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MED627 > Sleep > Flashcards

Sleep Flashcards

1
Q

what are the prevalence rates of sleep disorders

  1. general sleepiness
  2. insomnia
  3. OSA
  4. delayed sleep phase syndrome
  5. narcolepsy
  6. sleep walking
  7. sleep terrors
A
  1. general sleepiness: 0.5-36%
  2. insomnia: 4-19%
  3. OSA: 2-4% (middle aged adults)
  4. delayed sleep phase syndrome: 7% of adolescents
  5. narcolepsy 0.03-0.16%
  6. sleep walking: 1-15% adults
  7. sleep terrors: 3% children
    sleep disorders are quite prevalent w 2.2 million affected people in South Yorkshire
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2
Q

what are the consequences of poor sleep?

A
  1. mortality: accidents
    - 1 in 6 crashes related to fatigue/sleepiness -> 100,000 crashes per annum in US, $12.5 billion per annum
  2. morbidity: obesity, metabolic syndrome (CPAP reduces the effect Drager et al. 2007), depression, (may result in suicide)
  3. poor performance: at work, >24hrs of sleep deprivation = 10% blood ETOH conc., personal relationships
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3
Q

what are the various treatment options for sleep disorders?

A
  1. pharmacotherapy,
  2. behavioral therapy,
  3. continuous positive airway pressure (CPAP), dental appliances
  4. surgical therapy
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4
Q

why are sleep disorders under diagnosed?

A
  • 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
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5
Q

what is the difference b/w sleep and coma?

A

both are unconsciousness states however, a person can aroused by sensory or other stimuli in sleep unlike coma

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6
Q

what are the hypothesis based on necessity of sleep

A
  1. somatic theory: healing of bod, other endocrine functions
  2. metabolic theory: detoxification (ROS removal), regeneration (energy?)
  3. cognitive theory: learning, brain development (plasticity)
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7
Q

what does a sleep cycle consist of?

A
  • 4 stages

- REM sleep

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8
Q

describe the neurophysiology of sleep/ sleep stages

A
  1. 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
  2. Stage 2
    EEG: low voltage, mixed frequency, sleep spindles, K complexes
    EMG: tonic activity, low level
  3. Stage 3
    EEG: delta rhythm, high amplitude waves, low frequency
    EOG: none, reflects EEG
    EMG: tonic activity, low level
  4. Stage 4
    EEG: delta rhytm
    Polysomnographic profiles define two states of sleep:
    REM and NREM (further subdivided into 3 stages)
  5. REM
    EEG: low voltage, mixed frequency, theta activity, slow alpha activity
    EOG: phasic REMs
    EMG: tonic suppression, phasic twitches
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9
Q

what are the stages of REM?

A
  1. Tonic stage (desyncronised EEG:low voltage, frequency ↑, muscle atonia)
  2. Phasic stage (rapid eye movements:fast, saccadic eye movements, irregular breathing, heart rate ↑, myoclonus, apnea, hyperpnea, dreaming!)
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10
Q

what is neurochemicstry of wakefulness and sleep?

A

Reticular formation -> Basal forebrain, thalamus, post. Hypothalamus -> Cholinergic, serotonergic, monoamine., histamergic.

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11
Q

what are the difference b/w aminergic and cholinergic amounts during wake, sleep and REM?

A
  1. wake - both high
  2. sleep - both low
  3. REM
    aminergic low
    cholinergic high
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12
Q

what are the two theories for the mechanism of sleep?

A
  1. Passive theory: excitatory areas of RAS (reticular activating system) in upper BS fatigue -> become inactive
  2. active inhibitory process: stimulation of centre below midpontine of BS -> inhibit excitatory areas of RAS -> sleep
    ascending arousal system
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13
Q

what are the differences b/w circadian timing and ultradian timing?

A

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

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14
Q

what are the key steps in diagnosis of sleep problems?

A
  1. history
  2. 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
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15
Q

what are the outpatient and in patient neurophysiological studies

A
  • outpatient: pulse oximetry, ambulatory EEG, respiratory monitoring (limited), actigraphy
  • in patient: Polysomnography (sleep study) - prolonged EEG video telemetry, respiratory monitoring, movement detection (EMG, actigraphy)
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16
Q

what is the international classification of sleep disorders?

A
  • 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
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17
Q
  • 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
A
  • 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
18
Q

what is the treatment for insomnia?

A
  • Exclude other sleep disorders
  • Good sleep hygiene
  • Short term prescription (4 weeks) of hypnotic sedatives (eg zolpidem,
    temazepam)
  • CBT
  • Often difficult to treat
19
Q

why is insomnia important?

A
  • cause it is most expression of mental disease (depression, anxiety)
  • Fava et al. 2007 treating insomnia also enhances treatment of depression
20
Q

how effective is CBT as a treatment for insomnia?

A
  • 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
21
Q

what is hypersomnia? what are its other names?

A
  • significant episodes of sleep even after 7hrs of sleep and more
  • also known as hyper somnolence and excessive daytime somnolence
22
Q

what are the differential diagnosis of hypersonic?

A
  1. sleep disordered breathing:
    - OSA syndrome
    - central sleep apnoea
    - obesity hypoventilation syndrome
  2. central origin hypersomnia:
    - narcolepsy w and w/o cataplexy
    - secondary narcolepsy (MS,PD,head injury, encephalitis, tumour)
    - idiopathic hypersomnia
    - recurrent hypersomnia (Klein levin syndrome)
  3. insufficient sleep syndrome
  4. drug induced hypersomnia
23
Q

what is apnea-hypogea index (AHI), why is it used and what do the values represent?

A
  • 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
24
Q

how does the prevalence of sleep apnea w age?

A
  • increases w increase in age
  • children (2-8yrs) - 2-3%
  • middle aged adults - 5-7%
  • older adults (>65yrs) - >15%
25
Q

what are the day and nigh symtptpms of OSAHS (obstructive sleep apnoea hypopnea syndrome)

A
  • 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
26
Q

what are the risk factors for developing OSAHS

A
  • Obesity
  • Age
  • gender:male
  • family history of OSAHS
  • Alcohol before bedtime
  • Race
  • Smoking
  • Sedatives
  • Craniofacial anomalies
  • Hypothyroidism, acromegaly
27
Q

what are the benefits of 1. CPAP

  1. mandibular advancement devices (MAD) and mandibular repositioning splints (MRS) and
  2. surgery in OSA?
A
  1. RCT evidence, CPAP improves: sleepiness, cognition, health status, driving, BP
  2. 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
  3. CT 1998, maxillomandibular advacemnet (surgery) improves AHI, vigilance similar to CPAP
28
Q

what is narcolepsy and its clinical features?

A
  • 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
29
Q

what is epidemiology of narcolepsy?

A
  • NY journal,2003: third neurological disease following PD and MS
  • most common in middle-aged population 20-50, rare in children and elderly
30
Q

cataplexy in narcoplexy

  • what is it
  • duration
  • factors worsenenign it
  • parts of body affected
  • consciousness?
A
  • 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?)
31
Q

what is the pathophysiology causes of narcolepsy?

A
  • 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)
32
Q

how to diagnose narcolepsy?

A
  1. min 2 symptoms
    - HLA +ve more likely to
  2. PSG: exclude other abnormalities
  3. MSLT
33
Q

what is treatment for narcolepsy and w cataplexy?

A

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

34
Q

what is parasomnia? and its different types?

A
  • abnormal behaviour or experience during sleep
    1. sleepwalking
    2. sleep terrors
    3. sleep bruxism
    4. REM sleep behaviour disorder (RBD)
35
Q

how to differentiate parasomnia and epilepsy?

A

refer

36
Q

what are the different types of movement disorders of sleep?

A
  1. restless leg syndrome (RLS)
  2. periodic limb movements of sleep (PLMS)
  3. propriospinal myoclonus
  4. rhythmic movement disorder of sleep (common in children -> bang their hand, usually, autistic)
37
Q

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?

A
  • 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
38
Q

what is diagnostic criteria for RLS? (URGE)

A

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

39
Q

what are the treatment options for RLS and PLMS?

A
  • Iron
  • dopamine agonists
  • L-dopa
  • Clonazepam
  • Pregabalin
  • Gabapentin
  • Opiates
40
Q

what is the significance of driving in sleeping disorder?

A
  • 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

MED627 (6 decks)

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