Sleep Flashcards
Polysomnography
full/level1 sleep study
Provides information on sleep architecture
components of polysomnogram
EEG EMG (submentalis, ant. tibilalis) EOG (electro-occulogram) ECG Airflow (nasal pressure, thermistor) Respiratory effort digital oximetry
Ambulatory sleep studies
DIgital/level 3 useful only for sleep apnea no information on sleep stages, sleep/wake cycle measures: - airflow - respiratory effort - digital oximetry - +/- body position
Sleep staging
amplitudes and waveforms scored in 30 second epochs
EEG
Eye movements (rolling at sleep onset, rapid in REM sleep)
Muscle tone (EMG) - lessens with drowsiness and sleep depth, absent in REM
Normal sleep
Sleep latency
Non-REM sleep
Stages I, II, III
I: still input from environment
II: medium sleep
III: deep sleep
REM sleep
phasic: eye movements, twitches, variable autonomic activity
Tonic: EMG suppression, high arousal threshold, elevated brain temperature, poikilothermia, penile tumescence
Sleep apnea often worst during REM since muscles are relaxed
EEG patterns
Stage 1: theta
2: sleep spindles and mixed EEG
Stage 3: more delta waves
REM: low-voltage, high-frequency waves
Hypnogram
~ 90 min cycles between REM and non-REM
Elderly: shorter cycles, shallow sleep
Stage I of sleep
light sleep
transitional stage passed through from wake to sleep and sleep to wake
usually ~5% of TST
when increased –> indicates sleep disruption
Stage II of sleep
most of the night spent in this stage
Stage III of sleep
deepest - hard to awaken
Sleep drunkenness: sleep inertia when awakened; parasomnias occur from this stage
Most restorative
often reduced by benzodiazepines
maintained by zopiclone, zaleplon, zolpidem
Stage REM
dream sleep; ver narrative
tonic/phasic stages
tonic: voluntary muscle atonia
phasic: movements
Latency to stage REM shortened causes
REM rebound: first night of CPAP, drug/medication withdrawal
Depression (psychotic > milder forms)
Narcolepsy
Sleep and aging
more stage I, less stage III
more awakening
brain shrinks a bit - less deep sleep??
Complaints of normal elderly about sleep
insomnia relative advance of sleep phase shallow sleep less restorative dream content often unpleasant daytime sleepiness
Melatonin pathway
Inhibited by light
stimulated by darkness
Retinohypothalamic tract –> SCN –> made in pineal gland to go to superior cervical ganglion
Sleep disturbances commonly seen in the elderly
Respiratory sleep disorders
Restless legs/periodic limb movements
REM sleep behaviour disorder
Respiratory sleep disorders
Primary snoring
upper airway resistance syndrome
OSA - hypopnea syndrome
–> apnea: cessation of airflow >=10 seconds
–> hypopnea: decrease in airflow >=10 seconds
- respiratory effort persists
Central sleep apnea - no respiratory effort
Mixed sleep apnea
OSA night time symptoms
snoring witnessed apneas choking dyspnea restlessnes snocturia diaphoresis reflux drooling
OSA daytime symptoms
sleepiness, fatigue morning headaches poor concentration decreased libido/impotence decreased attention depression decreased dexterity personality changes
OSA risk factors
Obesity neck circumference over 40 cm macroglossia dental overjet and retrognathia high/narrow hard palate elongated/low lying uvula enlarged tonsils, adenoids crossbite/dental malocclusion prominent tonsillar pillars enlarged nasal turbinates deviated nasal septum narrow mandible narrow maxilla
Central sleep apnea
similar daytime symptoms to OSA typically have history of: - cardiac disease - stroke - opioid use
Restless legs syndrome features
urge to move limbs often associated with paresthesias/dysesthesias
symptoms worse of present only during rest
partially/temporarily relieved by activity
nocturnal worsening of symptoms
Diagnosis usually made clincially, but may be confirmed through the Standarized Immobilization Test
Associated features of restless legs syndrome
response to dopaminergic therapy in almost all cases
periodic limb movements occur during sleep/wakefulness in 80-90% of patients
usually progressive with age
no clear medical/physical pathology (primary form)
Demographics of restless legs syndrome
5-10% of adults of Northern European studies
lower in Indian/Asian studies
treatment typically sought after age 40
1.5-2x more common in women
Predisposing factors of restless legs syndrome
Fe deficiency
peripheral neuropathy
sedating antihistamines, dopamine antagonists, and most antidepressants (not buproprion)
family affected in >50%
increased risk (3-6x) in 1st degree relatives
Causes of secondary RLS
pregnancy –> dilutional anemia
end-stage renal disease
Fe deficiency (involved in dopamine synthesis?0
)
Treatment of RLS
underlying factors (anemia, renal disease, neuropathy) Medication options: - gabapentin, pregabalin - dopamine agonists - clonazepam - opioids in very severe cases
Periodic limb movement disorder essential features
EMG from the polysomnogram demonstrates repetitive, highly stereotyped limb movements that meet recording criteria = inter-movement interval of 5-90 seconds
PLM index exceeds 5/hour (children) and 15 (adults)
clinical sleep disturbance or a complaint of daytime fatigue
Periodic limb movement disorder treatment
only if clinically indicated (clear sleep disruption)
same option as RLS
REM sleep behaviour disorder essential features
presence of REM sleep without atonia
at least one of the folllowing:
- sleep related injurious, potentially hazardous, or disruptive behaviours by history
- abnormal REM sleep behaviours documented during PSG
Absence of EEG epleptiform activity during EEG
Associated features of RSBD
dream enactment typically occurs >90 min after sleep initaition
episode ends when individual awakens quickly, becomes alert, and reports dream
injury common secondary to violent dream enactment
sleepwalking uncommon
may have prodrome of sleep talking, yelling, twitching
patients often present after injury to self or bed partner
RSBD onset/course
gradual/rapid onset, progressive
delayed emergence of neurodegenerative disorder is very common (2/3 later develop Parkinson’s)
can be simply a symptom of narcolepsy
RSBD pathology
alpha-synucleinopathy
protein aggregates in vulnerable populations of neurons and glial cells
Predisposing/precipitating factors of RSBD
underlying neurological disorder, especialyl alpha-synucleinopathies (Parkinson’s LBD, multiple system atrophy)
narcolepsy
stroke
medications/withdrawal
Management of RSBD
safety first - remove obstacles, etc
Medication - best evidence clonazepam, effective in preventing violent dream enactment in most cases
Sleep and AD
disruption common in AD (19-44%)
Related to patient institutionalization
Negative impact on patient and caregivers’ QOL
Better management of sleep in AD
priority for improving comprehensive management of patients with AD
No long-term data
no data on behavioural interventions
Features of sleep in AD
similar to but worse than disturbances seen in non-dementing elderly increased freq/duration of awakenings increased stage I decreased stage III, REM sleep increased daytime napping sleep disturbances associated with: - increased memory/functional impairment - more rapid cognitive decline More severe in more demented patients
Mechanism of sleep disturbance in AD
Loss/damage to neuronal pathways that initiate and maintain sleep
Degenerative changes in brainstem regions/pathways that regulate sleep-wake cycles
Changes in cortical tissue that generate EEG low-wave activity during sleep
Changes in hypothalamic-suprachiasmatic nucleus and other parts of the circadian timing system
severe: day-night reversal occurs
Sleep apnea and AD
significant correlation between dementia and sleep apnea severity
apnea associated with increased nocturia
worsens with sedative medications
Sleep disturbance in AD treatments
Buspirone: anxiety/depressive
SSRI: depressed/non-specific mood
Agitation: benzo, anti-psychotic
Insomnia:trazodone, zopiclone, benzodiazepines,
use safest, most effective drug at lowest dose, short duration
Watch out for side effects: falls, fractures, confusion, etc
Behavioural interventions in sleep disturbance in AD
no empirical studies in this population
Physical environment/institutional routines
reduce daytime napping
address care-giver concerns about “upsetting routine”
Ideal hypnotic
rapid absorption short half-life no drug-drug interactions no tolerance to effect free from side effects (memory, psychomotor) no rebound cheap
Rebound insomnia
Transient exacerbation of insomnia commonly occurs when sedative/hypnotic medications are withdrawn
Sleep hygiene basic rules
sleep only as much as needed to feel rested, get out of bed
keep regular sleep schedule
avoid forcing sleep
Exercise regularly >=20 min, preferably 4-5 hours befor bedtime
avoid caffeinated beverages after lunch
avoid alcohol near bedtime
avoid smoking
don’t go to bed hungry
adjust bedroom environment
avoid prolonged use of light-emitting screens befoe bedtime
stimulus control!!
Rx sleep onset insomnia
Short-acting
Zaleplon, zolpidem, triazolam, lorazepam
Ramelteon: melatonin agonist - more effective in sleep onset rather than sleep maintenance insomnia
Adverse effects milder in melatonin agonists than benzodiazepines
Rx sleep maintenance insomnia
Longer-acting preferable
Zolpidem extended release, eszopiclone, temazepam, estazolam, low dose doxepin
- may increase risk for hangover sedation
Benzodiazepine MOA in insomnia
binds several subtypes of GABAa receptors
reduce time to onset of sleep
prolonged stage II
prolong total sleep time
may slightly reduce amount of REM
decrease anxiety, impair memory, have anticonvulsive properties
Short acting genzo
triazolam
Intermediate acting benzo
estazolam
lorazepam
temazepam
Long acting benzo
flurazepam
quazepam
Nonbenzodiazepine receptor agonists
more targeted action at one GABA type A receptor
greater specificity - less anxiolytic and anticonvulsant
improve subject/veobjective sleep outcomes
decrease sleep latency & number of awakenings, while improving sleep duration and sleep
Zaleplon
very short halflife
effective for sleep-onset insomnia
not indicated for long-term use
Zolpidem
1.5-2.4 half life
for sleep onset insomnia
not indicated for long-term use
Eszopiclone
longest half life of approved nonbenzos
effective for both sleep onset/maintenance insomnia
not limited to short-term use, little evidence for abuse/dependance
Zolpidem extended release
1.5-2.4 half life
improve both sleep onset/maintenance insomnia without hangover effects
not limited to short-term use, little evidence for abuse/dependence in most patients
