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Sleep-Wake Cycle And Disorders Flashcards

1
Q

Rapid eye movement (REM) sleep

paradoxical sleep

A

Period of de-synchronized EEG activity during sleep

  • rapid eye movements
  • muscular paralysis of major muscle groups occurs (cant roll over but peripheral muscles may move)
  • *classical dreaming occurs here
  • penile/clitoral tumescence

Physiological effects:

  • loss of motor tone
  • increased brain oxygen use
  • BP/pulse changes (usually gets higher, but can be higher in pathology or drugs. Gets lower in Non-REM sleep)
  • increased ACh
    • is believed to be the site of memory formation

starts with occurrence every 90 minutes of sleep and increases throughout the night

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2
Q

Non-REM sleep

A

Synchronized EEG activity. 4 stages and is the deepest form of sleeping

4 stages:

1) awake:
- open eyes = beta waves
- closed eyes = alpha waves
- both are very low amplitude but high frequency

2) N1 sleep:
- Light sleep and produces theta waves

3) N2 sleep:
- produces sleep spindles and K-complexes
- *site of bruxism occurring during sleep

4) N3 sleep
- deepest non-rem sleep
- delta waves (high amplitude, low frequency)
- *site of sleep walking, night terrors and bed wetting “wee and flee”

characteristics:

  • slow waves
  • moderate muscle tones (can roll over)
  • slow/absent eye movements
  • NO genital activity
  • less dreaming
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3
Q

What are used to measure sleep?

A

EEG

Electromyogram
- measuring muscle paralysis

Electrooculogram
- detects eye movements

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4
Q

Major differences between REM and non-REM sleep

A

REM:

  • beta waves
  • lack of muscle tone
  • rapid eye movements
  • penile erection or vaginal secretion
  • dreams occur

Non-REM (slow-wave sleep)

  • theta/delta waves
  • moderate muscle tone
  • slow or absent eye movements
  • no genital activity
  • less dreaming and more nightmares/night terrors
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5
Q

What stage is the most common stage to be in throughout the night while sleeping?

A

REM sleep (25%)

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6
Q

What is the most common non-REM sleepover stage while sleeping?

A

N2 (45%)

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7
Q

How does REM sleep change over the course of a lifetime?

A

Decreases

  • starts at 50% in newborns with total of 16 hrs on average
  • adults (20s) = 20% with total of 8hrs on average
  • elderly (60-70) = 15% with total of 6 hrs on average

common that stage 4 sleep just completely disappears in elderly populations

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8
Q

What is the key structure required for control of circadian rhythm?

A

The suprachiasmatic nucleus (SCN) area of the hypothalamus
- located just above the optic chiasm

Contains the biological clock that is responsible for organizing many of the body’s circadian rhythms

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9
Q

Pineal gland function in circadian rhythm

A

Endocrine gland that produces melatonin (serotonin-derived hormone)

  • modulates sleep patterns
    • production is triggered by darkness and fatigue
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10
Q

How does cortisol secretion work during sleep?

A

Decreases in 1st phase of sleep (N1)

Arises back up again once you begin to wake up

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11
Q

Reticular Activating System (RAS)

A

Neural circuit from the brain stem up to the thalamus that controls awakening and alertness

  • uses NE as the primary transmitter
  • damage to center = cant awaken = coma
  • over stimulation = cant fall asleep

NE is associated with decreased REM sleep

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12
Q

Raphe nucleus

A

Serotonin neurons extending from raphe nucleus throughout the limbic system and forebrain

  • primary neurotransmitter is serotonin
  • active during sleep onset and begin to force someone into sleep
  • serotonin neurons fire less as sleep prolongs, but is needed to both initate sleep and awaken someone from deep sleep -> REM sleep
  • damage = cant fall asleep
  • overstimulation = immediate sleep

holds almost all of the brains serotonergic neurons

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13
Q

Adenosine’s effect on sleep control

A

Neuromodulator that is released by neurons engaging in high levels of metabolic activity
- is believed to play a primary role in initiation of sleep (due to build up over the day)

caffeine is an antagonist of adenosine receptors = slows the build up of adenosine

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14
Q

ACh effect on sleep (dorsal pons/basal forebrain)

A

Long known to produce arousal and sleeplessness

  • increase ACh in the dorsal pons and basal forebrain = desynchronization of the cortical regions of the cerebral cortex
  • *increases REM sleep
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15
Q

Histamine effect in sleep

A

Originate in the hypothalamic tuberomammillary nucleus (TMN)

  • promote and stabilize wakefulness and attention
  • inhibts non-REM sleep

anti-histamines = sedation

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16
Q

Orexin (hypocretin-1)

A

Involved in wakefulness and auroral and produced in the hypothalamus

loss of orexin neurons causes narcolepsy

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17
Q

How to diagnose sleep disorders

A

Sleep logs

Sleep inventory (questionnaire)

Blood tests (rule out medical and thyroid problems)

Sleep study/polysomnography
- EEG oxygen levels and movements/patterns during sleep

18
Q

What questions should you ask for sleep disorders?

A

Onset

Duration

Frequency

Course

Aggravating factors

Past and current treatments (and responses if any)

19
Q

Insomnia

A

Chronic inability to sleep despite adequate opportunity to do so
- 9-15% of population

Primary insomnia:

  • sleep is disrupted for prolonged periods not attributable to psychological factors. Tends to physical medical casues
  • less common

Secondary/situational insomnia:

  • transitory and usually has an attributable cause
  • much more common
20
Q

DSM-5 for insomnia

A

Unsatisfying sleep quality or quantity with 1 or more of the following disabilities
1) sleep initiation (sleep latency > 30 minutes)

2) sleep maintenance (wake time after sleep onset > 30 minutes)
* should be less than 12 times *

3) early-morning awakening (awake 30 minutes before scheduled time and before total sleep time = 6.5)
* very common in depression*

4) functional distress or improvement

Must be at least 3 nights a week for at least 3 months

not better explained by another sleep-wake disorder or due to substance use

21
Q

How to measure sleep efficiency

A

Time asleep/time in bed

- < 85% is poor sleep efficiency

22
Q

Behavioral sleep medicine

A

Identification of psychological factors that develop sleep disorders

Then apply validated treatments for sleep disorders
- cognitive and/or behavior therapies

  • non-pharmacological treatment in insomnia is effective and should be considered first line before using medications*
  • all sleep disorder treatment should include sleep hygiene as an adjunct as well
23
Q

CBT in insomnia (CBTi)

A

Stepwise procedure to first improve sleep quality and then quantity

1) restrict time spent in bed to amount of sleep that is currently feasible, slowly increase sleep overtime
- also try to “re set” the biological clocks and align bedtime and rise time with specific times

2) use therapy strategies fro reducing sleep interference (worries mange stress, calming mind)
3) expose the patient to bright light upon waking

24
Q

OTC sleep medications

A

Some combination of Diphenhydramine/ Benadryl

Provides anti-H1 activity to induce sedation and drowsiness
- contraindicated in prostate cancer patients

Sometimes used in combo w/ acetaminophen or alcohol

causes hangover effects and anti-cholinergic side effects

tolerance develops quickly and becomes an habitual issue, bad since it can stress the liver out

25
Sedative/hypnotic drugs | Benzos, NBDRs and Z-drugs
Z-drugs are 1st line pharmacological agents for insomnia - administered for 4 weeks and not every night. tapered off slowly to avoid adverse effects: rebound insomnia, hangover effects, dependence and anterograde amnesia DONT mix with alcohol *Benzos are contraindicated in patients with chronic insomnia*
26
Ramelton
Newest drug in use and mimics the body regulation of the hormone melatonin. - best used for people with problems in initiating sleep - not good for those with trouble staying asleep *not a lot of evidence, but only minor dependence compared to benzos*
27
Obstructive sleep apnea
- Loud snoring that is then preceded by periods of apnea and then waking up to snore again (subconsciously) Extremely high rate of under diagnosis Likely a leading cause in secondary insomnia Risk factors: - age > 40 - obesity - males > females Treatment: - CPAP/BIPAP machine - *benzos, Z-drugs, and barbiturates are contraindicated*
28
Central sleep apnea
Brain doesn’t send proper signals that control breathing. Similar to obstructive sleep apnea except: - snoring is less common and not loud - chest pain is present - low tolerance for exercise Treatment: - address underlying neurological disorder - stop opioid medications (if on) - BIPAP/CPAP machine
29
Nightmare vs sleep terror
Nightmare = bad dream during REM sleep - patient can remember the nightmare - more likely in patients with PTSD and isolation behaviors Sleep terror = recurrent episodes of the person awakes suddenly in stage 4 sleep (NON-REM) in a panic, but no recollection of the night terror in the morning. - patient has complete amnesia of the night terrors - most common in little kids and often subside by 10 yrs of age - very uncommon in adults (2%) and are often indicative of underlying neurologic disorders
30
Nightmare treatment:
Non PTSD-associated nightmares = Image-reversal therapy is 1st-line - visualize the end of nightmare and it usually goes away PTSD-associated nightmares: image-reversal therapy with CBTi and Prazosin (a1/2 blocker, which decreases NE levels)= 1st-line - DONT use clonazepam and venlafaxine
31
Night terror treatment
Usually self-limited (goes away as they get older) Otherwise no treatment. Can try therapy if intense as well as educate the parents or guardians about sleep terrors - often looks way worse then they actually are
32
Somnambulism (sleepwalking)
Occurs in non-REM sleep - preforms activities that are usually performed during a state of full consciousness - dont try to wake up just take them back to bed if possible. * black box warning for Z-drugs because they increase sleepwalking and sleep driving = death* - don’t prescribe these drugs to patients with history of sleep walking
33
REM behavioral disorder treatments
Sleep behavior disorder where the patient acts out their dream in it’s entirety. Can get violent. Modify the sleep environment (especially if injury is possibility) Medications = clonazepam (not in elderly, sleep apnea or dementia patients) - melatonin (rameltion) can be an adjuvant agent
34
Sleep paralysis
Abnormal awakening from REM sleep where muscle paralysis is still active with hallucinations - tell them to “count back from 20 when this happens” usually it goes away Hypnapompic (sleep hallucinations right after wakening up) Hypnagogic (sleep hallucinations right before going to sleep)
35
Changes to REM sleep based on pathology and medications/drugs
Elderly: decreases in REM and N3 sleep Depression: increases REM sleep time, but latency is decreased (wake up earlier and is called insomnia) - “ Shitty REM” Narcolepsy: decreases REM latency Alcohol and barbiturates/benzos = decrease REM and N3 sleep - hence why benzos can be used in sleep walking/night terrors NE agonists = decreases REM sleep
36
What controls the extraocular movements in REM sleep?
The paramedian pontine reticular formation (PPRF)
37
What is the standard hypnogram patterns
- Goes through REM -> N3 -> REM throughout the night - REM sleep increases over time - deep sleep decreases over time
38
Norepinephrine effect on sleep
Long known that catecholamine agonists produce arousal and sleeplessness in the brain - specifically in the locus coeruleus* - decreased NE neuron firing rates in the locus coeruleus occurs as sleep deepens and prolongs
39
What TCA can be used for insomnia?
Doxepin
40
What drug is an orexin receptor antagonist that is rather new and is indicated insomnia?
Suvorexant - antagonizes orexin receptors - not used often in practice - contraindicated in narcolepsy
41
Narcolepsy
Excessive daytime sleepiness w/ recurrent episodes of rapid-onset overwhelming sleepiness - at least 3 times a week for at least 3 months - feels refreshed when awakening from sleep (compared to insomnia, OSA and MDD) Caused by a decrease in orexin (hypocretin-1) neurons Often shows hypnagogic and hypnopompic hallucinations as well as sleep paralysis - also can present w/ or without cataplexy Treatment: - good sleep hygiene - daytime = stimulants - night time = sodium oxybate (GHB)
42
Enuresis
Nighttime urinary incontinence > 2 times a week for at least 3 months - MUST be older than 5 years old Treatment: - behavioral modification = 1st line (scheduled voids, nighttime fluid restriction) and positive reinforcement) - refractory only = oral desmopressin (ADH analog) is preferred over imipramine (although both can be used

Mental Health (46 decks)

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