Brian Chow Sleep Powerpoint Flashcards
what % of total nighttime sleep is NREM
75%
what % of total sleep is REM
25%
when does slow wave sleep/N3 occur in the night
in first half of the sleep period
when does REM occur
more frequently during last THIRD of the sleep period
what is another term for N3 sleep
slow wave sleep
what does sleep architecture look like on a sleep histogram
what % of sleep is stage 2 sleep
50%
how many types of NREM sleep are there
W, N1, N2 and N3/SWS
what % of sleep is N3/SWS
20%
what % of sleep is N1
5%
list the 8 elements included in polysomnography
EEG–> brainwaves (central and occipital leads)
EOG–> eye movements
EMG–> muscle tone (chin and legs)
ECG–> heart
breathing–> airflow (nose/mouth) and effort (thoracic, abdo)
SaO2
snore microphone
digital AV recording
how do you conduct a multiple sleep latency test
do this after PSG
4-5 x 20 min naps at 2 hour intervals
check for average sleep onset latency
sleep onset REM periods
what is considered “pathological sleepiness” on a MSLT
fall asleep in 8 min or less and 2 or more SOREMPs (sleep onset REM periods)
what is the state of physiological arousal during NREM sleep
HYPOarousal –> low HR, low BP, low resting muscle tone
what is N1 sleep
light sleep–> slow rolling eye movements (hypnic jerks)
what stage of sleep is the most physically restorative
N3 (SWS)
physically restorative, consolidates declarative memory
are most difficult to rouse in this state
what happens to N3 sleep as we age
decreases
what waves are seen in EEG in the following phase? what frequency are these waves?
Awake
BETA waves
13-30 Hz
what waves are seen in EEG in the following phase? what frequency are these waves?
Drowsy
ALPHA waves
8-12 Hx
what waves are seen in EEG in the following phase? what frequency are these waves?
N1 sleep
THETA waves
3-7 Hz
what waves are seen in EEG in the following phase? what frequency are these waves?
N2 sleep
SLEEP SPINDLES and K COMPLEXES
12-14 Hz
what waves are seen in EEG in the following phase? what frequency are these waves?
N3 sleep
DELTA waves
0.5-2 Hz
which stage of sleep shows the slowest frequency waves on EEG
N3/SWS
which stage of sleep (NOT awake) shows the highest frequency waves on EEG
N2
which stage of sleep is associated with sleep spindels and K complexes
N2
with is a mnemonic to remember EEG waveform in various stages of sleep
BATS eat KD
beta, alpha, theta, sleep spindles and k complexes, delta
what type of waves are seen on EEG in REM sleep
SAWTOOTH waves
theta
slow alpha
why is REM called “paradoxical sleep”
because looks like awake on EEG
in what stage of sleep do you dream
REM
what is the physiological state of the body in REM sleep
HYPERarousal of autonomic state
HR, BP, RR show increased variability, can be irregular
brain–> increased glucose metabolism, blood flow, cerebral temp
poikilothermic condition prevails
penile erection
skeletal muscles are in NEAR TOTAL PARALYSIS
when do you have your first REM cycle
90 minutes after falling asleep
how long is your first REM cycle compared to later cycles
first is short (under 10 min) then later ones are longer (15-45 min)
have REM cycles every 90-100 minutes
in what stage of sleep are skeletal muscles in a state of near total paralysis
REM
what do the various brain waves look like in different stages of sleep (image)
in what stage of sleep do you see slow, rolling eye movements
N1
in what stage of sleep are there no eye movements
N2, N3
in what stage of sleep are there bursts of eye movements
REM
what brain areas are related to NREM sleep
anterior hypothalamus
thalamus
basal forebrain
nucleus tractus solitarius (medulla)
dorsal raphe nucleus (midbrain)
what brain areas are related to REM sleep
PONTINE RETICULAR FORMATION
midbrain
medulla
hypothalamus
what brain area controls the ONSET of sleep
hypothalamis
what brain area helps initiate REM sleep
pons
what brain area regulates the transition between sleep and wakefulness
reticular formation
what brain area is active during dreaming
hippocampus and amygdala
hippocampus=memory
amygdala=emotion
what brain area prevents sensory signals from reaching the cortex during sleep
thalamus
what neurotransmitter is associated with the pons
acetylcholine
what neurotransmitter is associated with the raphe nucleus
serotonin
what neurotransmitter is associated with the locus ceruleus
norepinephrine
where is orexin released from
hypothalamus
where does orexin act
locus ceruleus–> wakefulnes pathway
raphe nuclei–> wakefulness pathway
ventral tegmental area–> reward pathway
nucleus accumbens –> reward pathway
what are the two primary factors that control the physiological need for sleep
homeostasis –> PROCESS S
circadian rhythm–> PROCESS C
what is process S
“sleep drive”
homeostatic control of physiological need for sleep
tendency to sleep increases the further from last sleep you are
what is process C
controlled by “biological clock”–> the circadian rhythm
what brain area controls the circadian rhythm
SUPRACHIASMATIC NUCLEUS in the anterior hypothalamus
receives PHOTIC and NON-PHOTIC inputs
synchronizes circadian rhythm to environmental cues
list the WAKE promoting neurotransmitters
norepinephrine
dopamine
orexin (hypocretin)
histamine
glutamate
list the SLEEP promoting neurotransmitters
acetylcholine–> REM
which neurotransmitter is both awake and sleep promoting
serotonin
what does the suprachiasmatic nucleus do
regulates the timing of nocturnal melatonin secretion from the pineal gland via the superior cervical ganglion
how does exposure to light during the biological night affect melatonin production
exposure to light SUPPRESSES melatonin production
when do melatonin levels peak
middle of the night–> decline to low daytime amounts
starts being produced in the evening
what produces melatonin
pineal gland
how does total sleep change across the lifespan
decreases
how does REM sleep change across the lifespan
wayyyy more in kids up until about age 2-4, then steadily decreases into old age
how does NREM sleep amount change over the lifespan
decreases (not as dramatically as REM)
does NEED for sleep change over the lifespan
no–> need for sleep stays the same
how does the following sleep parameter change (increased or decreased) as someone ages:
REM sleep
declines after age 65
how does the following sleep parameter change (increased or decreased) as someone ages:
sleep fragmentation
increases
how does the following sleep parameter change (increased or decreased) as someone ages:
total sleep time
decreases
how does the following sleep parameter change (increased or decreased) as someone ages:
ability to sleep
decreases
how does the following sleep parameter change as someone ages:
natural circadian rhythm
phase ADVANCE (earlier to sleep and wake)
how does the following sleep parameter change (increased or decreased) as someone ages:
sleep efficiency
decreased
how does the following sleep parameter change (increased or decreased) as someone ages:
SWS
decreased
how does the following sleep parameter change (increased or decreased) as someone ages:
sleep latency
increased
how does the following sleep parameter change (increased or decreased) as someone ages:
total sleep time
decreased
how much sleep is recommended for a newborn
14-17 hours
how much sleep is recommended for a school age child
9-11 hours
how much sleep is recommended for a teen
8-10 hours
how much sleep is recommended for adults
7-9 hours
how much sleep is recommended for an odler adult
7-8 hours
what factors, and their related etiologies, can result in excessive daytime sleepiness
- lack of sleep (inadequate quantity)
–> insufficient time in bed - inadequate quality of sleep
–> sleep apnea, PLMS, environment - intrinsic sleepiness
–> narcolepsy, idiopathic hypersomnia - medical/psych disorder
–> mood disorder, medical, meds - circadian rhythm disturbance
–> shift work, delayed sleep phase etc
what factors, and their related etiologies, can result in nocturnal spells
- NREM sleep arousal disorder (parasomnia)
–> night terror type, sleep walking type - REM sleep arousal disorder (parasomnia)
–> nightmares, REM sleep behaviour disorder - seizure disorder
- psychiatric
–> panic attacks etc
how is cortisol release affected by insomnia
increased HPA activity with insomnia–> cortisol–> this normalizes with treatment of insomnia
why should you avoid excessive time in bed
can lead to sleep fragmentation
why should you not have a clock in your bedroom
watching clock leads to worry, rumination
why should you avoid caffeine, alcohol, nicotine
all can impact sleep and activate RLS
alcohol can worsen OSA
why should you reduce HS fluid intake
reduces nightime awakenings related to full bladder
why should you eat a light bedtime snack
promotes sleep by reducing hypoglycemia
list 7 strategies that fall under “sleep hygiene”
limit time in bed
regular sleep schedule–> esp. awakening time
no clock in bedroom
avoid caffeine, nicotine, alcohol
eat light bedtime snack
reduce HS fluid intake
dont try to fall asleep, or take worries to bed
why does having a regular sleep schedule help with sleep
strengthens homeostatic process and circadian synchrony
what is the goal of stimulus control in the treatment of insomnia
aim to re-associate sleep stimuli with falling asleep
what are elements of stimulus control in the treatment of insomnia
only go to bed when SLEEPY
only use BEDROOM for SLEEP
if unable to sleep, GET OUT OF BED
arise at SAME TIME every morning
DO NOT NAP during the day
why does sleep restriction work for insomnia
limits time in bed to ACTUAL sleep time
creates mild sleep deprivation and results in more consolidated and efficient sleep
how does sleep restriction work/how do you do it
maintain sleep log–> determine average total sleep time
decrease allowable time in bed to usual sleep time (NOT less than 5 hours)
change time in bed by 15 min increments weekly–> if sleep efficiency is above 85%, then increase by 15 min. If sleep efficiency below 85%, decrease by 15 min
wake time is kept constant and bedtimes are adjusted
what is the goal of CBT for insomnia
change the underlying beliefs that perpetuate insomnia that maintain maladaptive sleep behaviours
what are 6 basic cognitive strategies for insomnia
keep realistic expectations
do not blame insomnia for all impairments
do not give too much importance to sleep
do not catastrophize after a poor nights sleep
never TRY to fall asleep
develop tolerance to the effects of insomnia
list 3 first line NON pharmacological interventions for insomnia
sleep hygiene education
stimulus control therapy
sleep restriction therapy
list 2 second line NON pharmacological interventions for insomnia
cognitive training
relaxation training
when is pharmacological treatment appropriate for insomnia
SHORT term and TRANSIENT insomnia
NOT indicated for chronic insomnia
what are the prescribing principles when Rx for insomnia
lowest effective dose
intermittent dosing (2-4x per week)
short term prescribing (less than 4 weeks)
gradual discontinuation (reduce rebound insomnia)
meds with shorter half life–> minimize daytime sedation
how do you assess for hypersomnolence disorder
PSG–> rule out BRSD, PLMD, narcolepsy
use the epworth sleepiness scale
MSLT
what is the gold standard for testing daytime sleepiness
MSLT
what score on the epworth sleepiness test suggests hypersomnolence disorder
men are above 11
female are above 9
how do you treat hypersomnolence disorder
stimulants
modafinil–> less potential for abuse, no peripheral sympathomimetic action
ritalin, dexedrin–> abuse potential, can cause irritability, headaches, insomnia, excessive sweating
how many hours in bed is characteristic of someone with kleine-levin syndrome
18-20 hours in bed or asleep
list the characteristic features of kleine-levin syndrome
recurrent periods of SLEEPINESS
disinhibition
derealization
indiscriminate HYPERSEXUALITY
compulsive OVEREATING, acute weight gain
non specific neuro findings–> decreased deep tendon reflexes, nystagmus, dysarthria
is there any familial aggregation in kleine-levin syndrome
no
what is the course of kleine-levin syndrome
may continue with periodic course of decades
often resolves with middle age
are more men or women affected by kleine-levin syndrome
more men (3x)
what does the epworth sleepiness scale ask
how likely someone is to fall asleep doing various activities
what is the narcolepsy “pentad” (5 features)
- excessive daytime SLEEPINESS
–> may fall asleep without warning, in unusual situations - cataplexy
- hypnagogic/pompic hallucinations
- sleep paralysis
- disturbed nocturnal sleep
what % of those with narcolepsy have cataplexy
75%
what % of those with narcolepsy have hypnagogic/pompinc hallucinations
50-66%
what % of those with narcolepsy will have sleep paralysis
50-66%
list 3 non pharmacologic interventions for narcolepsy
scheduled napping
lifestyle adjustment
psychological counselling
what pharmacologic intervention can you use for the daytime sleepiness associated wtih narcolepsy
modafinil (could also consider ritalin or dexedrine)
what pharmacologic intervention can you use for the cataplexy associated wtih narcolepsy
sodium oxybate/GHB (also improved daytime sleepiness)
SSRIs, TCAs–> try SSRIs first before above as its safer
why might you use SSRIs to treat narcolepsy
are REM suppresants–> helps with sleep paralysis, hypnagogic/pompic hallucinations, cataplexy
list 4 physical exam findings common in OSA
often overweight
increased neck size
if normal weight, often have a structural abnormality like adenotonsillar enlargement
nasal airway obstruction even when awake (noisy breather)
are those with central sleep apnea likely to be overweight
less likely to be overweight
what are two sequelae of breathing related sleep disorders
HTN
can develop right heart failure/cor pulmonale
how do you assess breathing related sleep disorders
overnight PSG
how do you manage OSA
weight loss
avoid sleeping on back
tennis balls
nasal CPAP
nasal surgery
uvuloplasty
oral devices
what should you avoid in OSA
use of sedative meds and alcohol as can exacerbate OSA
what population is more likely to have non-24 hour circadian rhythm disorder
blind people
what population is more likely to have irregular sleep wake disorder
institutionalized or demented patients
what is the clinical presentation of irregular sleep wake disorder
chronic insomnia and excessive sleepiness and disorganzied sleep rhythm with 3+ sleep bouts in a 24 hour period–> total sleep time NORMAL for age
management of delayed sleep phase disorder
chronotherapy
melatonin in early evening (5-6 hours before sleep)
bright light in the MORNING
management of advanced sleep phase disorder
bright light in EARLY EVENING
management of non-24 hour sleep wake disorder
sleep wake scheduling
melatonin at bedtime
management of irregular sleep phase disorder
sleep wake scheduling
bright light exposure during the day and bright light therapy in the morning
what is the primary management of NREM sleep arousal disorders
educating and reassuring patients
maintain safety and avoid precipitates
when might you consider meds for NREM sleep disorders and what meds would you consider
in difficult cases
antidepressants–> SSRIs, TCAs
benzos–> historically, but now would avoid as can worsen symptoms (per brian chow sleep powerpoint)
what do you do to treat PTSD assoc nightmares
prazosin
can also do non pharm–> IRT, ERRT, EMDR, hypnosis
what types of psychotherapy might help in nightmare disorder
conflict resolution
image rehearsal therapy
progressive deep muscle relaxation
systematic desensitization
what is primary treatment for nightmare disorder
primarily nonpharm–> reassurance and psychotherapy
what meds can be used in nightmare disorder
in severe cases can use REM suppressant like SSRIs
how do you manage REM sleep behaviour disorder
- ensure safety of patient and partner–> address sleep environment
- CT/MRI head–> rule out lesions
- PSG–> rule out sleep disordered breathing, confirm REM without atonia
- pharmacological–> clonazepam, melatonin, dopamine agonists
what is the most commonly used pharmacological treatment for REM sleep behaviour disorder
clonazepam 0.5-2mg
BUT we recently read updated guidelines that said melatonin high dose (like up to 12mg) is as good if not better than clonazepam so would likely start with that
what 3 types of medication can be used to treat REM slepe behaviour disorder
clonazepam (increases threshhold for arousal)
melatonin
dopamine agonists
what do you expect to see on PSG in REM sleep behaviour disorder
REM without atonia
what is a mnemonia to remember the features of restless leg syndrome
URGE
Urge to move legs
Rest makes symptoms worse
Gets better with movement
Evening is time of worst symptoms
what is the prevalence of RLS
5-10%
what is the hypothesized mechanism behind RLS
brain DOPAMINE dysfunction
involves CIRCADIAN fluctuations in dopamine
deficiencies in other substances likely play a role
deficiency in what substance may play a role in RLS
iron
what neurotransmitter is hypothesized to be implicated in RLS
dopamine
list 6 factors that exacerbate RLS
caffeine
tobacco
alcohol
DA blockers
SSRIs
mirtazapine
do SSRIs help RLS or make it worse
make it worse
what is another term for periodic limb movement disorder
nocturnal myoclonus
what is periodic limb movement disorder
repetitive leg movements DURING SLEEP about which patient is usually unaware
20-40 sec apart
cause awakenings and fragmentation
bed partner reports “kicking”
how do you manage RLS/periodic limb movement disorder–> first step
correct underlying deficiencies or stop causative agent
list nonpharmacological interventions for periodic limb movement disorder/RLS
decrease alcohol, nicotine, caffeine consumption
hot baths
applying hot/cold compresses
massage
keep the mind alert
good sleep hygiene
what are two first line pharmacologic agents for periodic limb movement disorder/RLS
ropinirole
pramipexole
both are dopamine agonists
(can also use levodopa but not first line)
list all medications that can be used to treat periodic limb movement disorder/RLS
dopamine agonists–> ropirinole, pramipexole = FIRST LINE, also levodopa
gapabentin (recent studies)
benzos
opioids (low dose oxycodone_)
how does alcohol affect sleep ACUTELY
decreases sleep latency
increases SWS initially, then decreased in second half of sleep
decreased REM in first 2-4 hours of sleep period
REM rebounds in 2nd half of sleep period
intense DREAMS, nightmares
sleep FRAGMENTATION
how does chronic alcohol use affect sleep
INCREASED sleep latency
decreased sleep efficiency
decreased SWS
decreased REM
decreased TOTAL sleep time
how does alcohol withdrawal affect sleep
disrupted continuity of sleep
increased REM assoc with vivid dreaming
after acute withdrawal, chronic users may experience LIGHT, FRAGMENTED sleep for WEEKS TO YEARS
assoc with PERSISTENT decrease in SWS
alcohol exacerbates which sleep disorders
OSA
PLMD
RLS
parasomnias
RBD
SWS
opioids cause what ACUTE sleep changes
decreased total sleep time
decreased REM
decreased SWS
how does chronic opioid use affect sleep
same as with acute changes but these changes are minimized
how does opioid withdrawal affect sleep
insomnia
decreased REM and SWS
which sleep disorders are exacerbated by opioids
OSA
CSA
how does acute cannabis use affect sleep
decreased sleep latency
decreased REM
increased SWS
how does chronic cannabis use affect sleep
TOLERANCE to sleep induction effects and to SWS effects
decrease total sleep time
decreased sleep efficiency
decreased REM sleep
how does cannabis withdrawal affect sleep
starts after 2-3 days and lasts 2-7 weeks
REM REBOUND with increased dreaming and nightmares
decreased SWS
how do sedative/hypnotic/anxiolytic drugs affect sleep acutely
increased sleepiness
decreased wakefulness
how does chronic use of sedative/hypnotic/anxiolytic drugs affect sleep
tolerance–> with subsequent return of insomnia
how does sedative/hypnotic/anxiolytic drug withdrawal affect sleep
withdrawal and rebound insomnia
what sleep disorder is associated with benzo receptor agonists
parasomnias
(also sedative/hypnotic/anxiolytic drugs increase frequency and severity of apneas)
how do stimulants affect sleep acutely
insomnia
decreased total sleep time, REM and SWS
increased sleep latency
increased sleep continuity disturbance
how does chronic stimulant use affect sleep
increased sleep latency
decreased total sleep time
decreased sleep efficiency, REM, SWS
how does stimulant withdrawal affect sleep
excessive sleepiness
how does depression affect the following sleep parameter:
REM sleep
SHORTENED REM latency (under 60 min until first REM cycle rather than 90 min)
more REM sleep, increased REM density
shift to predominance of REM in first half of sleep (rather than SWS in first half)
how does depression affect the following sleep parameter:
SWS
decreased SWS
how does depression affect the following sleep parameter:
sleep continuity
disturbed sleep continuity, early morning awakenings
what effect does one night of total sleep deprivation have on patients with depression
one night with total sleep deprivation can temporarily alleviate depression in 40-60% of patients
how does mania affect sleep
TRUE reduction in need for sleep
awakens refereshed after 2-4 hours
what two changes in sleep are noted in patients with GAD
increased sleep latency
increased sleep fragmentation
what % of patients with PTSD have nightmares
96%
nightmares may also occur in NREM sleep, especially N2
may have MOTOR ACTIVITY with nightmares
how does PTSD affect the following sleep parameter:
N1
increased
how does PTSD affect the following sleep parameter:
SWS
decreased
how does PTSD affect the following sleep parameter:
REM
higher REM density but disrupted REM continuity
how does PTSD affect the following sleep parameter:
movements in sleep
PLMs occur frequently
what two changes are seen in sleep in those with panic disorder
paroxysmal AWAKENINGS upon entering N3/SWS
nocturnal panic attacks
how does SCZ affect the following sleep parameter:
REM
short REM latency
decreased REM sleep early during exacerbations
how does SCZ affect the following sleep parameter:
total sleep
decreased
how does SCZ affect the following sleep parameter:
NREM
decreased NREM during EXACERBATIONS
what is the most consistently found sleep abnormality in SCZ
short REM latency
name 3 changes to sleep seen in dementia
decreased REM sleep
decreased SWS
decreased melatonin
name Freuds 4 “distorting operations” in dream interpretation
condensation
displacement
visualization
symbolism
in Freud’s dream interpretation, what is the following operation:
condensation
one dream object stands for several ideas
in Freud’s dream interpretation, what is the following operation:
displacement
a dream objects emotional significance is separate from its real object or content, and attached to an entirely different one that does not raise the censors suspicions
in Freud’s dream interpretation, what is the following operation:
visualization
a thought is translated into visual images
in Freud’s dream interpretation, what is the following operation:
symbolism
a symbol replaces an action, person or idea
what stage of sleep is most likely affected in the following disorder:
sleep terror
1st third of the night, during SWS–> N3
what stage of sleep is most likely affected in the following disorder:
nightmare disorder
2nd half of night, during REM sleep
(less commonly can have during NREM)
what stage of sleep is most likely affected in the following disorder:
sleepwalking disorder
1st third of night, during SWS–> N3
what stage of sleep is most likely affected in the following disorder:
REM sleep behaviour disorder
REM sleep
is there often a family history of sleep terror or sleepwalking?
yes
what is the typical duration for a sleep terror
1-10 min
what is the typical duration for a sleepwalking episode
5-10 min (above 30 min is rare)
what is the typical duration for a nightmare (in nightmare disorder)
5-15 min
what is the typical duration for an episode of REM sleep behaviour disorder
seconds to 20 min
what are the symptoms of nightmare disorder
ABRUPT arousal with PANICKY scream/cry
autonomic and behavioural manifestations of intense fear
NO clear dream recall
what are the symptoms of sleepwalking disorder
automatisms
getting out of bed
walking
what are the symptoms of nightmare disorder
SUDDEN awakening with anxiety and VIVID DREAM RECALL
on awakening, QUICKLY become ALERT AND ORIENTED
what are the symptoms of REM sleep behaviour disorder
limb movements, kicking, punching, talking
potential for injury of self/bed partner
on awakening, QUICKLY become ALERT and ORIENTED
are there any symptoms post-episode in nightmare disorder or sleepwalking disorder
if are awakened during the spell, are CONFUSED and DISORIENTED for SEVERAL MINUTES
NO clear dream recall
usually does NOT awaken fully
AMNESIA of episode in the morning
are there any symptoms post-episode in nightmare disorder
VIVID recall of dream
anxiety may interfere with falling back asleep
are there any symptoms post-episode in REM sleep behaviour disorder
vivid recall of dream with theme of VIOLENCE
what are some possible pathophysiologies for nightmare disorder and sleepwalking disorder
alcohol, sedatives
sleep deprivation
emotional stress
sleep-wake schedule disruptions
predisposing psychopathology
what are some possible pathophysiologies for nightmare disorder
medications
daytime stress
predisposing psychopathology
what are some possible pathophysiologies for REM sleep behaviour disorder
PONTINE lesions
synucleinopathies
drug induced (i.e SSRIs, TCA, MAOI)
alcohol withdrawal
paraneoplastic syndrome
treatment for nightmare disorder and sleepwalking disorder
reassurance, ensure safety
avoidance of precipitants
psychotherapy
in difficult cases, consider SSRI, TCA
treatment for nightmare disorder
avoid stress
sleep hygiene
tx psych illnesses
prazosin, REM suppresant
IRT
name 3 antidepressants that have been known to cause nightmares
venlafaxine
duloxetine
buproprion
what effect do SSRIs have on REM sleep behaviour disorder and PLMs/RLS
can induce REM sleep behaviour disorder and PLMD/RLS
which antidepressant does not cause RLS/PLMD
buproprion