrad of symptoms Partial or complete muscle weakness - Excessive daytime sleepiness (± 100%) -Face - Cataplexy (± 85%) -Neck - Hypnagogic hallucinations (±60%) - Legs/knee - Sleep paralysis (±60%) - Total body
Patients aware of their surroundings
Pentad – Fragmented nocturnal sleep (±50%) Last from several seconds to 2 minutes
Slurred speech may be present
Elicited by emotion or stress.
Hypnagogic or Hypnopompic Sleep Paralysis Hallucination
Vivid, frightening dreams Transient unable to move before sleep onset or just after awakening. Sensation of flying
Occur at the time of transition from wakefulness into sleep or the reverse. Clinical Presentation Associated Features
Psychosocial problems
Sleep attacks on a background of chronic sleepiness or Depression fatigue Headaches Restorative sleep Frequent Misdiagnoses Frequent napping, usually refreshing - Major depression Memory lapses - Thyroid disorder Impaired attention / concentration - Chronic fatigue syndrome - Decreased work performance - Schizophrenia - Increased drowsiness (accidents) - Recreational drug use Visual disturbances - Poor sleeping habits
Epidemiology Epidemiology
Prevalence - 168 to 799 per100,00 Associated with obesity
Incidence – 0.74 per 100,000 person-years for Narcoleptics with lower CSF hypocretin-1 had higher BMI narcolepsy with cataplexy when compared to those narcoleptics with higher CSF hypocretin-1 levels
Incidence – 1.37 per 100,000 person-years for narcolepsy with or without cataplexy Increased incidence of narcolepsy when birth is in first half of the year, especially in the spring and during March (France, US, Canada) M > F
Sleep, Vol. 30, No. 1, 2007 Sleep, Vol. 30, No. 1, 2007
Etiology Etiology
Unknown Narcolepsy without cataplexy can be caused by a localized loss of hypocretin cells
Familial – 40-fold increase in first degree relatives 1 CSF hypocretin levels can be normal even when there is a substantial loss of hypocretin cells. Loss of Hypocretin -containing hypothalamic neurons
1- Sleep, Vol. 27, No. 6, 2004 SLEEP, Vol. 32, No. 8, p. 993-8, 2009 Etiology Etiology
In the area of isolated narcolepsy, there are reports, in the ↑ HLA-DQB1*0602 but also ↑in 12-38% of normal northern hemisphere, that narcoleptic patients are more often population born in March and less often born in September.
HLA-DQB1*0602 present in 88-98% of patients with 1 cataplexy It raises the possibility that prenatal or early postnatal Auto immune component: environmental influences may influence the subsequent development of the disorder. -Is Associated with a polymorphism in the T-cell receptor alpha gene 2 -↑anti-TRIB (tribbles) 2 antibodies 2
Environmental factors
? Association with H1N1 infection or vaccination 3
1-Am J Hum Genet 2001;68:686-99 2-Sleep, Vol.33, No. 7, 2010 3-Sleep, Vol. 33, No. 11, 2010 SLEEP, Vol. 27, No. 6, 2004
Immunologic Relation Onset of symptoms
Compared to controls, ASO (anti-streptolysin O)and ADB Usually begin by puberty (anti DNAse B) titers were highest close to narcolepsy onset, and decreased with disease duration Peak of age onset is 15 to 25 y/o Suggest that selected streptococcal infections may lead to the destruction of hypocretin neurons via molecular mimicry or superantigen interactions with the HLA-TCR Second smaller peak is between 35-45 y/o and near complex, or that infections could simply make it menopause in women. permissive for other, more specific factors to trigger narcolepsy
Streptococcal infections are probably a significant ± 15 year delay – onset to diagnosis environmental trigger for narcolepsy
SLEEP, Vol. 32, No. 8, p. 979-83, 2009
Diagnostic Evaluation PSG Findings
History Short sleep latency
- Sleepiness, cataplexy, other disassociated REM sleep Sleep onset REM period in 50% of narcoleptics features Sleep fragmentation (REM and NREM) Polysomnography (PSG) - Increased number of arousals - Exclude other causes of hypersomnia - Increased stage 1 sleep - Identify and treat associated conditions - Low sleep efficiency Multiple Sleep Latency Test (MSLT) Frequently associated with periodic leg movements - Objective sleepiness - Sleep onset REM periods (SOREMPs) MSLT Factors Affecting MSLT
Standardized protocol Sleep disruption and other sleep disorders
Four to five 20-minute naps Sleep deprivation / extension
Stop test 15 minutes after sleep onset Circadian factors / shift work
Always performed after a nocturnal polysomnogram Hypnotic agents / alcohol After appropriate withdrawal of any psychotropic drugs Caffeinated substances
Psychological stimulation Measures sleep latency and SOREM
Diagnostic Criteria Differential Diagnosis of Hypersomnia
Complaint of EDS occurring almost daily for 3 months OSA
± history of cataplexy Insufficient sleep syndrome
Confirmed by mean SL ≤ 8 min + 2 or more SOREMPs Delayed or advanced sleep phase (considering diagnostic polysomnography and MSLT) Shift work Alternative - CSF hypocretin-1 level ≤ 110pg/ml or 30% Jet lag of normal control values Major depression No other better explanation for the hypersomnia Chemical dependency (ETOH and others) Genetic testing (DQB1*0602) – non diagnostic Idiopathic hypersomnia
PLMD
Malingering and secondary gain
Secondary Narcolepsy Treatment in Adults
3rd ventricular lesions (hypothalamus, and midbrain by Avoid shift in sleep schedule tumors) Avoid heavy meals and alcohol intake Acute disseminated encephalomyelitis Regular timing of sleep Hypothalamic sarcoidosis Naps during the daytime Histiocytosis X Pharmacotherapy Multiple sclerosis
Parkinson’s disease Pharmacology Pharmachotherapy: Hypersomnia
Alpha-1b-noradrenergic antagonists (Prazosin) worsen Stimulants cataplexy - Effective treatment for EDS Alpha-2 receptor antagonists (yohimbine) reduced - Establish accurate diagnosis prior to treatment cataplexy Treatment objectives Central dopamine D2 receptor agonists suppress cataplexy - Alleviate daytime sleepiness - Not to enhance performance on attention tasks Atropine and scopolamine, which cross the blood-brain barrier, and are muscarinic receptor blocker, decrease Effective medications: cataplexy Sodium oxybate, Modafinil; Armodafinil; Methylphenidate; Pemoline; Methamphetamine; Dextroamphetamine
Treatment of Hypersomnia Pharmachotherapy
Modafinil, Armodafinil (no anti catapletic activity) Sodium oxybate Amphetamine (may have some anti catapletic activity)
Sodium Oxybate - 4.5 to 9 g/day Catapletic attacks - when switching from amphetamine - Two divided doses to modafinil or armodafinil
Rx in children: modafinil, armodafinil and methylphenidate.
Sodium oxybate Pharmachotherapy: Hypersomnia
Primarily indicated for the treatment of cataplexy Modafinil - 200 to 800 mg/day Improves also daytime sleepiness - starting at 4 weeks and having a maximal effect at 8 weeks Armodafinil - 50 to 250 mg /day Adverse effects: nausea, headache, dizziness or somnolence, pain, enuresis, and viral infection
Nonsignificant decreases in hypnagogic hallucinations and sleep paralysis also reported starting 1 month after treatment
Sleep 2003;26:31-5 Pharmachotherapy: Pharmachotherapy: Hypersomnia Hypersomnia
Methylphenidate Dextroamphetamine / Methamphetamine - 5 to 100 mg/day - 5 to 100 mg/day - Short half life formulation, variable dosing - Short and long half life formulation - Used alone or in combination - Most efficacious - Sympathomimetic effects, mood alterations - Sympathomimetic effects, mood alterations
Adverse Effects of Stimulants Rx of Cataplexy or REM phenomena
Irritability, Personality Changes, and Psychosis Tricyclic antidepressants
Insomnia - Protriptyline (10 to 60 mg/day)
Aggressiveness - Clomipramine / Imipramine (25 to 150 mg/day)
Rapidity of Thought - Anti-cholinergic side effects
Tremor and Jitteriness Selective serotonin re-uptake inhibitors - Fluoxetine / Paroxetine (20 to 60 mg/day) Hypertension - Better tolerated but higher dose often needed Tolerance and Drug Dependence Miscellaneous treatments - Venlafaxine (75 to 150 mg/day) - Sodium Oxybate (4.5 to 9 g/day) - MAO Inhibitors
Psychosocial and Educational Sleep Disordered Breathing Aspects
Refer to support groups (e.g. Narcolepsy Network)
National Narcolepsy Registry participation
Consider psychological impact
Possible work, school and family interventions
Medicolegal aspects (e.g. driving, Americans with Disabilities Act, confidentiality)
Disability benefits Prevalence of Moderate to Risk Factors associated with Severe SDB in the USA OSA
Stroke 1
Death from any cause 1, 2 Men Women Arterial hypertension 1, 3
Atrial fibrillation 4 30 – 49 y/o 10 % 3 % Motor vehicle accidents 5
Pulmonary Hypertension 6 50 – 70 y/o 17 % 9 % Nocturnal Asthma 6
Insulin Resistance 6
1 – NEJM. 2005 Nov 10;353(19):2034-41 2 -Sleep. 2008 Aug;31(8):1079-85 3 – NEJM. 2000 May 11;342(19):1378-84 4 – Circulation. 2004 Jul 27;110(4):364-7 5 - Respiration. 2009;78(3):241-8 Am J Epidemiol. 2013 May 1;177(9):1006-14. 6 - NEJM, Vol. 334, No.2, P. 99-104, 1996
Snoring Obstructive Apnea
Heavy snoring increases risk of carotid atherosclerosis
Mild Snoring – 0 to 25 % night snoring had 20% prevalence of carotid atherosclerosis
Moderate Snoring – > 25 to 50 % night snoring had 31% prevalence of carotid atherosclerosis
Severe Snoring - > 50% night snoring had 64% prevalence of carotid atherosclerosis
Independent of age, HTN, smoking h/o, sex, nocturnal hypoxemia and OSA severity but patient’s with heavy snoring were patient’s with greater BMI, greater degree of dyslipidemia, greater AHI
Sleep, Vol. 31, No 9, 1207-13. 2008
Central Apnea Hypopnea Cheyne-Stokes Respiration Sleep Apnea: Clinical Features
Daytime fatigue / sleepiness Snoring Observed apnea Choking awakenings Obesity Craniofacial abnormalities Nocturia Non-restorative naps Headache
Sleep Apnea: Common Causes Sleep Apnea: Other Causes
Nasal obstruction Down’s syndrome
Adenotonsilar hypertrophy Pharyngeal flap for cleft palate
Retrognathia Hypothyroidism
Obesity
Physical Exam SDB Screening
Tongue/Palate
S (snore) T (tired) O (obstruction) P (pressure)
1234 B (BMI) greater than 35 A (age) 50 years old or Tonsil older N (neck) greater than17 inches or a female greater than 16 inches G (gender) - Male
1234 Severity of OSDB Obstructive Sleep Apnea
Increased risk Mild – AHI ≥ 5 and < 15 events per - Hypertension (greater association with OSA if hypersomnia is hour present) 1 - Insulin resistance 2 - Pulmonary hypertension 2 Moderate – AHI ≥ 15 and < 30events 2 per hour - Cardiac arrhythmias - CAD / MI 2 - Nocturnal asthma 2 Severe – AHI ≥ 30 events per hour -CVA 2 - Right and left ventricular failure 2
1. SLEEP, VOL. 31, NO. 8. P 1127-32 Sleep 1999, 22:667-689 2. NEJM, VOL. 334, NO.2, P. 99-104, 1996
The Sleep Health Heart Study The Sleep Heart Health Study
Men > 40 and < 70 y/o with AHI >30 were 68% more likely to develop coronary heart disease (MI, revascularization procedure or coronary heart disease death) than those with AHI < 5 but not in men >70 y/o or women of any age
Men with AHI > 30 but not women were 58% more likely to develop heart failure than those with AHI < 5
Circulation. 2010; 122:352-360 Circulation. 2010;122:352-360
The Sleep Health Heart Study The Sleep Heart Health Study
Mean age 65 ± 12 years
AHI < 5 had LV mass index of 41.3 g/m2
AHI > 30 had LV mass index of 44.1 g/m2
Sleep Apnea: Associated with echocardiographic evidence of increased LV mass and reduced LV systolic function
Circulation. 2010;122:352-360 Circulation. 2008; 117:2599-2607 Sleep apnea and SCD Atrial Fibrillation and OSA
70
Braunwald Heart Diseases OSA, obesity and the risk of incidence of Atrial fibrillation – J Am Coll Cardiol 49-565, 2007
Resistant HTN SDB and Arrhythmias
OSA independent risk Patients with untreated OSA have a higher recurrence of Atrial Fibrillation after cardioversion than patients factor for resistant without a polysomnographic diagnosis of sleep apnea. hypertension
Appropriate treatment with CPAP in OSA patients is associated with lower recurrence of AF – 82 % VS 42%. recurrence in 12 months post cardioversion.
53% recurrence in patients not tested with PSG.
CHEST 2007; 132:1858–1862 Circulation. 2003;107:2589-2594
OSA and Heart Failure Wisconsin Sleep Cohort SDB and Mortality – 18 year f/up OSA seen in 11 % to 37 % of patients with HF 1
38% Males – 31 % Females diagnosed with OSA in pts with Increased all –cause mortality risk was significantly HF 1 increased with SDB severity Cheyne – Stokes respiration associated with CHF and Results unchanged after accounting for EDS poor prognosis Mean observation period – 13.8 years OSA associated with significant increase in likelihood of CHF Average age of deaths – 61.1 years
Circulation. 2008; 118 Sleep, Vol. 31 No. 8, p 1071-8. 2008 Wisconsin Sleep Cohort Sleep Monitoring Device SDB and Mortality – 18 year Types f/up Type I (Attended PSG) All cause mortality - Minimum of 7 channels AHI < 5 - 2.85 per 1000 person-year - Documents body position, leg movement AHI 5 < 15 - 5.40 per 1000 person-year - Intervention is possible during test AHI 15 < 30 - 5.42 per 1000 person-year Type II (HSAT): AHI ≥ 30 - 14.6 per 1000 person-year - Minimum of 7 channels
Cardiovascular death - Monitors sleep stage
Without SDB – 26% Type III (HSAT): With Severe SDB – 46% - Minimum of 4 monitored channels including ventilation CPAP was protective or airflow
Sleep, Vol. 31 No. 8, p 1071-8. 2008
HSAT Devices by SCOPER Categorization
Scheme based upon sensors used to measure:
Sleep
Cardiovascular
Oximetry
Position
Effort
Respiratory
JCSM, Vol. 7, No. 5. P.531-548. 2011 JCSM, Vol. 7, No. 5. P.531-548. 2011
Billing Codes for HSAT Indications for HSAT
Type II device In patients with high pre test probability of moderate to G0398 - $196 ($65.9 for 26; $130.1 for TC) severe OSA (without comorbidities or other sleep 95806 - $195 ($64.8 for 26; $130.8 for TC) disorders)
Type III device In patients where in lab-PSG is not possible due to immobility, safety, or critical illness. G0399 - $147 ($59.7 for 26; $87.7 for TC)
95806 - $195 ($64.8 for 26; $130.8 for TC) To monitor the response of non CPAP treatment for OSA
Type IV device
G0400 - $98 ($53.4for 26; $45.3 for TC)
95801 - $101($50.7for 26; $50.8 for TC)
Predicted CMS for the year of 2016 JCSM. 2007. Vol. 3 (7). P.737-747. Indications for HSAT Contra Indication for HSAT
If significant co-morbid medical conditions is present, like: - Moderate to severe pulmonary disease In conjunction with a comprehensive sleep evaluation - Supervised by a Board Certified or Eligible Sleep - Neuromuscular disease Physician 1 - Congestive heart failure Other sleep disorders, like: Board certification improves outcomes in patients with - Central sleep apnea OSA. 2 -PLMD - Insomnia - Parasomnias - Circadian rhythm disorders -Narcolepsy
Not indicated for general screening of asymptomatic
1 - JCSM. 2007. Vol. 3 (7). P.737-747. patients 2 - JCSM. 2006; Vol. 2. P. 133-142. JCSM. 2007. Vol. 3 (7). P.737-747.
Validation of a Portable Results Monitoring System for the Diagnosis of OSAS 82 pts recruited – 10 were pts without suspicion of OSA Type III (Stardust II ) 2 pts data were dropped due to incomplete rec. results Referred for EDS, Snoring, Witnessed apnea 10 pts had technical problems during HST recording Age – 47 ± 14 2 records HST data were lost due to equipment M:F % - 57:43 malfunction
BMI kg/m2 - 28 ± 5 8 recordings had loss of data including SpO2 and belt signal but > 80% of recording was still available Neck circumference, cm – 36.6 ± 4.9 22 (26.8%) - Suboptimal Studies SBP - 129 ± 17 and DBP – 85 ± 15
ESS – 10.4 ± 5.8
Snore reported – 87%
EDS reported – 88%
SLEEP 2009;32(5):629-636. SLEEP 2009;32(5):629-636.
Results Factors that may affect type 3 PSGs accuracy
Sensitivity decreased and specificity increased in direct Data loss relation with increase in AHI Poor data quality
↓ % of supine sleep Good agreement if AHI ≥ 30 AHI calculate by TIB and not TST
Underestimation of hypopneas Diagnostic agreement of PSG vs HST– 83%
Overestimation of AHI comp PSG vs HST– 20%
Underestimation of AHI comp PSG vs HST– 5%
SLEEP 2009;32(5):629-636. Otolaryngol Head Neck Surg. 2006 Feb;134(2):204-9. Factors that may affect type Non Diagnostic HST 3 PSGs accuracy
False negative rates may be as high as 17% in unattended HST.
Perform in-laboratory PSG in patients with high pretest probability for the diagnosis of OSA if:
- HST study was inadequate
- HST fails to establish the Dx of OSA
Otolaryngol Head Neck Surg. 2006 Feb;134(2):204-9.
Effect of recording duration Effect of recording duration on the diagnostic accuracy of on the diagnostic accuracy of OCST for OSA OCST for OSA
SLEEP 2014;37(5):969-975. SLEEP 2014;37(5):969-975.
Effect of recording duration An Integrated Health- on the diagnostic accuracy of Economic Analysis of OSA by OCST for OSA Pietzsch et al
Conclusion: at least 300 min recording time during out-of- center sleep testing is needed for accurate diagnosis of obstructive sleep apnea and determination of obstructive sleep apnea severity.
SLEEP 2014;37(5):969-975. JCSM, Vol. 34, No. 6. P695- 709. 2011 An Integrated Health- Treatment modalities Economic Analysis of OSA by Pietzsch et al Lifestyle changes:
Considering AHI ≥ 15 Fitness
False positive studies Diet
22% of patients may experience a technical failure or a Avoid sleep deprivation negative ambulatory study Positional therapy: Lateralposition or Elevated HOB Full-night PSG is cost-effective and is the preferred diagnostic strategy for adults suspected to have Protriptyline and fluoxetine moderate-to-severe OSA when all diagnostic options are Bariatric surgery available PAP via mask
Oral appliances
JCSM, Vol. 34, No. 6. P.695- 709. 2011 NEJM, Vol. 334, No.2, P. 99-104, 1996
Treatment modalities PAP Compliance Predictors
Surgical - SE Improvement – 6.12 +/- 2.25 hours/night of CPAP use Upper airway bypass (tracheostomy) - SE NOT Improved – 4.09 +/- 2.52 hours/night of CPAP UPPP use Laser assisted uvulo-palatectomy
Radiofrequency Initial experience with CPAP treatment improvement in Palatal implants sleep during CPAP titration may be crucial factors in determining future use of CPAP Retrolingual pharynx: mandibular advancement, lingual plasty and resection, mandibular osteotomy, genioglossus advancement with hyoid myotomy & suspension (GAHM), and maxillary & mandibular advancement osteotomy(MMO)
SLEEP, Vol. 26, No. 3, p. 308-311. 2003
First Night Use and Long term Symptoms and Severity of SDB PAP Compliance Predicting PAP Compliance
Problems after the first night reported: 1
- YES - PAP compliance of – 2.4 hours/night Snoring history 1 - NO - PAP compliance of – 5.0 hours/night
Compliance of > 4 hours per night in the first 3 night: 2 AHI > 30 1 - YES – PAP of 84% compliant by 30 days - NO – PAP of 26% compliant by 30 days History of hypersomnia - ??? 1,2 Long-term adherence to CPAP can be predicted as early as 3 days following CPAP initiation 2
First Night use of CPAP seems the most important predictor of ensuing machine use 1
1- SLEEP, Vol. 27, No. 1, p. 134-138. 2004 1 - AJRCCM , 159:1108-14. 1999 2- SLEEP, Vol. 30, No. 3, p. 320-324. 2007 2 - SLEEP, Vol. 27, No. 1, p. 134-138. 2004 Type of PAP device and C-Flex Technology Compliance VS Regular CPAP
BPAP is as effective and has same compliance as CPAP Severe OSA
Mean PAP of 11.6 cmH2O
CPAP use – 5.6 +/- 1.4 hrs/night 3 months compliance
BPAP use – 5.6 +/- 1.7 hrs/night Median Compliance:
C-Flex – 5.51 hrs/night
CPAP use > 4 hrs/night – 80.5 % of days Regular CPAP – 5.89 hrs/night
BPAP use > 4 hrs/night – 77.6 % of days
SLEEP, Vol. 26, No. 7, p. 864-869. 2003 SLEEP, Vol. 33, No.4, p. 523-529. 2010
APAP VS Fixed CPAP Tongue-retaining Device
Mean APAP pressure: 6.3 +/- 1.4 cmH2O
Mean CPAP pressure: 8.1 +/- 1.7 cmH2O
Compliance after 18 months:
APAP – 4.9 +/- 2.1 hrs/night
CPAP - 4.9 +/- 1.9 hrs/night
Similar side effects:
Dry mouth
Runny nose
Mask leak
Pressure felt too high
Claustrophobia
SLEEP, Vol. 30, No.2, P. 189-194. 2007
Mandibular Advancement Mandibular Advancement with Oral Appliance with Oral Appliance
Treatment adherence – median of 77% of nights at 1 year 1
Minor adverse effects - Minor tooth movement and small changes in the occlusion developed in some patients after prolonged use, but the long-term dental significance of this is uncertain
OAs are less efficacious than CPAP in reducing the apnea hypopnea index (AHI)
OAs have also been compared favorably to surgical modification of the upper airway (uvulopalatopharyngoplasty, UPPP)
SLEEP, Vol. 29, No. 2, 2006 Nasal EPAP Device Nasal EPAP Device
SLEEP, Vol. 34, No. 4, 2011 SLEEP, Vol. 34, No. 4, 2011
Nasal EPAP Device Nasal EPAP Device
SLEEP, Vol. 34, No. 4, 2011 SLEEP, Vol. 34, No. 4, 2011
UPPP Tonsillar Hypertrophy
Surgical success - 50% or greater reduction in the apnea- hypopnea index and a postoperative apnea-hypopnea index of less than 20 events per hour
Overall success rate of UPPP was 78%
Success rates for:
Mild (AHI<15) - 90%
Moderate (AHI 15-29) - 73%
Moderate-severe (AHI 30-59) - 81%
Severe (AHI ≥ 60) - 74%
SLEEP, Vol. 29, No. 12, 2006 , P. 1537 -41. Hypoglossal Nerve Stimulator Pre-op UPPP Post-op UPPP •Synchronous stimulation
NEJM 370;2. 2014. P. 139-149
Hypoglossal Nerve Stimulator Hypoglossal Nerve Stimulator
NEJM 370;2. 2014. P. 139-149 NEJM 370;2. 2014. P. 139-149
NEJM 370;2. 2014. P. 139-149 NEJM 370;2. 2014. P. 139-149 Adverse Events Palatal Implants Overall rate of serious adverse events was less than 2%.
2 serious device-related adverse event requiring repositioning and fixation of the neurostimulator to Polyethelene stays placed into uvular tissues resolve discomfort.
Total of 33 serious adverse events not considered to be Adds rigidity to upper airway related to the implantation procedure or implanted devices Indicated for snoring, not OSA 18% of the participants had temporary tongue weakness after surgery
40% of the participants reported some discomfort associated with stimulation
In 9 pts , a tooth guard was used to resolve tongue soreness or abrasion related to the device
NEJM 370;2. 2014. P. 139-149
Palatal Implants: Positions of Devices in the Soft Palate
Wai-kuen Ho, FRCSEd; William I. Wei, FRCS; Ka-fai Chung, MRCPsych Arch Otolaryngol Head Neck Surg. 2004;130:753-758