Sleep Flashcards
what are the prevalence rates of sleep disorders
- general sleepiness
- insomnia
- OSA
- delayed sleep phase syndrome
- narcolepsy
- sleep walking
- sleep terrors
- general sleepiness: 0.5-36%
- insomnia: 4-19%
- OSA: 2-4% (middle aged adults)
- delayed sleep phase syndrome: 7% of adolescents
- narcolepsy 0.03-0.16%
- sleep walking: 1-15% adults
- sleep terrors: 3% children
sleep disorders are quite prevalent w 2.2 million affected people in South Yorkshire
what are the consequences of poor sleep?
- mortality: accidents
- 1 in 6 crashes related to fatigue/sleepiness -> 100,000 crashes per annum in US, $12.5 billion per annum - morbidity: obesity, metabolic syndrome (CPAP reduces the effect Drager et al. 2007), depression, (may result in suicide)
- poor performance: at work, >24hrs of sleep deprivation = 10% blood ETOH conc., personal relationships
what are the various treatment options for sleep disorders?
- pharmacotherapy,
- behavioral therapy,
- continuous positive airway pressure (CPAP), dental appliances
- surgical therapy
why are sleep disorders under diagnosed?
- 95% of people w sleep problem - unidetiied and under diagnosed as few heath are providers qs patients about sleep and lil content in med schools
- interestingly, top 10 diagnosis in a clinic by intern was associated w sleep
- hypertension, diabetes mellitus, hyperlipidemia - top 3 causes associated w OSA
what is the difference b/w sleep and coma?
both are unconsciousness states however, a person can aroused by sensory or other stimuli in sleep unlike coma
what are the hypothesis based on necessity of sleep
- somatic theory: healing of bod, other endocrine functions
- metabolic theory: detoxification (ROS removal), regeneration (energy?)
- cognitive theory: learning, brain development (plasticity)
what does a sleep cycle consist of?
- 4 stages
- REM sleep
describe the neurophysiology of sleep/ sleep stages
- Stage 1
EEG: low voltage, mixed frequency, may be theta rhythm 2-7 Hz, up to 50-75uV range
EOG: slow rolling eye movements
EMG: tonic activity - Stage 2
EEG: low voltage, mixed frequency, sleep spindles, K complexes
EMG: tonic activity, low level - Stage 3
EEG: delta rhythm, high amplitude waves, low frequency
EOG: none, reflects EEG
EMG: tonic activity, low level - Stage 4
EEG: delta rhytm
Polysomnographic profiles define two states of sleep:
REM and NREM (further subdivided into 3 stages) - REM
EEG: low voltage, mixed frequency, theta activity, slow alpha activity
EOG: phasic REMs
EMG: tonic suppression, phasic twitches
what are the stages of REM?
- Tonic stage (desyncronised EEG:low voltage, frequency ↑, muscle atonia)
- Phasic stage (rapid eye movements:fast, saccadic eye movements, irregular breathing, heart rate ↑, myoclonus, apnea, hyperpnea, dreaming!)
what is neurochemicstry of wakefulness and sleep?
Reticular formation -> Basal forebrain, thalamus, post. Hypothalamus -> Cholinergic, serotonergic, monoamine., histamergic.
what are the difference b/w aminergic and cholinergic amounts during wake, sleep and REM?
- wake - both high
- sleep - both low
- REM
aminergic low
cholinergic high
what are the two theories for the mechanism of sleep?
- Passive theory: excitatory areas of RAS (reticular activating system) in upper BS fatigue -> become inactive
- active inhibitory process: stimulation of centre below midpontine of BS -> inhibit excitatory areas of RAS -> sleep
ascending arousal system
what are the differences b/w circadian timing and ultradian timing?
duration
1. circadian: 24hrs
2. ultradian: >24hrs
region of brain
1. circadian: hypothalamus (suprachiasmatic nucelus), pineal gland (melatonin)
2. ultradian: prepontin nuclei, raphe nuclei, locus coerulus
what are the key steps in diagnosis of sleep problems?
- history
- sleep quality measurement
- no single gold standard test available
- combination of objective and subjective tests (depending on the availability)
2a. Subjective
- the epworth sleepiness scale
- Parkinson’s disease sleep scale (PDSS)
2b. Objective
- multiple sleep latency test (MSLT)
- Maintenance of Wakefulness Test (MWT)
- Vigilance Tests: Psychomotor Vigilance Test: PVT, Osler test
what are the outpatient and in patient neurophysiological studies
- outpatient: pulse oximetry, ambulatory EEG, respiratory monitoring (limited), actigraphy
- in patient: Polysomnography (sleep study) - prolonged EEG video telemetry, respiratory monitoring, movement detection (EMG, actigraphy)
what is the international classification of sleep disorders?
- American academy of sleep medicine 2005
1. Insomnia
2. Hypersomnia: sleep disordered breathing, central origin hypersomnia
3. Circadian Rhythm disorders
4. Parasomnias
5. Movement disorders of sleep
- what is insomnia?
- where is it most common?
- duration of the sleep disorder to confirm insomnia
- symptoms associated
- likehood cause for transient and chronic insomnia
- PSG/MSLT results
- inability to achieve and maintain sleep
- common: in industrialised world
- duration: >1m
- symptoms associated w fatigue, poor memory+ concentration in short term sufferers
- transient insomnia associated w stress, shift works, jet lag, pain, alcohol, drug withdrawal
- chronic insomnia associated w depression, alcohol/drug abuse, excess caffeine, physical illness, cat naps
- PSG/MSLT results: normal in chronic cases
what is the treatment for insomnia?
- Exclude other sleep disorders
- Good sleep hygiene
- Short term prescription (4 weeks) of hypnotic sedatives (eg zolpidem,
temazepam) - CBT
- Often difficult to treat
why is insomnia important?
- cause it is most expression of mental disease (depression, anxiety)
- Fava et al. 2007 treating insomnia also enhances treatment of depression
how effective is CBT as a treatment for insomnia?
- it is the first choice pf treatment for insomnia - 70-80% benefit from CBT
- sleep improvements after CBT are well sustained over time
- it is effective across a range of insomnia (not just primary insomnia)
- cost-effective
what is hypersomnia? what are its other names?
- significant episodes of sleep even after 7hrs of sleep and more
- also known as hyper somnolence and excessive daytime somnolence
what are the differential diagnosis of hypersonic?
- sleep disordered breathing:
- OSA syndrome
- central sleep apnoea
- obesity hypoventilation syndrome - central origin hypersomnia:
- narcolepsy w and w/o cataplexy
- secondary narcolepsy (MS,PD,head injury, encephalitis, tumour)
- idiopathic hypersomnia
- recurrent hypersomnia (Klein levin syndrome) - insufficient sleep syndrome
- drug induced hypersomnia
what is apnea-hypogea index (AHI), why is it used and what do the values represent?
- number of apnea and hyponeas per 1 sleeping hr
- measures the severity of sleep disordered breathing
- normal: <5
- mild: 5-15
- moderate: 16-30
- severe: >30
how does the prevalence of sleep apnea w age?
- increases w increase in age
- children (2-8yrs) - 2-3%
- middle aged adults - 5-7%
- older adults (>65yrs) - >15%
what are the day and nigh symtptpms of OSAHS (obstructive sleep apnoea hypopnea syndrome)
- day: excessive daytime sleepiness, unrefreshign sleep, memory problems,headcahe, depression, decreased libido, stomach ache
- night: snoring, apnea, choking-gasping, arousals, swatting, dry mouth, palpitation, nycturia
what are the risk factors for developing OSAHS
- Obesity
- Age
- gender:male
- family history of OSAHS
- Alcohol before bedtime
- Race
- Smoking
- Sedatives
- Craniofacial anomalies
- Hypothyroidism, acromegaly
what are the benefits of 1. CPAP
- mandibular advancement devices (MAD) and mandibular repositioning splints (MRS) and
- surgery in OSA?
- RCT evidence, CPAP improves: sleepiness, cognition, health status, driving, BP
- several CT: MAD/MRS can reduces AHI, sleepiness, BP, symptoms in mild to moderate OSA
- however, 2 RCT (2002,2004) showed CPAS gives better outcomes than MRS - CT 1998, maxillomandibular advacemnet (surgery) improves AHI, vigilance similar to CPAP
what is narcolepsy and its clinical features?
- excessive daytime sleepiness due to poor nocturnal sleep quality
Clinical features - several night time awakening (thus, sleepy in the clinic)
- dreams immediately after falling asleep
- hypnagogic (sleep onset) and hypnopompic (upon awakening) hallucinations: auditory, visual, somesthetic, feeling os threatening stranger in room, scared, fearful to get out of bed
- sleep paralysis (secs-mins): inability to move limbs, head or beathe normally, associated w REM intrusion, terminated when the patient is moved
what is epidemiology of narcolepsy?
- NY journal,2003: third neurological disease following PD and MS
- most common in middle-aged population 20-50, rare in children and elderly
cataplexy in narcoplexy
- what is it
- duration
- factors worsenenign it
- parts of body affected
- consciousness?
- sudden drop in muscle tone triggered by emotions (laughter>joking>anger»»sex)
- duration: secs-mins, occasionally hours ‘status cataplecticus’ due to withdraw of anti-cataplectic drugs
- poor sleep and fatigue worsen it
- may affect all started muscles or limited to face or affect entire body
- consciousness retained (compared to epilepsy?)
what is the pathophysiology causes of narcolepsy?
- dysregulation of normal sleeping pattern
1. intrusion of REM into wakefulness
2. imbalance b/w adrenergic (↓), serotinergic (↓) and Ach(↑) tone
3. hypocretin (NP) mutations found in mice but not identified in humans yet however, reduced human CSF hypocretin found in typical cataplexy (as well as other neurological diseases)
how to diagnose narcolepsy?
- min 2 symptoms
- HLA +ve more likely to - PSG: exclude other abnormalities
- MSLT
what is treatment for narcolepsy and w cataplexy?
narcolepsy
1. planend naps: early afternoon, good sleep hygiene
2. stimulants: med like modafinil (400mg effective than 200mg as they have lower EPSS, 1998), methylphenidate, amphetamines
Cataplexy
1. SSRIs: fluoxetine
2. NA reuptake inhibitory
3. NA and serotonin reupatke inhibitory: fewer side effects than TCI
4. TCA: imipramine, clomipramine (block reupatke of NA+ serotonin)
- but side effects (anti-ach) dry mouth, dizziness, impotence, weight gain
5. sodium oxybate: Placebo controlled trial 2002, 9g SO reduces cataplexy attacks by 70% (side effect: too much Na+)
6. hypocretin agonists being developed. further, to cinsider hypocretin neuron transplant
what is parasomnia? and its different types?
- abnormal behaviour or experience during sleep
1. sleepwalking
2. sleep terrors
3. sleep bruxism
4. REM sleep behaviour disorder (RBD)
how to differentiate parasomnia and epilepsy?
refer
what are the different types of movement disorders of sleep?
- restless leg syndrome (RLS)
- periodic limb movements of sleep (PLMS)
- propriospinal myoclonus
- rhythmic movement disorder of sleep (common in children -> bang their hand, usually, autistic)
what is RLS and its features? and what are its two types and what are they associated w? why is history poorly understood for primary RLS?
- sensorimotor disorder of extremities
- irresistible urge to move legs -> relived by movement of legs
- worsen towards evening
- common but frequently undiagnosed
1. primary RLS - genetic association
- earlier onset
- more severe than secondary causes
- natural history poorly understood: long delays in seeking attention, few longitudinal studies
2. secondary RLS associated w - iron deficiency
- end stage renal failure
- pregnancy
- drugs: TCA, anti-psychotics
what is diagnostic criteria for RLS? (URGE)
U - urge to move legs (+ uncomfortable sensations in legs)
R - resting or inactivity worsens it (e.g. lying or sitting)
G - getting up relives unpleasant sensations in legs
E - evening or night worsens it
what are the treatment options for RLS and PLMS?
- Iron
- dopamine agonists
- L-dopa
- Clonazepam
- Pregabalin
- Gabapentin
- Opiates
what is the significance of driving in sleeping disorder?
- important medicolegal aspect of sleep medicine
- several case control studies, 1 prospective and 1 cross sectional study in the late 90s have shown an association b/w crash risk and OSA
- UK police stats: sleepiness accounts for 15-20% of accidents on monotonous roads , includes running off road, lane drifting, running into back of vehicle in front
