Harrison + Bennett Sleep Notes Flashcards
how much more sleep do women need compared to men
15-30 more minutes
what is muscle tone like in NREM sleep
normal
how frequent must symptoms occur to meet criteria for RLS
3+ times per week for 3+ months
how does prevalence of RLS change with age
increases with age
in which population is RLS more common
caucasian
lower in asian, african american
how does pregnancy affect risk of RLS
prevalence during pregnancy is 2-3 x higher than gen pop
is there a genetic basis for RLS
yes–> some alleles strongly associated
what is the underlying pathophysiology of RLS
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
how do you diagnose PLMD
PSG–> can only be diagnosed with PSG
what % of those with RLS have PLMs when sleep recordings taken over multiple nights
90%
does RLS require a sleep study to diagnose
no
list the main medical disorders that are comorbid or etiologically related to RLS
CV disease
HTN
narcolepsy
migraine
parkinsons
MS
peripheral neuropathy
OSA
DM
fibromyalgia
osteoporosis
obesity
thyroid disease
cancer
iron deficiency
pregnancy
chronic renal failure (uremia)
is gabapentin first line for RLS
no–> second line (along with pregabalin)
the dopamine agonists are first line
prevalence of REM sleep behaviour disorder
0.5% in general population
M>F
what is the population most overwhelmingly affected by REM sleep behaviour disorder
males older than 50
what is the presumed etiology of REM sleep behaviour disorder
thought to be due to loss of spinal inhibition in REM
list risk factors for REM sleep behaviour disorder
TBI
farming and pesticide exposure
lower education
aggravated by SSRI use
what is the usual course of REM sleep behaviour disorder
usually progressive
how does REM sleep behaviour disorder usually change as the underlying synucleinopathy progresses (if associated with one)
actually usually improves as the dementia worsens
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
narcolepsy or med induced REM sleep behaviour disorder
what % of those with narcolepsy also have REM sleep behaviour disorder
about 30%
what are the 2 NREM parasomnias
sleep terrors
sleepwalking
is someone alert quickly after waking up from a REM sleep behaviour disorder
yes
is someone alert quickly after waking up from a NREM sleep behaviour disorder
no–confused, amnestic of the event
what medical condition, that is fairly treatable, can mimic or worsen REM sleep behaviour disorder
OSA
what type of investigation is needed to diagnose REM sleep behaviour disorder
VIDEO polysomnography–> ESSENTIAL for the dx of REM sleep behaviour disorder
which medication is now favored for treatment of REM sleep behaviour disorder
high dose melatonin–> favored over clonazepam which used to be the first line tx
typical dose range for melatonin = 3-12mg
what % of those with a REM sleep behaviour disorder will go on to develop a parkinsons plus syndrome
90%
how many obstructive apneas or hypopneas per hour of sleep are required to make the dx of OSA
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
define mild OSA
apnea hypopnea index is less than 15
define moderate OSA
apnea hypopnea index is 15-30
define severe OSA
apnea hypopnea index is above 30
what is the most common breathing related sleep disorder
OSA
what is the prevalence of OSA
1-2% of children
2-15% of middle age adults
more than 20% of older adults
are more men or women affected by OSA
men:women 3:1
risk factors for OSA
first degree relative doubles risk
genetic disorders like marfans
small jaw
large neck
smoking
alcohol use
obesity
how long do episodes of apnea/hypopnea tend to last
10-30 sec but can be longer
what disorder may be diagnosed in error, when the underlying problem is actualyl sleep apnea
depression
what physical symptom is common in the mornings for those with OSA
morning headaches
having OSA increases risk for what adverse events in life
HTN, afib and other arrythmias, HF, stroke, TIAs, CAD
DM, DLD
depression
MVAs
poor job perofrmance
work related accidents
dementia
what is the standard treatment for OSA
CPAP
what is a mnemonic for risk factors/questions to ask about for OSA
STOP BANG
snoring
tired
observed apnea
“pressure”
BMI
age
neck size
gender (m)
what is cheyne stokes breathing
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
what is criterion A for hypersomnolence disorder
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
how is severity of hypersomnolence disorder assessed
depends on number of days per week the person has difficulty maintaining daytime alertness
what % of cases of hypersomnolence disorder are associated with viral infection
10%
head trauma 6-18 months prior is also a risk factor
is sleep efficiency impaired in hypersomnolence disorder
no, 90% have good sleep efficiency, but still experience “sleep inertia”
how do you treat hypersomnolence disorder
trial of modafinil, methylphenidate, amphetamines for symptom management
what is criterion A for insomnia disorder
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
what is the prevalence of insomnia disorder
5%
list risk factors for insomnia disorder
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
what proportion of those with insomnia disorder have difficulties with initiation?
1/3 have difficulty with initiation
1/3 with maintenance or both
1/3 with non-restorative sleep
what sleep latency is considered “initial insomnia”
greater than 20-30 min
what is the most common type of insomnia in the pediatric population
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
should you treat behavioural insomnia pharmacologically
NO
what are the 3 principles to treating bed time resistance/behavioural insomnia
- creating an emotional state of calmness and safety
- consistent limit setting
- 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
what % of those c/o insomnia could have a mood disorder
up to 40%
what % of GAD patients have insomnia
up to 70%
what % of those with depression complain of insomnia
up to 90%
what investigations should you consider in someone with suspected insomnia disorder
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
list first line pharmacological treatments for insomnia disorder
- benzo-receptor agonists–>
temazepam
(US FDA has also approved some other benzos with funny names) - non-benzo receptor agonists–>
zopiclone, zolpidem, eszopiclone, zaleplon
list second line agents for pharmacological tx of insomnia disorder
trazodone
doxepin
mirtazapine
and other sedating SSRIs
what are some off label medications that are sometimes used for treating insomnia disorder
olanzapine, quetiapine, risperidone
melatonin, tryptophan, valerian root
gabapentin, pregabalin
how do benzos affect sleep
increases N2 sleep–> decreases SWS, REM
after 6-7 weeks, only get an hour more of sleep
what effect do the Z drugs have on sleep
LESS EFFECT on sleep architecture
mild INCREASE in SWS
less rebound insomnia than benzos
do not use more than 5 mg in elderly
how do suvorexant and lemborexant work
they are orexin ANTagonists
orexin promotes wakefulness–antagonists would do opposite
lemborexant increases NREM sleep
should you use antipsychotic to treat chronic insomnia
no
how does melatonin affect sleep
increased REM density
increased N2
decreased SWS
*take 6 hours before middle of sleep
what would you use kava kava for
insomnia
is CBT-insomnia first line
YES–> is effective and should be offered as first line tx
Effects are more DURABLE than medications
can also reduce depression sx
what are the components of CBT-I
sleep hygiene education
sleep restriction
stimulus control
relaxation based intervention
cognitive restructuring
are sleep terror episodes common in childhood
yes–> 36.7% at 18 mo, 20% at 30 months but not necessarily the DISORDER
drops to 2.2% in adulthood
what is the natural course of sleep terrors
will usually start in childhood and resolve by adolesence
can develop it in adulthood however and this course usually waxes and wanes
are there any anticipatory autonomic changes seen prior to the arousals in NREM sleep terrors
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
treatment of sleep terrors
clonazepam low dose
can also use SSRIs, TCAs in tx of NREM parasomnias
what % of those with sleep walking have family hx of same
up to 80%
what medications can cause NREM parasomnias
Z drugs–> should be avoided in patients with parasomnias
if an adult presents for sleep walking but has no hx of sleep walking as a kid, what should you consider
other etiology like OSA, nocturnal seizures or medication effect
criterion A for nightmare disorder
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”)
what is the prevalence of frequent nightmares
1-2%
are more males or females affected by nightmare disorder
females
what is the course of nightmare disorder
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
what do you see on EEG during a sleep terror
slow wave sleep pattern most likely
are night terrors dreams
no, technically not dreams
are more of a sudden reaction of fear that occurs during the transition from one sleep stage to another
peak age for sleep terrors
1-4 years
peak age for nightmares
3-12 years
treatment of nightmare disorder
image rehearsal therapy (IRT)
what is criterion A for narcolepsy
recurrent, irresistible NEED FOR SLEEP 3+ a week for 3+ months
in addition to criterion A, criterion B for narcolepsy lists 3 other symptoms–how many are required and what are they
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
what is cataplexy
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
how do you measure hypocretin deficiency
in the CSF–> needs to be less than 1/3 of normal to dx narcolepsy
are there genetic narcolepsy syndromes
yes–> autosomal dominant cerebellar ataxia, deafness and narcolepsy + autosomal dominant narcolepsy, obesity and T2DM
when do symptoms usually start in autosomal dominant cerebellar ataxia, deafness and narcolepsy
late onset–> age 30s-40s
eventually develop dementia
what other medical illnesses can cause narcolepsy
whipples disease
sarcoidosis
traumatic
tumoral desctruction of hypocretin neurons
how do you measure severity for narcolepsy
● 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)
prevalence of narcolepsy
0.03%
what is narcolepsy type 1
with cataplexy
with is narcolepsy type 2
without cataplexy
what is the prevalence of narcolepsy in first degree relatives of someone with the disorder
increases to 1% which is a 40x increase over general population risk
what is almost always the cause of narcolepsy-cataplexy
loss of hypothalamic hypocretin producing cells causing orexin/hypocretin deficiency
can be due to autoimmune causes, TBI, viral infections, strep infection
when does narcolepsy typically start
adolescence
bimodal–> 15-25 then again ages 30-35
what % of those with narcolepsy also have vivid hypnagogic or hypnopompinc hallucinations
30%
what is thought to cause cataplexy
thought to be due to REM INTRUSION –> intrusion of REM sleep paralysis into a state of wakefulness
are respiratory function or eye muscles affected by cataplexy
no
what investigations should you do when narcolepsy is suspected
hypocretin/orexin
genotyping
PSG
what is the gold standard test for narcolepsy
hypocretin/orexin n the CSF–> need to do LP
what % of those with narcolepsy+cataplexy have an implicated gene
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
