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20. Sleep-Wake Disorders > Harrison + Bennett Sleep Notes > Flashcards

Harrison + Bennett Sleep Notes Flashcards

1
Q

how much more sleep do women need compared to men

A

15-30 more minutes

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2
Q

what is muscle tone like in NREM sleep

A

normal

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3
Q

how frequent must symptoms occur to meet criteria for RLS

A

3+ times per week for 3+ months

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4
Q

how does prevalence of RLS change with age

A

increases with age

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5
Q

in which population is RLS more common

A

caucasian

lower in asian, african american

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6
Q

how does pregnancy affect risk of RLS

A

prevalence during pregnancy is 2-3 x higher than gen pop

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7
Q

is there a genetic basis for RLS

A

yes–> some alleles strongly associated

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8
Q

what is the underlying pathophysiology of RLS

A

thought to be due to disturbances in the central DOPAMINERGIC system –> reduction of D2 receptor binding is seen in CAUDATE and PUTAMEN on spect/pet

also improves with dopamine agonist therapy

low brain iron concentrations, disturbances in iron metabolism and disturabnces in brain iron transport are also thought to be involved

in CSF samples, iron and ferritin values are LOWER and transferrin levels are HIGHER in individuals with RLS

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9
Q

how do you diagnose PLMD

A

PSG–> can only be diagnosed with PSG

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10
Q

what % of those with RLS have PLMs when sleep recordings taken over multiple nights

A

90%

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11
Q

does RLS require a sleep study to diagnose

A

no

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12
Q

list the main medical disorders that are comorbid or etiologically related to RLS

A

CV disease

HTN

narcolepsy

migraine

parkinsons

MS

peripheral neuropathy

OSA

DM

fibromyalgia

osteoporosis

obesity

thyroid disease

cancer

iron deficiency

pregnancy

chronic renal failure (uremia)

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13
Q

is gabapentin first line for RLS

A

no–> second line (along with pregabalin)

the dopamine agonists are first line

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14
Q

prevalence of REM sleep behaviour disorder

A

0.5% in general population
M>F

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15
Q

what is the population most overwhelmingly affected by REM sleep behaviour disorder

A

males older than 50

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16
Q

what is the presumed etiology of REM sleep behaviour disorder

A

thought to be due to loss of spinal inhibition in REM

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17
Q

list risk factors for REM sleep behaviour disorder

A

TBI

farming and pesticide exposure

lower education

aggravated by SSRI use

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18
Q

what is the usual course of REM sleep behaviour disorder

A

usually progressive

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19
Q

how does REM sleep behaviour disorder usually change as the underlying synucleinopathy progresses (if associated with one)

A

actually usually improves as the dementia worsens

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20
Q

if you see a patient who is young and female, and they seem to have sx of REM sleep behaviour disorder, what other disorders should you consider first

A

narcolepsy or med induced REM sleep behaviour disorder

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21
Q

what % of those with narcolepsy also have REM sleep behaviour disorder

A

about 30%

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22
Q

what are the 2 NREM parasomnias

A

sleep terrors

sleepwalking

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23
Q

is someone alert quickly after waking up from a REM sleep behaviour disorder

A

yes

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24
Q

is someone alert quickly after waking up from a NREM sleep behaviour disorder

A

no–confused, amnestic of the event

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25
Q

what medical condition, that is fairly treatable, can mimic or worsen REM sleep behaviour disorder

A

OSA

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26
Q

what type of investigation is needed to diagnose REM sleep behaviour disorder

A

VIDEO polysomnography–> ESSENTIAL for the dx of REM sleep behaviour disorder

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27
Q

which medication is now favored for treatment of REM sleep behaviour disorder

A

high dose melatonin–> favored over clonazepam which used to be the first line tx

typical dose range for melatonin = 3-12mg

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28
Q

what % of those with a REM sleep behaviour disorder will go on to develop a parkinsons plus syndrome

A

90%

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29
Q

how many obstructive apneas or hypopneas per hour of sleep are required to make the dx of OSA

A

5+ per hour of sleep (seen on PSG) + nocturnal breathing disturbances (i.e snoring) or daytime sleepiness/fatigue etc

OR

PSG evidence of 15+ apneas or hypopneas per hour of sleep regardless of other symptoms

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30
Q

define mild OSA

A

apnea hypopnea index is less than 15

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31
Q

define moderate OSA

A

apnea hypopnea index is 15-30

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32
Q

define severe OSA

A

apnea hypopnea index is above 30

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33
Q

what is the most common breathing related sleep disorder

A

OSA

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34
Q

what is the prevalence of OSA

A

1-2% of children

2-15% of middle age adults

more than 20% of older adults

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35
Q

are more men or women affected by OSA

A

men:women 3:1

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36
Q

risk factors for OSA

A

first degree relative doubles risk

genetic disorders like marfans

small jaw

large neck

smoking

alcohol use

obesity

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37
Q

how long do episodes of apnea/hypopnea tend to last

A

10-30 sec but can be longer

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38
Q

what disorder may be diagnosed in error, when the underlying problem is actualyl sleep apnea

A

depression

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39
Q

what physical symptom is common in the mornings for those with OSA

A

morning headaches

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40
Q

having OSA increases risk for what adverse events in life

A

HTN, afib and other arrythmias, HF, stroke, TIAs, CAD

DM, DLD

depression

MVAs

poor job perofrmance

work related accidents

dementia

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41
Q

what is the standard treatment for OSA

A

CPAP

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42
Q

what is a mnemonic for risk factors/questions to ask about for OSA

A

STOP BANG

snoring
tired
observed apnea
“pressure”
BMI
age
neck size
gender (m)

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43
Q

what is cheyne stokes breathing

A

A pa ttern of periodic crescendo-decrescendo varia tion in tidal volume that results in central apneas and hypopneas at a frequency of 5+ events per hour, accompanied by frequent arousal

often associated with heart failure

44
Q

what is criterion A for hypersomnolence disorder

A

A. Self-reported excessive sleepiness despite a main sleep period lasti ng at least 7 hours, with at least 1+:
–Recurrent periods of sleep or lapses into sleep within the same day
–A prolonged main sleep episode of more than 9 hours per day that is non-restorati ve (unrefreshing)
–Difficulty being fully awake a fter abrupt awakening

45
Q

how is severity of hypersomnolence disorder assessed

A

depends on number of days per week the person has difficulty maintaining daytime alertness

46
Q

what % of cases of hypersomnolence disorder are associated with viral infection

A

10%

head trauma 6-18 months prior is also a risk factor

47
Q

is sleep efficiency impaired in hypersomnolence disorder

A

no, 90% have good sleep efficiency, but still experience “sleep inertia”

48
Q

how do you treat hypersomnolence disorder

A

trial of modafinil, methylphenidate, amphetamines for symptom management

49
Q

what is criterion A for insomnia disorder

A

A predominant complaint of DISSATISFACTION with sleep QUALITY or QUANTITY, associated with 1+ of:
1. Difficulty INITIATING sleep
2. Difficulty MAINTAINING sleep, characterized by frequent awakenings or problems
returning to sleep aft er awakenings
3. EARLY MORNING awakening with inability to return to sleep

*occurs despite adequate opportunity for sleep

50
Q

what is the prevalence of insomnia disorder

A

5%

51
Q

list risk factors for insomnia disorder

A

female

advanced age

family hx of insomnia disorder

anxiety/worry prone personality or cognitive style

increased arousal predisposition

noise

light

high/low temp

high altitude

excessive caffeine use

irregular sleep schedules

52
Q

what proportion of those with insomnia disorder have difficulties with initiation?

A

1/3 have difficulty with initiation
1/3 with maintenance or both
1/3 with non-restorative sleep

53
Q

what sleep latency is considered “initial insomnia”

A

greater than 20-30 min

54
Q

what is the most common type of insomnia in the pediatric population

A

behavioural insomnia–> “bed time resistance”

may refuse to sleep, want to be rocked, or sleep in parents bed

methods that demand children “cry it out” can actually impeded development of healthy self regulation –> soothing with an aim toward learning self soothing provides better long term results for emotional growth and resilience

55
Q

should you treat behavioural insomnia pharmacologically

A

NO

56
Q

what are the 3 principles to treating bed time resistance/behavioural insomnia

A
  1. creating an emotional state of calmness and safety
  2. consistent limit setting
  3. establishing good bedtime habits–> i.e wind down period and sequence of activities that begin 30-60 min before bed time and promote good sleep hygiene
57
Q

what % of those c/o insomnia could have a mood disorder

A

up to 40%

58
Q

what % of GAD patients have insomnia

A

up to 70%

59
Q

what % of those with depression complain of insomnia

A

up to 90%

60
Q

what investigations should you consider in someone with suspected insomnia disorder

A

PSG–> increased stage 1 sleep, decreased stage 3

quantitative EEG–> higher frequency EEG power around sleep onset and during NREM sleep–> suggests INCREASED CORTICAL AROUSAL

bloodwork–> ?increased activation of HPA axis

61
Q

list first line pharmacological treatments for insomnia disorder

A
  1. benzo-receptor agonists–>
    temazepam
    (US FDA has also approved some other benzos with funny names)
  2. non-benzo receptor agonists–>
    zopiclone, zolpidem, eszopiclone, zaleplon
62
Q

list second line agents for pharmacological tx of insomnia disorder

A

trazodone

doxepin

mirtazapine

and other sedating SSRIs

63
Q

what are some off label medications that are sometimes used for treating insomnia disorder

A

olanzapine, quetiapine, risperidone

melatonin, tryptophan, valerian root

gabapentin, pregabalin

64
Q

how do benzos affect sleep

A

increases N2 sleep–> decreases SWS, REM

after 6-7 weeks, only get an hour more of sleep

65
Q

what effect do the Z drugs have on sleep

A

LESS EFFECT on sleep architecture

mild INCREASE in SWS

less rebound insomnia than benzos

do not use more than 5 mg in elderly

66
Q

how do suvorexant and lemborexant work

A

they are orexin ANTagonists

orexin promotes wakefulness–antagonists would do opposite

lemborexant increases NREM sleep

67
Q

should you use antipsychotic to treat chronic insomnia

A

no

68
Q

how does melatonin affect sleep

A

increased REM density

increased N2

decreased SWS

*take 6 hours before middle of sleep

69
Q

what would you use kava kava for

A

insomnia

70
Q

is CBT-insomnia first line

A

YES–> is effective and should be offered as first line tx

Effects are more DURABLE than medications

can also reduce depression sx

71
Q

what are the components of CBT-I

A

sleep hygiene education

sleep restriction

stimulus control

relaxation based intervention

cognitive restructuring

72
Q

are sleep terror episodes common in childhood

A

yes–> 36.7% at 18 mo, 20% at 30 months but not necessarily the DISORDER

drops to 2.2% in adulthood

73
Q

what is the natural course of sleep terrors

A

will usually start in childhood and resolve by adolesence

can develop it in adulthood however and this course usually waxes and wanes

74
Q

are there any anticipatory autonomic changes seen prior to the arousals in NREM sleep terrors

A

NO–> NREM sleep arousals begin suddenly from sleep, without anticipatory autonomic changes

this is different from nightmare disorder, where there ARE autonimic changes before the arousal

75
Q

treatment of sleep terrors

A

clonazepam low dose

can also use SSRIs, TCAs in tx of NREM parasomnias

76
Q

what % of those with sleep walking have family hx of same

A

up to 80%

77
Q

what medications can cause NREM parasomnias

A

Z drugs–> should be avoided in patients with parasomnias

78
Q

if an adult presents for sleep walking but has no hx of sleep walking as a kid, what should you consider

A

other etiology like OSA, nocturnal seizures or medication effect

79
Q

criterion A for nightmare disorder

A

Repeated occurrences of EXTENDED, extremely DYSPHORIC, and WELL REMEMBERED dreams that usually involve efforts to avoid threats to survival, security, or physical integrity and that generally occur during the SECOND HALF of the major sleep episode

(typically “story like”)

80
Q

what is the prevalence of frequent nightmares

A

1-2%

81
Q

are more males or females affected by nightmare disorder

A

females

82
Q

what is the course of nightmare disorder

A

increases from ages 10-13 for both M and F, but continues to increase to ages 20-29 for females (while decreasing for males)

prevalence decreases steadily with age for both sexes but gender difference remains

83
Q

what do you see on EEG during a sleep terror

A

slow wave sleep pattern most likely

84
Q

are night terrors dreams

A

no, technically not dreams

are more of a sudden reaction of fear that occurs during the transition from one sleep stage to another

85
Q

peak age for sleep terrors

A

1-4 years

86
Q

peak age for nightmares

A

3-12 years

87
Q

treatment of nightmare disorder

A

image rehearsal therapy (IRT)

88
Q

what is criterion A for narcolepsy

A

recurrent, irresistible NEED FOR SLEEP 3+ a week for 3+ months

89
Q

in addition to criterion A, criterion B for narcolepsy lists 3 other symptoms–how many are required and what are they

A

need 1+ of:
1. cataplexy at least a few times per month
2. hypocretin (orexin) deficiency
3. PSG showing REM sleep latency less than or equal to 15 min or MSLT showing mean sleep latency of 8min or less and 2 or more sleep onset REM period

90
Q

what is cataplexy

A

in those with long standing narcolepsy, brief (seconds to minutes) episodes of SUDDEN BILATERAL LOSS OF MUSCLE TONE with MAINTAINED CONSCIOUSNESS that are PRECIPITATED by LAUGHTER/JOKING

or

in kids or those within 6 months of onset, SPONTANEOUS GRIMACES or JAW OPENING episodes with TONGUE THRUSTING or a GLOBAL HYPOTONIA without any emotional triggers

91
Q

how do you measure hypocretin deficiency

A

in the CSF–> needs to be less than 1/3 of normal to dx narcolepsy

92
Q

are there genetic narcolepsy syndromes

A

yes–> autosomal dominant cerebellar ataxia, deafness and narcolepsy + autosomal dominant narcolepsy, obesity and T2DM

93
Q

when do symptoms usually start in autosomal dominant cerebellar ataxia, deafness and narcolepsy

A

late onset–> age 30s-40s

eventually develop dementia

94
Q

what other medical illnesses can cause narcolepsy

A

whipples disease

sarcoidosis

traumatic

tumoral desctruction of hypocretin neurons

95
Q

how do you measure severity for narcolepsy

A

● Mild: Infrequent cataplexy (less than once per week), need for naps only once or twice per day, and less disturbed nocturnal sleep

● Moderate: Cataplexy once daily or every few days, disturbed nocturnal sleep, and need for mul tiple naps daily

● Severe: Drug-resistant cataplexy with mul tiple a ttacks daily, nearly constant sleepiness, and disturbed nocturnal sleep (i.e., movements, insomnia, and vivid dreaming)

96
Q

prevalence of narcolepsy

A

0.03%

97
Q

what is narcolepsy type 1

A

with cataplexy

98
Q

with is narcolepsy type 2

A

without cataplexy

99
Q

what is the prevalence of narcolepsy in first degree relatives of someone with the disorder

A

increases to 1% which is a 40x increase over general population risk

100
Q

what is almost always the cause of narcolepsy-cataplexy

A

loss of hypothalamic hypocretin producing cells causing orexin/hypocretin deficiency

can be due to autoimmune causes, TBI, viral infections, strep infection

101
Q

when does narcolepsy typically start

A

adolescence

bimodal–> 15-25 then again ages 30-35

102
Q

what % of those with narcolepsy also have vivid hypnagogic or hypnopompinc hallucinations

A

30%

103
Q

what is thought to cause cataplexy

A

thought to be due to REM INTRUSION –> intrusion of REM sleep paralysis into a state of wakefulness

104
Q

are respiratory function or eye muscles affected by cataplexy

A

no

105
Q

what investigations should you do when narcolepsy is suspected

A

hypocretin/orexin

genotyping

PSG

106
Q

what is the gold standard test for narcolepsy

A

hypocretin/orexin n the CSF–> need to do LP

107
Q

what % of those with narcolepsy+cataplexy have an implicated gene

A

99%–> HLA-DQBI*06:02

its present in 20-25% of gen pop and in 40% of those with narcolepsy but no cataplexy

might consider genotyping before CSF hypocretin LP

20. Sleep-Wake Disorders (3 decks)

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