Sleep Disorders Flashcards

1
Q

What are the EEG waves for a fully awake person? What happens when they get sleepy?

A

Fully awake = low voltage, rapid waves

Sleepy = alpha waves [8-12hz]

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2
Q

A persons EEG shows low voltage theta waves [3-7Hz]. They do NOT have rapid eye movements. What stage of the sleep cycle are they in?

A

Stage 1 NREM sleep

-lightest stage of sleep

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3
Q

A person’s EEG shows sleep spindles [high frequency bursts] and K-complexes [slow triphasic waves]. What stage of the sleep cycle are they in?

A

Stage 2 NREM sleep

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4
Q

A person’s EEG shows high voltage, low frequency delta wave predominance. What stage of the sleep cycle are they in?

A

Stage 3 or 4 NREM sleep

-aka “slow wave sleep”

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5
Q

A person’s EEG shows low voltage theta waves and they are demonstrating rapid conjugate eye movements. What stage of the sleep cycle are they in?

A

REM

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6
Q

What is sleep latency?

What is REM latency?

A

Sleep latency is the amount of time it takes from attempting sleep to getting to stage 2 sleep [spindles/kcomplexes].

REM latency is the amount of time from onset of sleep to first REM sleep which is usually about 90 minutes

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7
Q

When does the majority of REM sleep occur?

When does the majority of delta sleep [stages 3 and 4] occur?

A

REM cycles every 90minutes and lasts longer with each successive episode so the majority of REM occurs later in the night and earlier in the morning.

Delta sleep occurs most frequently in the first half of the night.

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8
Q

What stage of sleep is the most predominant stage of sleep throughout the night?

A

Stage 2

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9
Q

In addition to sleep latency and REM latency, what 3 medical conditions are studied with polysomnography [sleep studies]?

A
  1. Apnea index = measure the number of times a patient holds their breath for over 10 sec per hour
  2. Myoclunus index = measures periodic limb movements per hour
  3. nocturnal penile tumescence= measures the spontaneous occurrence of penile erection during REM sleep to differentiate psychological from physio ED
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10
Q

What are the physiological changes associated with REM sleep?

A

“paradoxical sleep”- high brain/physio activity

  1. INCREASED pulse, BP, oxygen consumption, RR
    - greater than or similar to wakefulness
  2. significantly decreased muscle tone
    - except this stage of sleep is when males get penile erections
  3. normal dreaming
    - if awakened in this stage, the person will be alert and able to recall the dream
  4. poikilothermia
    - temperature variation depends on the environment
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11
Q

What are the physiological features of NREM sleep?

A

peaceful sleep with diminished physiological function
- restorative function because it is increased with starvation or exercise

If one is awakened during slow wave NREM sleep, she will be confused/disoriented and unable to recall clear dream content.

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12
Q

You wake up your boyfriend and he is instantly alert and describing the dream he was just having. What stage of the sleep cycle was he in when you woke him?

A

REM

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13
Q

You wake up your boyfriend and he is disoriented and confused. He cannot recall any clear dream content. What stage of the sleep cycle was he in?

A

NREM slow wave sleep

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14
Q

How does sleep content change with age?

A

Newborns have 50% REM, adults 25% REM

Elderly have decreased REM and decreased slow wave sleep so overall quantity and quality are diminished –> complaints of non-restorative sleep

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15
Q

What is the effect of depression on sleep?

A

It can cause insomnia or hypersomnia but either way:

  1. decreased REM latency [enter REM in less than 90min]
  2. REM moves to first half of the night [where deep, slow wave, restorative sleep should be]
  3. increased % of total sleep is REM
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16
Q

If a person doesn’t have external cues, what is the normal human sleep/wake rhythm?

A

25-hr cycle

some require less than 6 hrs, others require over 9

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17
Q

What does prolonged, profound sleep deprivation lead to in ANYONE?

A

hallucinations and confusion

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18
Q

What happens with brief REM deprivation [person is wakened everytime they lapse into REM]?

A

Transient anti-depressant effect

[however, when the person is allowed to sleep w/o interruption again, the REM is increased and depression returns]

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19
Q

Where does melatonin secretion come from?

What is the effect on bright light on secretion?

A

Suprachiasmatic nucleus of hypothalamus is the circadian pacemaker for melatonin release.

Melatonin secretion by the pineal gland is inhibited by bright lights

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20
Q

Where is serotonin produced in the brain?

What is the effect if these nuclei are destroyed?

A

Serotonin is made in the dorsal raphe nucleus .

Destruction of the neurons leads to decreased sleep

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21
Q

Where in the brain is NE released?

What does stimulation of these neurons lead to?

A

NE is released from the locus ceruleus and stimulation of these neurons leads to decreased REM sleep and increased wakefulness

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22
Q

What part of the sleep cycle is affected by Ach?

A

Ach affects REM sleep.

Decreased Ach–> reduced REM sleep

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23
Q

What is the effect of dopamine from the substantia nigra on sleep?

A

Dopamine leads to wakefulness.

Antipsychotics–> sleepiness

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24
Q

What is dyssomnia?

What are examples?

A

Sleep disorder with disturbed:

  1. amount
  2. quality
  3. timing

primary insomnia, primary hypersomnia, narcolepsy, breathing-related sleep disorders, circadian rhythm sleep disorder, periodic limb movement disorder, restless leg syndrome

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25
Q

primary insomnia, primary hypersomnia, narcolepsy, breathing-related sleep disorders, circadian rhythm sleep disorder, periodic limb movement disorder, restless leg syndrome are all examples of what kind of sleep disorder?

A

dyssomnia

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26
Q

What is parasomnia? Examples?

A

Disruptive events that occur during sleep or sleep/wake transition.

Nightmares, sleep terror, sleepwalking, parasomnia NOS [REM sleep behavior disorder, sleep paralysis, bruxism, sleep-talking]

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27
Q

What causes narcolepsy?

A

deficiency in orexin [hypocretin] a neuropeptide that suppresses REM sleep and increases arousal circuits.

28
Q

A person has sudden sleep attacks and excessive daytime sleepiness. They will suddenly lose muscle tone [cataplexy]. This is often brought on by strong emotions.
In the sleep wake transition, the person has hallucinations [both falling asleep and waking]. She has sleep paralysis and atonia of REM sleep as she falls asleep and wakes.

What is the diagnosis?

A

Narcolepsy

  • cataplexy [loss of muscle tone]
  • intrusion of REM into sleep/wake transitions with
    hypnoGOgic hallucinations as they GO to sleep
    hypnoPOMPic hallucinations as they wake
    sleep paralysis
29
Q

What are 3 situations that can lead to circadian rhythm sleep disorder?

A
  1. delayed sleep phase - natural sleep cycle leads them to go to sleep very late and wake up very late
  2. jet lag -particular with west to east trips
  3. shift work
30
Q

A person has brief leg muscle contractions lasting 5-15 seconds recurring every minute during sleep as shown on a polysomnogram.
The person is not aware of the movements, but they do complain of mini-arousal, non-refreshing sleep and excessive daytime sleepiness.
What is this sleep disorder?
What phases of sleep are most commonly effected?

A

Periodic limb movement disorder

-affects stages 1,2 and 3/4

31
Q

A person complains of delayed sleep onset because they feel prickling, tingling, burning in their legs when trying to fall asleep.
They have an intense urge to get up and move/walk which gives them transient relief.
What sleep disorder is present and what disorder often accompanies it?

A

This is restless leg syndrome and it is often accompanied by periodic limb movement disorder

32
Q

A patient awakens rapidly with full orientation and alertness with detailed recall of dream content. The dream is scary and distressing.

What is the sleep disorder?
What stage of the sleep cycle does it affect?

A

Nightmare disorder [dream anxiety disorder]

-REM sleep

33
Q

A child wakes up abruptly, screams and is sweating, with rapid HR. She is not alert and does not respond to reassurance/comfort. She falls back asleep rapidly. In the morning she has no memory of the dream or episode.

What is the sleep disorder and what stage of the sleep cycle is affected?
When in the night is it most likely to occur?

A

Sleep Terror Disorder and it occurs during delta sleep so it most likely occurs in the first 1/3 of the night

34
Q

A person arises out of sleep and walks, eats, dresses, talks and drives. The person is not alert and does not recall the events the next morning.

What sleep disorder is this?
What stage of the sleep cycle does it affect?
What age group does it affect most?

A

Somnambulism [sleepwalking]
It occurs when the person is in delta sleep [first 1/3 of the night]
It affects children > adults

35
Q

A man violent acts out dream content with punching, jumping, and throwing. When the person is awakened, he remembers the content of the dream.
What disorder is this and what stage of the sleep cycle is affected?

A

REM Sleep Behavior Disorder

-REM sleep but without the normal REM atonia

36
Q

What is obstructive sleep apnea?
What is obstructive sleep hypopnea?
What do they both result in?

A

Obstructive sleep apnea is the ABSENCE of airflow measured at the nose and mouth despite ongoing effort to breath that lasts 10 sec or longer.

Obstructive sleep hypopnea is a reduction in airflow [greater or equal to 30%] at the nose/mouth despite ongoing efforts to breath

Both result in decreased oxyhemoglobin saturation and change in EEG indicating arousal from sleep.

37
Q

What is central apnea? How does it differ from OSA and OSH?

A

no effort from the thoracic cage nor abdominal muscles during cessation of airflow for 10 sec or more.

In obstructive sleep apnea and obstructive sleep hypopnea, there is continued effort to breath despite reduction in airflow

38
Q

The apnea/hypopnea index [AHI] rates syndrome severity. What AHI score is mild, moderate, and severe OSA?

A
Mild = 5-15 events/hr
Moderate = 15-30 events/hr
Severe = >30 events/hr
39
Q

What criteria must be met for a patient to be diagnosed with OSAHS?

A

A OR B plus C

A. excessive daytime sleepiness that is not explained by other things

B. 2 or more of the following:

  • choking/gasping in sleep
  • recurrent awakenings
  • unrefreshing sleep
  • daytime fatigue
  • impaired concentration

C. overnight monitoring demonstrates 5 or more obstructed breathing events per hr sleep [apneas/hypopneas, respiratory effort related to arousal]

40
Q

What % of middle-aged causcasians have OSAHS?
What gender has higher risk?
What race?
What other factors?

A

5%
Males > females
AA have higher risk than whites
Menopause & obesity increase the risk

41
Q

What physiologically causes hypopnea or apnea to occur?

A

Negative intrathoracic pressure cause a suction force narrowing or closing the upper airway by moving the retropalatal or retrolingual closed

42
Q

What is the primary cause for airway closure during sleep?
What determinants lead to this?
WHEN are they most vulnerable?

A

Primary cause of closure is a small airway.

  1. craniofacial structure and function
  2. obesity

They are able to keep a patent airway when awake, but when asleep, decreased muscle tone, snoring and airway narrowing can result.

Because muscle tone plays a role, they are most vulnerable in supine positions during REM [when atonia occurs]

43
Q

What is the stimulus for resumption of normal breathing?

How is this identified by sleep pathologists?

A

Ventilatory-related arousal from sleep

It is seen on EEG and is precipitated by increased airway resistance

44
Q

Struggling against a partially or completely closed airway is associated with what 3 things?

A
  1. increased intrathoracic pressure
  2. increased vagal tone –>bradycardia followed by tachycardia
  3. hypoventilation
45
Q

Intermittent hypoxemia is a hallmark of OSAHS. What is the result?

A

It results in transcription and translation of biomarkers of oxidative stress like CRP and IL6 which lead to cardiovasular disease and alter metabolic function

46
Q

What are the ACUTE effects of OSA?

A
  1. increased hypoxic load
  2. increased mechanical load
  3. increased adrenergic load
  4. increased upper airway instability
47
Q

What are the cardio complications of OSAHS?

A
nocturnal dysrrhthmias
bradycardia
afib
nocturnal HTN
diurnal HTN **** [even when control for all other risk factors]
pulm HTN
CHF
MI
stroke
48
Q

What are the metabolic complications of OSAHS?

A

Leptin resistance

Insulin resistance

49
Q

What are the neuro-cognitive complications of OSAHS?

A
  1. daytime sleepiness
  2. car accidents
  3. work accidents
  4. neuropsych performance
  5. impaired quality of life
  6. memory/cognition impairment
50
Q

What has been demonstrated to have favorable impacts on the cardio, metabolic and neurocognitive co-morbidities of OSAHS?

A

adequate treatment especially with positive pressure

51
Q

What is the relationship between AHI and co-morbidities?

A

The more severe the OSAHS, the more co-morbidities. IT is a “dose-dependent” relationship

52
Q

What is leptin? What is the effect of OSAHS on leptin?

A

Leptin is an adipokine that inhibits neuropeptide Y [a stimulator of food intake].

OSAHS increases leptin levels which can lead to leptin resistance and increased food consumption

53
Q

Untreated OSAHS has a __________ impact on vigilance, executive function and coordination and a ______ impact on verbal and intellectual functioning.

A

Significant impact on vigilance, EF, coordination

Negligible impact of verbal, intellectual function

54
Q

There is an increase in the prevalence odds ratio for OSAHS in patient prescribed what?

A
  1. antidepressant

2. antihypertensive

55
Q

What lifestyle interventions can be used in the treatment of OSA?

A
  1. weight loss - sleep/breathing
  2. avoiding sleep deprivation
    - decrease daytime sleepiness
    - increase upper airway muscle tone
  3. stop alcohol/sedatives
    - increase upper airway tone
  4. head of bed elevation or lateral position of head
56
Q

How does positive pressure therapy improve sleep apnea?

A

Pneumatically splints the airway open during sleep, preferentially affecting lateral pharyngeal wall

57
Q

What are the 2 ways the positive pressure can be applied?

A
  1. CPAP- continuous positive air pressure
  2. BPAP- bilevel positive airway pressure
    - pressure is higher during inspiration than expiration [because normally the pressure is more neg in inspiration]
58
Q

What is patient adherence to CPAP?
How can you monitor compliance?
How can you improve patient compliance?

A

50% adherence.
Monitor compliance with “smart card” that stores prescribed pressure, nightly hours of use and pressure being generated.

Improve compliance by:

  1. make sure the masks fit
  2. treat nasal congestion/dryness with heated humidifiers in line
  3. desensitization if they are clostrophobic
59
Q

What is the goal of oral appliance therapy?

Why is it considered “second line”

A

To modify the position of the mandible and tongue to increase the upper airway size and decrease collapsibility.

It is second line because:

  1. requires multiple adjustments that take weeks or months to accomplish
  2. not 100% effective
  3. objective adherence can’t be measured
60
Q

What are the benefits of oral appliance therapy?

A
  1. decreased sleepiness and sleep disordered breatihing
  2. reduced BP
  3. patients prefer it to the masks [CPAP/BPAP]
61
Q

What are the 2 types of oral appliance therapy?

A
  1. Tongue retaining device [TRD]
    - suction applied to tongue to maintain protrusion and increase retrolingual airway
  2. mandibular advancement device [MAD]
    - sequential adjustments require weeks so not to be used in severe cases that need expedient results
62
Q

What are the contraindications for MAD oral appliance therapy for sleep apnea?

A
  1. insufficient tooth number, tooth mobility
  2. untreated peridontal disease
  3. TMJ
63
Q

What is palatal surgery alone used to treat?

What are the 2 types of surgery for OSAHS?

A

Palatal surgery for snoring

OSAHS

  1. tracheostomy- bypass the upper airway
  2. reconstruction of the upper airway
64
Q

Who gets tracheostomy for OSAHS?

A

patients with severe and pontentially life threatening cases for whom CPAP and BPAP didn’t work or they are intolerant.

65
Q

What are the 2 phases of reconstruction of the upper airway?

Which is more effective? What are drawbacks?

A

Phase I = palatoplasty and genioglossal advancement
*low morbidity, but less than optimal results

PHase II = maxillomandibular advancement
*more effective, but may have transient trauma and damage to the inferior alveolar nerve