Sleep disorders Flashcards
Sleep disorders are
common serious treatable under-diagnosed costly
prevalence rates insomnia obstructive sleep apnoea (OSA) delayed sleep phase syndrome narcolepsy sleep walking sleep terrors general sleepiness
insomnia - 4-19%
obstructive sleep apnoea (OSA) = 2-4% middle age adults
delayed sleep phase syndrome = 7% adolescents
narcolepsy = 0.03 - 0.16% (1 in 2000)
sleep walking = 1-15% adults
sleep terrors = 3 % children
general sleepiness = 0.5 - 36%
consequences of sleep disorders
mortality
accidents = 1in6 crashes possibly related to fatigue/ sleepiness = 100,000 crashes per annum = 1500 fatalities
Morbidity
- obesity (sleep problems = tend to be larger/ more overweight)
- metabolic syndrome = increase risk. Diabeters/ hypertension/ stress/ heart disease
-mental health = increased risk
–> depression (relative risk = 4, which means the risk is 4 x higher for those with sleep disorders)
–> suicide (rr = 1)
(could argue mental health is causing sleep disorder)
Poor Performance
- work = after 24 hours of sleep deprivation performance equivalent to people with 10% blood ETOH concentration
obstructive sleep apnoea crash risk odds:
2.3 ETOH : 7 OSA
(so, OSA way more likely to crash than drunk)
hypersomnolence = excessive daytime sleeping
Sleep disorders are treatable
- successful treatment modalities?
- % people that sleep ‘well’?
- what is ‘normal’ sleep?
- pharmacotherapy
- behavioural therapy
- continuous positive airway pressure (CPAP) = breathing therapy
- dental appliances
- surgical therapy
- -> 95% patients are underdiagnosed and unidentified
- few health care providers question about sleep
- rarely taught in medical schools
- only 50% people report they sleep well!
Sleep history of patient may explain disorder
- onset of symptoms
- childhood sleep history: hypersomnia/ insomnia, behavioural attacks in sleep, restlessness/ limb movement, sleep disordered breathing, dreams/ nightmares/ hallucinations, emotional trauma
- adult sleep history: bed time, sleep onset latency, arousals (attacks, breathing problems, kicking/ restlessness, dreams/nightmares/hallucinations, enuresis, sleeping with others, rising time, refreshment, daytime somnolence (Epworth sleepiness score), daytime dreams, cataplexy (strong emotion causes sudden collapse)
- past medical history
- drug history
- social history (alcohol, drugs etc)
- occupation
- driver
- alcohol
- family history
Scales can be used to work this out (3)
1) Epsworth sleepiness scale
- -> how likely are you to doze off or fall asleep in the following situations
scores: <11 normal, 12-14 mild sleepiness, 15-18 moderate, > 18 severe (out of 24)
2) restless leg syndrome rating scale
3) parkinson’s disease sleep scale (PDSS)
Objective measurement of sleep quality
- outpatient neurophysiology studies
- inpatient telemetry studies
- pulse oximetry (measure breathing via finger pulse) - info of pulse and oxygen saturation
- ambulatory EEG (measures brain wave function)
- limited outpatient respiratory monitoring
- actigraphy (measures movement)
polysomnography
prolonged video EEG telemetry
respiratory monitoring
movement detection - EMG, actigraphy
multiple sleep latency test (MSLT) –> length of time it takes someone to get to sleep and type of sleep (used in narcolepsy and hypersomnia)
-maintenance of wakefulness test (MWT)
- vigilance tests - psychomotor vigilance test : PVT/ Osler test
International classification of sleep disorders
insomnia (3 types)
- treatment and conclusions
initial = beginning of the night
- hypnic phenomena (can be bizarre if you hallucinate)= can result in phobia
-exploding head syndrome (noise)
middle of the night
- can be related to spouse/ snoring/ pain/ kids (history useful to establish cause)
- paralysis can be very distressing(can hallucinate during this)
- may be due to narcolepsy, as it may be a problem with REM (narcolepsy = REM disorder)
Terminal = end of the night
- associated with mental health eg. depression
up to 15% have insomnia symptoms
important to treat insomnia as it can also enhance treatment of depression
treatment = effective (CBT-I)
- can reduce: WASO, sleep onset latency, number of awakenings, increase total sleep time
conclusions:
70-80% patients benefit
sleep improvements following CBT are well sustained over time
CBT is effective across a range of insomnias (not just primary insomnia)
CBT is first choice treatment for chronic insomnia
CBT can be cost effective and might be simplified
There is a need for more effective dissemination of CBT approaches to the management of insomnia
Hypersomnia
-causes?
differential diagnosis of excessive daytime somnolence
sleep disordered breathing:
- obstructive sleep apnoea
–> airflow = low, but thoracic and abdominal effort = high
- central sleep apnoea
–> airflow = low, thoracic and abdominal effort(drive) = low too (= more to do with brain dysfunction as it is not obstructed, the patient just isn’t breathing properly)
- obesity hypoventilation syndrome
Hypersomnia of central origin (things that can cause hypersomnia)
- narcolepsy (with/ without cataplexy)
-secondary narcolepsy (MS, PD, head injury, tumour)
Idiopathic insomnia
Recurrent hypersomnia
- Klein Levin syndrome - v tired
Insufficient sleep syndrome
Drug induced hypersomnia –> prescribed or not
Hypersomnia due to medical conditions
Cataplexy –> when strong emotion is felt it tends to occur = ‘Sudden transient episode of muscle weakness accompanied by full conscious awareness’
Atonic seizure = much quicker than cataplexy eg. fall to ground much faster (v rapid and sudden)
non epileptic attack = slump
myoclonic jerks - brain causes body to jerk
frontal lobe seizure - abnormal posturing of limbs from sleep (v typical bodily position arises from this)
- clinical features of narcolepsy
- diagnosis
- pathophysiology
- treatment
- nocturnal sleep quality is poor - this contributes to excessive daytime sleepiness
- several night time awakenings
-dreams occur immediately after falling asleep - hypnagogic (sleep onset) hallucinations
- hypnopompic (upon waking) hallucinations
auditory, visual, somesthetic
feeling of a threatening stranger in the bedroom
scary
patients are fearful of going to bed
-sleep paralysis
=inability to move the limbs, head, or breather normally
terrifying, suffocating, duration:secs - mins
, associated with REM intrusion, can be terminated if patient is moved
age of onset has 2 peaks: - late adolescence and 40 ish
-certain vaccination caused surge in rates (gave insight into pathophysiology)
DIAGNOSIS
- at least 2 symptoms needed (EDS + 1 other)
- cataplexy is characteristic and pathognomonic (characteristic of narcolepsy)
- HLA DQB1* 0602
- night time sleep latency <8mins
- night time REM latency <20mins
PATHOPHYSIOLOGY
- intrusion of REM into wakefulness
- dysregulation of normal sleeping patterns
- imbalance between adrenergic (decrease) and serotinergic (decrease) and ACh (increase) tone
- -> extremely complex interaction
- hypocretin (orexins)
- they are neuropeptides (1&2)
- produced by neurons in the lateral hypothalamus
- projections to RAS, cortex, thalamus & brainstem
- mutation in gene coding for hypocretin 2 receptor in Dobermans and mice identified (not humans though)
- reduction in human CSF hypocretin has been found (in cases with typical cataplexy)
- loss of hypocretin (compound made in hypothalamus) = immune response thought to destroy hypocretin neurons = can’t produce hypocretin = sleepiness = can’t be corrected
NARCOLEPSY TREATMENT
- planned naps (good sleep hygiene)
- stimulants - modafinil, methylphenidate, amphetamines
CATAPLEXY
- antidepressants –> effective immediately (no delay)
- SSRIs
- noradrenaline and serotonin reuptake inhibitor (fewer side effects than tricyclics)
- side effects (anticholinergic = dry mouth, dizziness, impotence, weight gain
- sodiu oxybate = drug, slightly hypnotix, inhibits cataplexy and helps sleep better
cataplexy atonic seizure non epileptic attack myoclonic jerks frontal lobe seizure
Cataplexy –> when strong emotion is felt it tends to occur = ‘Sudden transient episode of muscle weakness accompanied by full conscious awareness’
- sudden drop in muscle tone triggered by emotions
- worsens with poor sleep and fatigue
- may affect all striated muscles
- may be limited to face or entire body
- consciousness is retained
- duration of attacks varies: secs - minutes
- attacks occasionaly last hours ‘status cataplecticus’ - precipitated by withdrawal of anticataplectic drugs
(emotional triggers = laughing, joking, anger, excitation, surprise, stress, startlement, sex)
Atonic seizure = much quicker than cataplexy eg. fall to ground much faster (v rapid and sudden)
non epileptic attack = slump
myoclonic jerks - brain causes body to jerk
frontal lobe seizure - abnormal posturing of limbs from sleep (v typical bodily position arises from this)
Parasomnias
- SWS parasomnia?
- REM parasomnia?
behavioural disturbances in sleep
non-REM and REM have different characterisitcs in parasomnias
- abnormal sleep parasomnia = SLOW WAVE SLEEP
–> sleep walkers/talkers / intercourse / eating / driving
(can use these as a sleep defence in court)
SWS parasomnias = disorder of arousal
- sleep terrors (Childhood), confusional arousals, sleep walking (complex behavioural automatisms = unconscious behaviours), sleep talking
- common in childhood (decrease with age)
- occurs in first 3rd of every night
- can be triggered by stress, sleep deprivation
- associated with amnesia for the event
- potentially injurious, violent behaviour
-usually not associated with EDS
TREATMENT:
- reassurance
- hypnotics eg. benzodiazapines
- antidepressants (can improve or worsen symptoms = v difficult to treat)
REM parasomnias:
- loss of normal generalised atonia in REM sleep
- violent dream enactment
- last 3rd of the night (more REM at latter)
- patient can remember the episode if awakened
- little confusion or disorientation
- PSG and video required for diagnosis
- associated with drug/ alcohol withdrawal, pontine tumours, GB syndrome, parkinsonism, alzheimers
TREATMENT: clonazepam 500 ug -1 mg
Epilepsy
stereotype to behaviour (spin same way round) certain posturing (motor seizure in hand) EEG normal (too subtle to pick up on)
Restless leg syndrome
- primary and secondary?
- symptoms?
- diagnostic criteria?
restless leg syndrome - sensorimotor disorder of extremeties - irresistible urge to move legs- relieved by movement of legs -worse towards evening -common yet frequently undiagnosed PRIMARY RLS - likely genetic predisposition - tends to be earlier onset and more severe than secondary causes - natural history poorly understood - long delays in people seeking attention - few longitudinal studies SECONDARY RLS - associated with: iron deficiency end stage renal failure pregnancy drugs --> tricyclics, antipsychotics (thought to be a dopamine depletion syndrome = why it can be made worse by drugs)
Diagnostic criteria:
U = urge to move legs
R - Rest = symptoms worsen during periods of rest
G - Getting up = symptoms partially or totally relieved by movement
E - Evening = symptoms are worse in the evening
Treatment
- iron
- DA agonist
- L Dopa
- Clonazepam
- Gabapentin
- Opiates
Periodic limb movements in sleep (PLMS)
stereotyped movements (part of RLS spectrum)
