sleep related breathing · pdf filesleep related breathing disorders ... usually most severe...

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Sleep Related Breathing Disorders

Elisabeth Brandauer, MD Department of Neurology, Innsbruck Medical University, Austria

Movement Disorders in SleepBarcelona, Jan 30-31

Abnormalities of respiration during sleep

Possible location of respiratorydisturbances :

• Central respiratory drive• Oropharyngeal muscles• Respiratory muscles• Ventilation

Possible consequences:

• Snoring• Apneas, Hypopneas• Hypoxemia• Hypercapnia

Apnea: drop in the peak thermal sensor excursion by >90% of baseline, duration at least 10 sec.

– obstructive apnea– central apnea– mixed apnea

Definitions

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Hypopnea:• The nasal pressure signal excursion drop by >30% of baseline, duration at least

10 sec.• There is a >3% oxygen desaturation from pre-event baseline or the event is

associated with arousal

Oxygen desaturation index(ODI):� number of desaturation per

hour of sleep

Apnea-hypopnea index (AHI):� Number of apneas and

hypopneas per hour of sleep

Classification

Obstructive Sleep ApneaDisorders

• Obstructive Sleep Apnea, Adult• Obstructive Sleep Apnea, Pediatric

Central Sleep Apnea Syndromes• Central Sleep Apnea with Cheyne-Stokes

Breathing• Central Apnea Due to a Medical Disorder

without Cheyne-Stokes Breathing• Central Sleep Apnea Due to High Altitude

Periodic Breathing• Central Sleep Apnea Due to a Medication

or Substance• Primary Central Sleep Apnea• Primary Central Sleep Apnea of Infancy• Primary Central Sleep Apnea of

Prematurity• Treatment-Emergent Central Sleep Apnea

Sleep Related Hypoventilation Disorders

• Obesity Hypoventilation Syndrome • Congenital Central Alveolar Hypoventilation

Syndrome • Late-Onset Central Hypoventilation with

Hypothalamic Dysfunction• Idiopathic Central Alveolar Hypoventilation• Sleep Related Hypoventilation Due to a

Medication or Substance• Sleep Related Hypoventilation Due to a

Medical Disorder

Sleep Related HypoxemiaDisorder

• Sleep Related Hypoxemia

Isolated Symptoms and Normal Variants

• Snoring• Catathrenia

Obstructive Sleep Apnea

�A. The presence of one or more of the following:

�The patient complains of sleepiness, nonrestorative sleep, fatigue, or insomniasymptoms�The patient wakes with breath holding, gasping or choking.�The bed partner or other observers reports habitual snoring, breathinginterruptions, or both during the patients sleep.�The patient has been diagnosed with hypertension, a mood disorder, cognitivedysfunction, coronary artery disease, stroke, congestive heart failure, atrialfibrillation, or type 2 diabetes mellitus

• (A and B) or C satisfy the criteria

�B. Polysomnography (PSG) or OCST (out-of-center sleep testing) demonstrates:

�Five or more predominantly obstructive respiratory events (obstructive and mixedapneas, hypopneas, or respiratory effort related arousals (RERAs) per hour of sleepduring PSG or per hour of monitoring in OCST

�C. PSG or OCST demonstrates:. The presence of one or more of the following:

�Fifteen or more predominantly obstructive respiratory events per hour of sleep duringa PSG or per hour of monitoring

International Classification of Sleep Disorders 3rd

American Academy of Sleep Medicine, 2014

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Predisposing Factors: � Obesity

� Male>female� Prevalence increases with age with a plateau reached app. at age 65

� Alcohol consumption and sedating medication� menopause

� Endocrine disorders (hypothyroidism, acromegaly)

� Maxillomandibular malformation, adenotonsillar enlargement� First degree relatives of OSA patients are twice as likely to have OSA

Demographics:� 9% of females and 24% of males between 30-60 years with criterion

AHI>5/h;

2% of females and 4% of males using the criterion AHI>5/h plus exzessive daytime sleepiness (Young et al. 1993)

� 3-7% of adult males, 2-5% of adult females (Punjabi 2008)



Pathophysiology:

� Reduced cross sectional area of the upper airway lumen due toexcessive bulk of soft tissues or craniofacial anatomy

� During inspiration negative pressure is generated in the lumen of theupper airway

� Activity of pharyngeal dilating muscles becomes insufficient in OSA

� Further reduction of activity in these muscles in REM sleep

� Event termination may occur with or without arousal:

� Some events resolve with augmentation of muscle tone fromchemical and mechanical stimuli

� Others resolve with arousals

Graduation: � Mild OSA: AHI > 5/h� Moderate OSA: AHI 15-30/h� Severe OSA: AHI > 30/h



� Clinical history

� Scales (e.g. Epworth Sleepiness Scale)

� OCST (out of center sleep testing)

� Polysomnography

� Testing daytime symptoms� Neuropsychological testing systems� Multiple Sleep Latency Test

Diagnostic steps

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OCST

Polysomnography

� Excessive daytime sleepiness, reduction in quality of life

� Risk of accidents sixfold higher (Teran-Santos et al. 1999)

� Cognitive impairment, depression

� Cardiovascular risks: systemic hypertension („non dipping“),coronary artery disease, congestive heart failure, stroke, cardiac arrhythmias,

� Hints on elevated levels of circulating inflammatorymediators related to repetitive episodes of oxygendesaturation and increased sympathetic nervous systemactivity

Complications

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� Weight reduction, prevention of alcohol andsedative medication

� Prevention of back position

� Positive airway pressure therapy

� Mandibular advancement devices

� Surgery (UVPP, surgery of tongue, tonsillectomy, hypoglossal nerve stimulation)

Therapy

� CPAP (continous positve airway pressure)� APAP (automatically adjusting positive

airway pressure)

Positive airway pressure therapy

Effect of CPAP therapy

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Central Sleep Apnea Syndromes

� Central Sleep Apnea with Cheyne-Stokes Breathing

� Central Apnea Due to a Medical Disorder withoutCheyne-Stokes Breathing

� Central Sleep Apnea Due to High Altitude PeriodicBreathing

� Central Sleep Apnea Due to a Medication orSubstance

� Primary Central Sleep Apnea

� Primary Central Sleep Apnea of Infancy

� Primary Central Sleep Apnea of Prematurity

� Treatment-Emergent Central Sleep Apnea



Common features

– AHI > 5/h– Number of central apneas/hypopneas > 50%

Abb: central apneas, Polysomnography

Central Sleep Apnea with Cheyne-Stokes breathing

– Presence of atrial fibrillation/flutter, congestiveheart failure or a neurological disorder

– Therapy: adaptive Servo-ventilation


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Due to medication orsubstances:� e.g opioids

Primary Central Sleep Apnea� rare� Arterial pCO2 drops below the hypocapnic apnea treshold� Frequent arousals from sleep predispose to central apneas

Treatment Emergent Central Sleep Apnea� Central apneas due to CPAP

treatment


� Obesity Hypoventilation Syndrome � Congenital Central Alveolar Hypoventilation Syndrome

� Late-Onset Central Hypoventilation with Hypothalamic Dysfunction

� Idiopathic Central Alveolar Hypoventilation

� Sleep Related Hypoventilation Due to a Medication or Substance� Sleep Related Hypoventilation Due to a Medical Disorder

Common features:� Insufficient sleep related ventilation, resulting in abnormally

elevated PaCO2

� Oxygen desaturation may be present, not necessarily

� Scoring Hypoventilation: rise of pCO2 > 55mmHg for> 10min orrise of pCO2 during sleep> 10mmHg and pCO2>50mmHg for>10min




Obesity Hypoventilation Syndrome

� Presence of hypoventilation during wakefulness(PaCO2>45mmHg)

� Obesity (BMI>30kg/m2)

� Hypoventilation is not primarily due to other disease

� OSA is often present (80-90%)

� Symptoms like in OSA, hypersomnolence is common

� Therapy: CPAP, adaptive Servoventilation

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Congenital Central Alveolar Hypoventilation (Ondine´s curse)

� Sleep related hypoventilation

� Mutation of gene PHOX2B

� Some central apneas may occur, but the predominant pattern isreduced flow/tidal volume

� Some patients may present phenotypically later in life


Sleep Related Hypoventilation due to a Medical Disorder

� Lung parenchymal or airway disease, pulmonary vascularpathology, chest wall disorder, neurologic disorder, muscleweakness

� Usually most severe in REM sleep


Sleep Apnea in Movement Disorders

� Parkinson´s Disease

� Multiple System Atrophy� Occurence of OSA, central sleep apnea, irregular and apneustic

breathing, Cheyne Stokes breathing pattern, stridor

� Due to damaged brainstem structures controlling respiration

� OSA occurs more frequently than central sleep apnea

Caig and Iranzo, 2012

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Sleep Apnea in Parkinsons disease

• Controversial results on prevalence of SDB in PD

n Manifest or subclinical sleep breathing disorders in 50% of PD patients, but

sleep structure not normalized with nCPAP treatment (Schäfer 2001)

• Moderate or severe obstructive sleep apnea syndromes in 20%(Arnulf 2002)

• 43 % sleep apnea syndrome, mostly mild or moderate with little oxygendesaturations (Diederich 2005)

• Significant correlation of heavy snoring and ESS in PD and controls• (Högl et al 2003, Braga Neto 2006)

• Sleep apnea in PD less frequent than in sick in hospital controls (Arnulf 2009)


• Pathophysiology: Upper airway obstruction present in 24-65% of PD

patients, thought to be related to hypokinesia and rigidity involving

the upper airway (Sabate 1996, Shill 2002)

• PD patients might be protected from OSA due to lower body weight

and muscle atonia during REM sleep

• Review of da Silva-Junior 2014: neither obstructive nor central

disordered breathing events were more frequent in PD patients


• Excessive daytime sleepiness does not correlate with AHI in

PD patients (da Silva-Junior 2014, review)

• SDB in PD does not seem to be a disease related process,

more an aging related conditon (da Silva-Junior 2014, review)

• CPAP treatment should be done when necessary, and it is

effective (Neikrug 2014)

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