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20. Sleep-Wake Disorders > Sleep Lecture from Dr. Gautam > Flashcards

Sleep Lecture from Dr. Gautam Flashcards

1
Q

what is the treatment for restless leg syndrome in children

A

iron + gabapentin

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2
Q

which disorders are associated with alpha-intrusion

A

GAD
PTSD
trauma
fibromyalgia/chronic pain

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3
Q

what is alpha intrusion

A

presence of alpha waves (“drowsiness”) during slow wave sleep

explains why people with anxiety/trauma describe “not sleeping at all”

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4
Q

how long of a period of sobriety is required for sleep to return to normal architecture

A

1 year at least

if someone has been an alcohol for several years, there are likely permanent changes to sleep architecture

*benzos are similar

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5
Q

what are the cutoffs points for pediatric OSA

A

normal 0-1

mild 1-5

moderate 5-10

severe > 10

on AHI scale per hour of sleep

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6
Q

which SSRI is most known to cause restless leg syndrome

A

fluoxetine

(SSRIs indirectly block dopamine)

if develop RLS on fluoxetine, usually does not go away

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7
Q

what are the first two things you need to rule out in someone presenting with night terrors

A

rule out OSA and night time seizures

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8
Q

how do you manage night terrors (if you know they’re not OSA or seizures)

A
  1. ensure safety (i.e doors locked, cant injure themselves)
  2. dont try to wake them up, sit with them
  3. 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”
  4. after a couple weeks it starts going away
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9
Q

what are the phases of sleep

A

NREM and REM

within NREM–> stage 1, stage 2, and slow wave sleep

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10
Q

what is the normal distribution between REM and NREM sleep in adults

A

75% NREM

25% REM

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11
Q

what % of sleep is spent with REM in normal neonates

A

50%

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12
Q

what sleep stages does a neonate go through while falling asleep

A

neonates fall DIRECTLY into REM

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13
Q

how does serotonin affect sleep stages

A

decreases time spent in REM

serotonin = shorter REM

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14
Q

how does norepinephrine affect sleep stages

A

NE = “REM OFF”

NE cells in the locus ceruleus–> increased firing leads to wakefulness and NREM

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15
Q

how does acetylcholine affect sleep stages

A

Ach = “REM ON”

Ach–> muscarinic agonists into pontine reticular formation–> REM on neurons–> more REM

(lower Ach during NREM)

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16
Q

where is melatonin released from

A

pineal gland

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17
Q

what affect does melatonin have on sleep

A

regulates circadian rhythms

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18
Q

do histamine neurons fire while asleep?

A

NO

fire while awake but NOT during NREM or REM

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19
Q

what affect do antidepressants have on sleep?

A

more serotonin–> more NREM and less REM

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20
Q

what affect does alzheimer’s have on sleep

A

fewer ACh neurons–> less REM and less slow wave sleep

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21
Q

what is the “pacemaker” of sleep

A

the suprachiasmatic nucleus (in hypothalamus)

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22
Q

what are the two Processes that regulate sleep cycles

A

Process S–> “sleep”–> accumulates during wakefulness

Process C–> “circadian”–> in hypothalamus and regulates temperature and sleep duration

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23
Q

if they were pitted against each other, would Process S win out or Process C?

A

Process S

(i.e if you have stayed awake for 40 hours, you WILL fall asleep even if middle of the day)

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24
Q

what is a mnemonic to remember which brain waves correlate with which sleep phase?

A

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

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25
Q

what physiological changes happen during REM with regard to:

  1. pulse, resp rate and BP
  2. cerebral blood flow
  3. response to increased pCO2
  4. skeletal muscles
  5. penis
  6. temperature
A

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)

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26
Q

how does the need for sleep change with age

A

need for sleep stays the same

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27
Q

how does the ability to sleep change with age

A

ability to sleep decreases, therefore there is a decrease in total sleep

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28
Q

how does increasing age affect sleep phase? latency? awakenings?

A

with increasing age there is:

phase advance (sleep earlier)

increased sleep latency

increased number of nocturnal awakenings

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29
Q

what sleep phases are affected by increasing age and in what way

A

marked reduction in N3/SWS (with compensatory increase in N1 and N2)

decreased REM overall, with redistribution–> increased number of shorter REM episodes

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30
Q

how does depression affect sleep phases?

A

less SWS

increased REM

shorter REM onset latency (quicker to REM)

poor sleep continuity

increased sleep latency + increased fragmentation and arousals

antidepressants suppress REM

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31
Q

what is the mechanism by which antidepressants suppress REM

A

increase monoamines–> monoamines tonically inhibit REM

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32
Q

how does schizophrenia affect sleep

A

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

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33
Q

how does dementia affect sleep

A

reduced REM and SWS

reduced melatonin

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34
Q

how does GAD affect sleep

A

increased sleep latency

increased sleep fragmentation

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35
Q

how does PTSD affect sleep

A

increased arousals and motor activity

increased N1

decreased SWS

higher REM density

nightmares

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36
Q

how does acute alcohol consumption affect sleep

A

decreased sleep latency

increased SWS

decreased REM in first half and REBOUND in second half (with more REM)

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37
Q

how does chronic alcohol consumption affect sleep

A

tolerance develops after ONE WEEK

increased sleep latency

decreased SWS + REM + efficiency + total sleep time

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38
Q

how long might effects of chronic EtOH consumption last on sleep

A

up to two years after abstinence

39
Q

how does EtOH withdrawal affect sleep

A

increased REM with vivid dreaming

disrupted continuity

40
Q

how does acute cannabis consumption affect sleep

A

increased SWS

decreased REM

decreased sleep latency

41
Q

how does chronic cannabis consumption affect sleep

A

decreased REM

tolerance to increased SWS

decrease in latency

42
Q

how does cannabis withdrawal affect sleep

A

REM rebound with reduced SWS

(people will report “crazy dreams” when stop cannabis–> due to REM rebound)

43
Q

how do opioids affect sleep

A

decreased total sleep time

decreased SWS and REM

exacerbation of OSA and CSA

44
Q

how do stimulants affect sleep

A

decreased time in SWS and REM

45
Q

is insomnia an indication for polysomnography

A

no–> PSG looks at sleep and if you have insomnia you are not sleeping

46
Q

list 6 indications for polysomnography

A
  1. sleep related breathing disorders
  2. sleep related movement disorders (i.e PLMD)
  3. uncertain diagnosis
  4. sleep related seizure disorder
  5. inadequate response to treatment
  6. sleep related behavioral issues
47
Q

list the 7 components/measurements that MUST be taken during polysomnography

A

EEG

EOG (extra-ocular movements)

chin EMG

airflow

arterial oxygen saturation

respiratory effort

ECG or HR

48
Q

list four other components of polysomnography that are optional but can be useful

A

anterior tibialis EMG (i.e for PLMD)

snoring microphone

expiratory CO2 sensor

video monitoring

49
Q

is polysomnography indicated in circadian rhythm disorders

A

no

50
Q

what two things are useful for treatment of circadian rhythm disorders

A

melatonin

light therapy

*sleep log also useful

51
Q

should you use melatonin or sedatives in dementia patients

A

ideally no–> risk of falls, confusion

52
Q

what is the most important sleep breathing disorder

A

OSA

53
Q

how is the severity of OSA graded in adults

A

based on AHI (apnea-hypopnea index)

mild–> 5-15

moderate–> 15-30

severe–> more than 30

(in kids, above 10 is considered severe OSA)

54
Q

what type of sleep study is needed to diagnose OSA

A

level 1 or 3

55
Q

what makes breathing related sleep disorders like OSA worse

A

muscle relaxants

alcohol

benzos

supine position

REM phase

56
Q

why do we care about OSA in psychiatry

A

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

57
Q

what can be some medical illness ramifications of OSA

A

HTN

Afib

impaired glucose tolerance

CHF

athersclerosis

stroke

58
Q

how is narcolepsy diagnosed

A

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)

59
Q

what do you find on polysomnography in narcolepsy

A

REM latency is less than 15 min

60
Q

what do you find on MSLT for narcolepsy

A

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)

61
Q

how do patients with narcolepsy usually present

A

complaining of hypersomnia but disturbed overnight sleep

62
Q

what are the two types of narcolepsy

A

with and without cataplexy

63
Q

other than hypersomnia and cataplexy what is another feature of narcolepsy

A

hypnagogic and hypnapompic hallucinations

64
Q

how do you treat the daytime sleepiness associated with narcolepsy

A

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)

65
Q

how do you treat the sleep paralysis and hypnagogic/pompic hallucinations associated with narcolepsy

A

SSRI (REM suppressing drugs)

66
Q

how do you treat the cataplexy associated with narcolepsy

A

SSRI (REM suppressant) or sodium oxybate (Xyrem)

sodium oxybate is very addictive

67
Q

what is the pentad (5) symptoms of narcolepsy

A
  1. excessive daytime sleepiness
  2. cataplexy
  3. hypnogogic/hypnopompic hallucinations
  4. sleep attacks
  5. disturbed nocturnal sleep
68
Q

are most cases of restless leg syndrome (RLS) primary or secondary

A

primary

69
Q

what is a mnemonic for remembering secondary RLS etiology

A

RAP RnB DT

Renal failure

Anemia (iron deficiency)

Pregnancy (normal)

Rheumatoid arthritis

B12 deficiency

Diabetes and diabetic neuropathy/peripheral nerve dysfunction

Thyroid abnormalities

70
Q

is restless leg syndrome exacerbated by menopause

A

no–> gets better–> because stop losing blood/less likely to be anemic

71
Q

list 4 things that may exacerbate restless leg syndrome

A

caffeine

alcohol

nicotine

medications (DA blockers, lithium, SSRI, mirtazapine)

72
Q

what medication should you consider using for depression in someone with restless leg syndrome

A

buproprion (because more dopaminergic)

73
Q

how to treat restless leg syndrome

A
  1. treat underlying condition (i.e anemia)
  2. dopaminergic agents
    –> levodopa (as PRN is less than 3/week)
    –> pramipexole (if more frequent symptoms, take regularly)
  3. other agents–> clonazepam, gabapentin, pregabalin, opioids
74
Q

what do you have to be careful of when you Rx pramipexole

A

impulsive behaviours

75
Q

does clonazepam actually treat restless leg syndrome

A

no–> just increases arousal threshhold so you sleep through movements

76
Q

what should you rule out first if you suspect a REM sleep behaviour disorder

A

underlying sleep related breathing disorder–> “pseudo RBD”

77
Q

REM sleep behaviour disorder is highly associated with what two other disorders

A

parkinsonism

lewy body dementia

often occurs 10-15 years before onset of the parkinsons/dementia

78
Q

what is first line treatment for REM sleep behaviour disorder

A

clonazepam (increases arousal threshold)

*if have comorbid OSA may use melatonin as first line to avoid exacerbating OSA

79
Q

what is second line for REM sleep behaviour disorder

A

melatonin > pramipexole

80
Q

how to treat Klein Levin syndrome

A

lithium can be used

81
Q

what is klein levin syndrome

A

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

82
Q

nightmares occur in what phase of sleep

A

REM

83
Q

how do nightmares differ from night terrors

A

nightmares–> REM, people remember content, normal arousal after waking up

night terrors–> NREM, people wake up confused, cannot remember the dream

84
Q

what is recommended for treatment of nightmares assoc with PTSD

A

prazosin (level A)

clonidine (level C)

85
Q

is venlafaxine recommended for treatment of PTSD assoc nightmare

A

no

86
Q

what are some psychotherapies that can be used for nightmares

A

CBT and its variants

image rehearsal therapy (level A)

87
Q

what are primary treatment goals for insomnia

A

improve sleep quality and quantity

improve insomnia related daytime impairments

88
Q

what is the pharmacologic treatment algorithm for insomnia (primary)

A

short term acting benzo receptor agonists or ramelton i.e zolpidem, temazepam

sedating antidepressants only if treating comorbid anxiety/depression (i.e trazodone, mirtazapine)

89
Q

what are three agents that help with sleep initiation

A

zaleplon

triazolam

ramelton

90
Q

what are three agents that help with sleep initiation and maintenanec

A

temazepam

eszopiclone

zolpidem

91
Q

what are two agents that help with sleep maintenance

A

suvorexant

doxepin

92
Q

list the four components of CBT for insomnia

A

sleep log

stimulus control

sleep restriction

cognitive therapy and psychoeducation regarding sleep hygiene

93
Q

what is the goal of the stimulus control in CBT-I

A

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

94
Q

in what disorder should you not restrict sleep

A

bipolar

20. Sleep-Wake Disorders (3 decks)

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