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Sleep Disorders

Terms in this set (140)

sleep definition
A reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment


Is a natural physiologic activity essential for good quality of life and indeed species survival
Why do we need to sleep?
To recover from fatigue

Memory consolidation

Tissue repair

Recover brain function at cellular and brain network levels
Sleep Deprivation
Physiologic effects
Alterations in immune function

Cardiovascular system

Circulating levels
Sleep Deprivation
Physiologic effects

changes in circulating levels of
growth hormone

thyroid stimulating hormone

thyroxine

cortisol

adrenaline
Sleep Deprivation

adverse effects
increasing sleepiness

cognitive defects

concentration

short and long term memory

effects on mood
Sleep Deprivation

adverse effects:
effects on mood
irritability

depression
How much sleep do we need?

teen
9 hours
How much sleep do we need?

adult
7-8 hours
How much sleep do we need?

older adults
same as young adults (9 hours)
we need to ______ lost sleep in a state of ________
make up

sleep debt
consequences of lack of sleep
impairment of judgement

diminished reaction time

daytime sleepiness

low productivity

incr risk of motor vehicle accidents
conditions that favor a good sleep environment
safe, quiet, comfortable

low-level stimuli will have little or no influence on the sleep quality of a healthy person
pain and sleep
effect of acute pain
an unexpected pain (tooth ache or back pain) can generate a clear awakening response that may trigger anxiety and impede subsequent sleep

once the cost of pain has been addressed, sleep will continue with no issues
Pain and Sleep
Effect of Chronic Pain
is sleep a simple diminution of brain activity?
NO

(It is not just a matter of our bodies "turning off " for several hours followed by ours bodies "turning back on" when we awake)
sleep is a series of _______________: sequence governed by a group of _______
PRECISELY controlled brain states

brainstem nuclei
sleep is a very _______ involving ___________ measured by ____________
active state

brain waves activity

an electroencephalogram (EEG)
types of sleep
Non-rapid eye movement (NREM)

Rapid eye movement (REM)
Non-rapid eye movement (NREM)

stages
light sleep (N1)

Deep sleep (N2)

Deepest sleep (N3) - Dominated by slow-wave brain activity
sleep architecture

% of sleep cycle
brain waves types
beta waves
alpha waves
theta waves
delta waves
beta waves
awake

here we are busily engaged in activities and conversation
alpha waves
very relaxed

deepening into meditation

low amplitude, high frequency but diminished compared to beta waves
theta waves
N2 stage

drowsy and drifting down into sleep and dreams

mid amplitude and slower waves
delta waves
N3 stage

deeply asleep and not dreaming

high amplitude, low frequency
Stage 1 Non REM (N-1)

arousal threshold
low
Stage 1 Non REM (N-1)

EEG
Decreased frequency: 4-8 Hz

increased amplitude (theta waves)
Stage 1 Non REM (N-1)

characteristics
light sleep (drowsy)

occasionally muscle twitching
Stage 1 Non REM (N-1)

duration
1-5 mins
Stage 2 Non REM (N-2)

arousal threshold
higher than N-1
Stage 2 Non REM (N-2)

EEG frequency
10-12 Hz oscillations called spindles

theta waves
Stage 2 Non REM (N-2)

characteristics
most of sleep spent here

slower RR and HR

slight decrease in body temperature

most bruxers brux here
Stage 2 Non REM (N-2)

duration
10-25 mins
Stage 3 Non REM (N-3)

arousal threshold
much higher

Hard to wake a person
Stage 3 Non REM (N-3)

EEG
brain begins to generate delta waves
Stage 3 Non REM (N-3)

characteristics
most "restorative" phase

deep sleep begins

decreased muscle tone

decreased HR, BP, RR, temperature
REM Sleep

aka
paradoxical sleep

dream sleep
REM Sleep

characteristics
Decreases with increasing age

Increased BP, HR, metabolism

pupillary constriction

dreaming occurs in this stage
REM sleep

movement
Rapid, ballistic eye movement

Paralysis of many large skeletal muscles EXCEPT diaphragm muscle

Twitching of the smaller muscles in fingers, toes and middle ear
sleep stages and waves summary
there are 5 stages instead of 4 because in the past NREM sleep was divided into 4 stages

the cycle occurs 3-4 times per night each lasting 80-120 mins
Sleep Cycle: REM Sleep
typically very short (<5 mins) during first sleep cycle and usually becomes longer over the night
sleep cycle: N-3
becomes shorter over the night and may not exist in later sleep cycles
Why Do We Sleep?
Sleep is dependent on:
Homeostatic drive for sleep

Circadian process for sleep
Sleep is dependent on:
Homeostatic drive for sleep
similar to other drive states (thirst, hunger)
Sleep is dependent on:

circadian process
Involves hormonal and neuroendocrine process

Entrained to the light/dark cycle
circadian process
Based in the hypothalamus

Suprachiasmatic nucleus

Entrained to cycles of light and darkness
circadian process

suprachiasmatic nucleus
Biologic clock

Promote wakefulness and opposes homeostatic drive for sleep

Control physiologic and hormonal processes
circadian process

suprachiasmatic nucleus: Control physiologic and hormonal processes
Body temperature

Cortisol

Melatonin

Thyroid hormone production
circadian process pathway
melatonin
Neurohormone produced by the pineal gland
melatonin

precursor
tryptophan (found in these foods)
melatonin

synthesis and release are stimulated by ______ and suppressed by _____
darkness
light
melatonin clinical uses
used in treatment of various conditions
- Jet lag
- Delayed sleep phase syndrome
- Sleep enhancement in healthy people
- Alzheimer's
- Cancer
- Circadian rhythm entrainment in the blind
melatonin release at different times of day
rise from 8-10 pm

peak at 2-4 am

gradually declines
melatonin release with age
decreases with age
Sleep Changes with Age
Increased awakenings and arousals

Decreased REM sleep

(Probably) decreased SWS

Fewer "cycles"

Reduced sleep efficiency
sleep hygiene
Regular wake and sleep times 7 days/week

At least 8 hours of sleep time per night

Avoid caffeine, nicotine, alcohol

Regular exercise but not within 5 hours of sleep time

No mentally stimulating activity prior to bedtime
primary sleep disorders
dyssomnias
dyssomnias
Insomnia
Hypersomnia
Narcolepsy
Obstructive sleep apnea
Circadian rhythm disorder
Sleep-Related Breathing Disorders
breathing with snoring at the mild end of spectrum

OSA at other end of spectrum
obstructive sleep apnea definition
Repetitive complete or partial collapse of the upper airway during sleep
OSA prevalence

adult population
2 - 5% of adult population (30 to 60 years of age)
OSA prevalence

children
0.7 - 3% of children (2 to 5 years of age)
OSA prevalence

gender
males more affected than females (2:1)
OSA prevalence

race
Higher prevalence
- African americans
- Hispanics
- Asian americans
upper airway definition
airway segment between nose, mouth, and main carina

made up of bony structures and soft tissues
upper airway

bony structures
mandible
maxilla
hyoid bone
upper airway

soft tissues
tongue
soft palate
parapharyngeal fat pads
pharyngeal muscles
lateral pharyngeal wall
upper airway is divided into ____ different areas
4 (nasopharynx, velopharynx, oropharynx, hypopharynx)
nasopharynx
behind nose
velopharynx
behind soft palate
oropharynx
behind oral cavity
hypo pharynx
behind the throat
Upper Airway Function
conditioning and cleaning of the air conducted to lower airways

important role in protection of the lower airways and formation of sound produced by vocal chords
upper airway functions require
the capacity for patency and closure of the upper airway
airway is patent when?
whenever there is an open pathway between patient lungs and outside world
etiology of OSA
Anatomically narrowed upper airway

Nasal cavity

Nasopharynx

Oropharynx
etiology of OSA

nasal cavity
septal deviation

enlarged turbinates
etiology of OSA

nasopharynx
- Hypertrophic adenoids and tonsils

- Elongated soft palate

- Elongated/ edematous uvula
etiology of OSA

oropharynx
- Enlarged tongue

- Excessive lymphoid tissue

- Redundant parapharyngeal folds
Signs & Symptoms of OSA
Described by the bed partner or parents

Snoring, snorting, gasping

Breath holding

Excessive daytime sleepiness

Difficulty with attention

Mood disturbance
clinical signs and symptoms of OSA
obesity

mandibular retrognathia

long soft palate

large tongue

high arched palate
clinical signs and symptoms of OSA

obesity increases risk of OSA _____fold
10-14
Obstructive Sleep Apnea
Predisposing Factors
age

obesity

gender

neck circumference

medications, alcohol

anatomic abnormalities
Obstructive Sleep Apnea
Predisposing Factors

age
40-60 years
Obstructive Sleep Apnea
Predisposing Factors

gender
male (8:1/ male:female)
Obstructive Sleep Apnea
Predisposing Factors

airway size
OSA

diagnosis
Epworth sleepiness scale
Apnea - Hypopnea Index (AHI)
Laboratory diagnosis (polysomnography)
Body mass index (BMI)
Neck circumference
Craniofacial evaluation
Intraoral evaluation
Imaging
gold standard for OSA diagnosis
polysomnography
OSA diagnosis: Epworth sleepiness scale
Measures subjective sleepiness

Eight questions / situations

Questions answered in a scale of 0 to 3

Not specific for sleep-related breathing disorders
OSA diagnosis: Epworth sleepiness scale

scoring
maximum possible score= 24

score>10= significant daytime sleepiness
OSA diagnosis: Epworth sleepiness scale

Eight questions / situations
OSA diagnosis: Epworth sleepiness scale

Questions answered in a scale of 0 to 3
0= no likelihood of falling asleep

3= 100% likelihood of falling asleep
Apnea - Hypopnea Index (AHI)
Average number of apnea and hypopnea events per hour of sleep

(sum of respiratory events/# hours slept)
Apnea - Hypopnea Index (AHI)

scoring
- Normal sleep: AHI < 5
- Mild OSA: AHI 5 - 15
- Moderate OSA: AHI 15-30
- Severe OSA: AHI > 30
Apnea - Hypopnea Index (AHI)

diagnosis of OSA made if AHI is what
>5 (with symptoms of excessive daytime sleepiness, weakness, nocturnal apnea, awakening with choking, breath holding)
Laboratory Diagnosis
polysomnography
polysomnography
- Overnight sleep study

- Monitoring multiple physiologic parameters
polysomnography

components
electroencephalogram (EEG)

electrooculogram (EOG)

electromyogram (EMG)

electrocardiogram (ECG)

pulse oximetry

nasal thermistor

chest and abdominal strain gauges
electroencephalogram (EEG)

monitors
brain waves
electrooculogram (EOG)

monitors
eye waves
electromyogram (EMG)

monitors
jaw muscular activity and leg movements
electrocardiogram (ECG)

monitors
heart rate/rhythm
pulse oximetry

monitors
blood oxygen saturation
nasal thermistor

monitors
nasal airflow CO2 levels
chest and abdominal strain gauges

monitors
breathing efforts
OSA diagnosis

body mass index (BMI)
Weight in Kg / Height inm²
OSA diagnosis

body mass index (BMI)

obese
BMI > 30
OSA diagnosis

neck circumference
Greater than 17 inches - 43 cm (M)

Greater than 16 inches 41 cm (W)
OSA diagnosis

craniofacial evaluation
- Mandibular retrusion

- Maxillary defficiency

- Inferior displacement of hyoid bone
OSA diagnosis

Intraoral evaluation
- Tonsillar hypertrophy

- Macroglossia

- Oropharyngeal narrowing
Mallampati Classification

determined by
looking at the anatomy of the oral cavity
Mallampati Classification

based on
the visibility of
-uvula
-faucial pillars
-soft palate
Mallampati Classification

used to predict _________ and provides an idea of _______
the ease of intubation

how severe OSA is
Mallampati Classification

class I
Mallampati Classification

class II
Mallampati Classification

class III
Mallampati Classification

class IV
OSA diagnosis

imaging
Lateral radiography
Acoustic reflection
Fluoroscopy
Optical coherence tomography
Nasopharyngoscopy
Dynamic and cone beam CT
Magnetic resonance imaging
Lateral radiography
measurements introduced by mcnamara to determine any upper airway obstruction

measures upper and lower pharyngeal width
Lateral radiography

upper pharynx
measured from 2 points:
- Posterior outline soft palate
- Posterior pharyngeal wall
Lateral radiography

lower pharynx
measured from 2 points:
- Intersection posterior border of the tongue and posterior border of the mandible
- Posterior pharyngeal wall
OSA management
Sound diagnosis
Positive airway pressure
Upper airway surgery
Oral appliances
OSA management:

CPAP machine advantage
Relieve of obstruction at all levels of the airway
gold standard treatment for OSA
positive airway pressure (CPAP machine)
OSA management:

CPAP machine disadvantages
- Patient's compliance
- Mask leaks
- Skin ulceration or irritation
- Rhinorrhea
- Nasal congestion
- Claustrophobia
OSA management

upper airway surgery
- Nasal reconstruction
- Tonsillectomy/ Adenoidectomy
- Uvulopalatopharyngoplasty (UPPP)
- Mandibular osteotomy /genioglossus advancement
- Hyoid myotomy suspension
- Maxillomandibular advancement
- Tracheostomy
Uvulopalatopharyngoplasty (UPPP)
removes excess tissues in the throat to make airway wider

decreases the severity of OSA
Mandibular osteotomy /genioglossus advancement
designed to place tension on the tongue and move it forward

improves the airway behind the back of the tongue during sleep
Hyoid Myotomy Suspension
hyoid bone and its muscle attachments to the tongue and airway are pulled forward

aim: to increase airway size and improve airway stability in the retrolingual and hypo pharyngeal airway
Maxillomandibular Advancement
advances the mandible to expand the airway
Oral Appliances
Primary treatment option
oral appliances

indications
for Patients who are unable to tolerate CPAP or who refuse to use CPAP
oral appliances MOA
increase the volume of the upper airway
-retropalatal area
-retroglossal area
types of oral appliances
mandibular advancement devices (MAD)

tongue-retaining devices (TAD)
oral appliances:
mandibular advancement devices (MAD)
engage and reposition the mandible and tongue (indirectly) forward

typically made of acrylic resin

composed of 2 pieces that cover upper and lower arches
Oral appliances
mandibular advancement devices (MAD)

examples
Oral appliances
tongue-retaining devices (TAD)
directly engage/suction the tongue and hold it in a forward position

made of silicone in the shape of a bulb
Oral Appliances Contraindications
Active TMJ disorder. Myofascial pain

Severe periodontal disease or dental caries

Fewer than 10 teeth per dental arch

Limited mandibular range of motion

Patients with seizure disorders
Role of Dentist in OSA Patients
Although OSA can be diagnosed only by a physician , a dentist may be called on to screen for OSA
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