Sleep Lecture from Dr. Gautam Flashcards
what is the treatment for restless leg syndrome in children
iron + gabapentin
which disorders are associated with alpha-intrusion
GAD
PTSD
trauma
fibromyalgia/chronic pain
what is alpha intrusion
presence of alpha waves (“drowsiness”) during slow wave sleep
explains why people with anxiety/trauma describe “not sleeping at all”
how long of a period of sobriety is required for sleep to return to normal architecture
1 year at least
if someone has been an alcohol for several years, there are likely permanent changes to sleep architecture
*benzos are similar
what are the cutoffs points for pediatric OSA
normal 0-1
mild 1-5
moderate 5-10
severe > 10
on AHI scale per hour of sleep
which SSRI is most known to cause restless leg syndrome
fluoxetine
(SSRIs indirectly block dopamine)
if develop RLS on fluoxetine, usually does not go away
what are the first two things you need to rule out in someone presenting with night terrors
rule out OSA and night time seizures
how do you manage night terrors (if you know they’re not OSA or seizures)
- ensure safety (i.e doors locked, cant injure themselves)
- dont try to wake them up, sit with them
- if need to treat, time the night terrors (is usually during first half of the night when there is more N3)
–> 10-15 min before the night terror usually starts, shake them gently to shift them from N3–> N2 to prevent the night terror (dont fully awaken them)
–> “scheduled awakenings” - after a couple weeks it starts going away
what are the phases of sleep
NREM and REM
within NREM–> stage 1, stage 2, and slow wave sleep
what is the normal distribution between REM and NREM sleep in adults
75% NREM
25% REM
what % of sleep is spent with REM in normal neonates
50%
what sleep stages does a neonate go through while falling asleep
neonates fall DIRECTLY into REM
how does serotonin affect sleep stages
decreases time spent in REM
serotonin = shorter REM
how does norepinephrine affect sleep stages
NE = “REM OFF”
NE cells in the locus ceruleus–> increased firing leads to wakefulness and NREM
how does acetylcholine affect sleep stages
Ach = “REM ON”
Ach–> muscarinic agonists into pontine reticular formation–> REM on neurons–> more REM
(lower Ach during NREM)
where is melatonin released from
pineal gland
what affect does melatonin have on sleep
regulates circadian rhythms
do histamine neurons fire while asleep?
NO
fire while awake but NOT during NREM or REM
what affect do antidepressants have on sleep?
more serotonin–> more NREM and less REM
what affect does alzheimer’s have on sleep
fewer ACh neurons–> less REM and less slow wave sleep
what is the “pacemaker” of sleep
the suprachiasmatic nucleus (in hypothalamus)
what are the two Processes that regulate sleep cycles
Process S–> “sleep”–> accumulates during wakefulness
Process C–> “circadian”–> in hypothalamus and regulates temperature and sleep duration
if they were pitted against each other, would Process S win out or Process C?
Process S
(i.e if you have stayed awake for 40 hours, you WILL fall asleep even if middle of the day)
what is a mnemonic to remember which brain waves correlate with which sleep phase?
BAT Kave D SAT
Beta–> awake, eyes open
Alpha–> drowsy, eyes closed
Theta–> NREM 1
K spindles–> NREM 2
Delta (high amplitude, slow wave)–> Slow Wave
Saw tooth, slow Alpha, Theta–> REM
what physiological changes happen during REM with regard to:
- pulse, resp rate and BP
- cerebral blood flow
- response to increased pCO2
- skeletal muscles
- penis
- temperature
pulse, respiratory rate and BP increase
cerebral blood flow increases
there is DECREASED ventilatory response to increased pCO2 (no increase in tidal volume)
near total paralysis of skeletal muscles–> except for resp and ocular muscles
penis almost always erect
poikilothermia (temp varies with surroundings)
how does the need for sleep change with age
need for sleep stays the same
how does the ability to sleep change with age
ability to sleep decreases, therefore there is a decrease in total sleep
how does increasing age affect sleep phase? latency? awakenings?
with increasing age there is:
phase advance (sleep earlier)
increased sleep latency
increased number of nocturnal awakenings
what sleep phases are affected by increasing age and in what way
marked reduction in N3/SWS (with compensatory increase in N1 and N2)
decreased REM overall, with redistribution–> increased number of shorter REM episodes
how does depression affect sleep phases?
less SWS
increased REM
shorter REM onset latency (quicker to REM)
poor sleep continuity
increased sleep latency + increased fragmentation and arousals
antidepressants suppress REM
what is the mechanism by which antidepressants suppress REM
increase monoamines–> monoamines tonically inhibit REM
how does schizophrenia affect sleep
most consistent finding–> short REM latency
total sleep and NREM reduced during exacerbations
REM sleep reduced early in exacerbations
sleep onset and maintenance insomnia–> CHARACTERISTIC feature of SCZ (regardless of treatment status)
SWS and REM sleep latency reduced (REM duration tends to stay the same)
both positive and negative symptom severity reduces REM latency and increase % of REM sleep
how does dementia affect sleep
reduced REM and SWS
reduced melatonin
how does GAD affect sleep
increased sleep latency
increased sleep fragmentation
how does PTSD affect sleep
increased arousals and motor activity
increased N1
decreased SWS
higher REM density
nightmares
how does acute alcohol consumption affect sleep
decreased sleep latency
increased SWS
decreased REM in first half and REBOUND in second half (with more REM)
how does chronic alcohol consumption affect sleep
tolerance develops after ONE WEEK
increased sleep latency
decreased SWS + REM + efficiency + total sleep time
how long might effects of chronic EtOH consumption last on sleep
up to two years after abstinence
how does EtOH withdrawal affect sleep
increased REM with vivid dreaming
disrupted continuity
how does acute cannabis consumption affect sleep
increased SWS
decreased REM
decreased sleep latency
how does chronic cannabis consumption affect sleep
decreased REM
tolerance to increased SWS
decrease in latency
how does cannabis withdrawal affect sleep
REM rebound with reduced SWS
(people will report “crazy dreams” when stop cannabis–> due to REM rebound)
how do opioids affect sleep
decreased total sleep time
decreased SWS and REM
exacerbation of OSA and CSA
how do stimulants affect sleep
decreased time in SWS and REM
is insomnia an indication for polysomnography
no–> PSG looks at sleep and if you have insomnia you are not sleeping
list 6 indications for polysomnography
- sleep related breathing disorders
- sleep related movement disorders (i.e PLMD)
- uncertain diagnosis
- sleep related seizure disorder
- inadequate response to treatment
- sleep related behavioral issues
list the 7 components/measurements that MUST be taken during polysomnography
EEG
EOG (extra-ocular movements)
chin EMG
airflow
arterial oxygen saturation
respiratory effort
ECG or HR
list four other components of polysomnography that are optional but can be useful
anterior tibialis EMG (i.e for PLMD)
snoring microphone
expiratory CO2 sensor
video monitoring
is polysomnography indicated in circadian rhythm disorders
no
what two things are useful for treatment of circadian rhythm disorders
melatonin
light therapy
*sleep log also useful
should you use melatonin or sedatives in dementia patients
ideally no–> risk of falls, confusion
what is the most important sleep breathing disorder
OSA
how is the severity of OSA graded in adults
based on AHI (apnea-hypopnea index)
mild–> 5-15
moderate–> 15-30
severe–> more than 30
(in kids, above 10 is considered severe OSA)
what type of sleep study is needed to diagnose OSA
level 1 or 3
what makes breathing related sleep disorders like OSA worse
muscle relaxants
alcohol
benzos
supine position
REM phase
why do we care about OSA in psychiatry
effects can mimic psychiatric disorders
OSA can exacerbate psychiatric conditions like mood disorders, increase aggression in schizophrenia, increase nightmares in PTSD, worsen cognition in NCD, and contribute to substance use relapse
what can be some medical illness ramifications of OSA
HTN
Afib
impaired glucose tolerance
CHF
athersclerosis
stroke
how is narcolepsy diagnosed
with polysomnography and multiple sleep latency test (MSLT)
can also make dx by evidence of cataplexy or hypocretin deficiency in CSF but this requires LP so dont rly do it (no real reason to rather than doing polysomnography etc)
what do you find on polysomnography in narcolepsy
REM latency is less than 15 min
what do you find on MSLT for narcolepsy
sleep latency is less than 8 min and REM onset occurs in at least two naps
(test involves multiple naps during the day after the polysomnography occurring every two hours)
how do patients with narcolepsy usually present
complaining of hypersomnia but disturbed overnight sleep
what are the two types of narcolepsy
with and without cataplexy
other than hypersomnia and cataplexy what is another feature of narcolepsy
hypnagogic and hypnapompic hallucinations
how do you treat the daytime sleepiness associated with narcolepsy
stimulant
used to always use MODAFINIL but recent warning of teratogenesis in pregnant women–> can also use i.e Ritalin
Modafinil reduces the number of sleep attacks and improves psychomotor performance
potentially can decrease catalepsy (per K+S)
how do you treat the sleep paralysis and hypnagogic/pompic hallucinations associated with narcolepsy
SSRI (REM suppressing drugs)
how do you treat the cataplexy associated with narcolepsy
SSRI (REM suppressant) or sodium oxybate (Xyrem)
sodium oxybate is very addictive
what is the pentad (5) symptoms of narcolepsy
- excessive daytime sleepiness
- cataplexy
- hypnogogic/hypnopompic hallucinations
- sleep attacks
- disturbed nocturnal sleep
are most cases of restless leg syndrome (RLS) primary or secondary
primary
what is a mnemonic for remembering secondary RLS etiology
RAP RnB DT
Renal failure
Anemia (iron deficiency)
Pregnancy (normal)
Rheumatoid arthritis
B12 deficiency
Diabetes and diabetic neuropathy/peripheral nerve dysfunction
Thyroid abnormalities
is restless leg syndrome exacerbated by menopause
no–> gets better–> because stop losing blood/less likely to be anemic
list 4 things that may exacerbate restless leg syndrome
caffeine
alcohol
nicotine
medications (DA blockers, lithium, SSRI, mirtazapine)
what medication should you consider using for depression in someone with restless leg syndrome
buproprion (because more dopaminergic)
how to treat restless leg syndrome
- treat underlying condition (i.e anemia)
- dopaminergic agents
–> levodopa (as PRN is less than 3/week)
–> pramipexole (if more frequent symptoms, take regularly) - other agents–> clonazepam, gabapentin, pregabalin, opioids
what do you have to be careful of when you Rx pramipexole
impulsive behaviours
does clonazepam actually treat restless leg syndrome
no–> just increases arousal threshhold so you sleep through movements
what should you rule out first if you suspect a REM sleep behaviour disorder
underlying sleep related breathing disorder–> “pseudo RBD”
REM sleep behaviour disorder is highly associated with what two other disorders
parkinsonism
lewy body dementia
often occurs 10-15 years before onset of the parkinsons/dementia
what is first line treatment for REM sleep behaviour disorder
clonazepam (increases arousal threshold)
*if have comorbid OSA may use melatonin as first line to avoid exacerbating OSA
what is second line for REM sleep behaviour disorder
melatonin > pramipexole
how to treat Klein Levin syndrome
lithium can be used
what is klein levin syndrome
recurrent episodes of severe hypersomnia associated with cognitive and behavioural disturbances such as confusion, de realizeation, apathy, compulsive eating and hypesexuality
episodes last a few days tos several weeks and are separated by weeks or months of normal sleep and behaviours
nightmares occur in what phase of sleep
REM
how do nightmares differ from night terrors
nightmares–> REM, people remember content, normal arousal after waking up
night terrors–> NREM, people wake up confused, cannot remember the dream
what is recommended for treatment of nightmares assoc with PTSD
prazosin (level A)
clonidine (level C)
is venlafaxine recommended for treatment of PTSD assoc nightmare
no
what are some psychotherapies that can be used for nightmares
CBT and its variants
image rehearsal therapy (level A)
what are primary treatment goals for insomnia
improve sleep quality and quantity
improve insomnia related daytime impairments
what is the pharmacologic treatment algorithm for insomnia (primary)
short term acting benzo receptor agonists or ramelton i.e zolpidem, temazepam
sedating antidepressants only if treating comorbid anxiety/depression (i.e trazodone, mirtazapine)
what are three agents that help with sleep initiation
zaleplon
triazolam
ramelton
what are three agents that help with sleep initiation and maintenanec
temazepam
eszopiclone
zolpidem
what are two agents that help with sleep maintenance
suvorexant
doxepin
list the four components of CBT for insomnia
sleep log
stimulus control
sleep restriction
cognitive therapy and psychoeducation regarding sleep hygiene
what is the goal of the stimulus control in CBT-I
to disrupt the aassociation between bedroom and not sleeping (classical conditioning)
dont go to bed until sleepy, and get up after 20 min if not sleeping–> rinse and repeat until asleep
+wake at same time every day
+no daytime naps
in what disorder should you not restrict sleep
bipolar
