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CNS / Insomnia > insomnia > Flashcards

insomnia Flashcards

1
Q

Which type of behavioral therapy for childhood insomnia is analogous to stimulus control?

A

Graduated extinction

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2
Q

Which of the following is true regarding the use of actigraphy to diagnose insomnia?

A

Compared with sleep logs, actigraphy provides similar information about total sleep time and sleep latency in response to treatment

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3
Q

In Genome Wide Association studies of insomnia symptoms, which gene, previously implicated in another sleep disorder, was associated with insomnia?

A

MEIS1, Restless Legs Syndrome

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4
Q

According to the AASM Clinical Practice Guideline for Pharmacologic Treatment of Insomnia, which of the following is true about the medications recommended for pharmacologic treatment of sleep maintenance insomnia?

A

None of the treatments decreased WASO more than 30 minutes

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5
Q

Among adults with insomnia symptoms or DSM-IV insomnia syndrome at baseline, what percent will have insomnia at least 1 year over the next 3 years?

A

74%

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6
Q

Compare zolpidem to doxepin

A

Zolpidem was associated with higher fall risk and more difficulty with arousal

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7
Q

What is the incidence of transient insomnia at one year

A

40%

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8
Q

What is the Incidence of different types of insomnia

A

Sleep onset insomnia 23%
Sleep maintenance insomnia 32%
Mixed insomnia 17%
Combined insomnia 29%

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9
Q

What is adjustment sleep disorder

A

Associated with a specific stress or

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10
Q

What is Psychophysiologic insomnia

A

Heightened arousal and learned sleep preventing associations

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11
Q

What is Paradoxical insomnia

A

Subjective report of severe sleepiness not congruent with the absence of sleep or minor degree of daytime impairment

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12
Q

What is Idiopathic insomnia

A

Onset in childhood or infancy

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13
Q

What is Inadequate sleep hygiene

A

Associated with activities that are inconsistent with optimal sleep

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14
Q

What is Behavioral insomnia of childhood

A

Result of inappropriate sleep associations or inadequate limit setting

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15
Q

What is the prevalence of chronic insomnia

A

10

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16
Q

Chronic Insomnia Disorder

A

A. The patient reports, or the patient’s parent or caregiver observes, one or more of the following:1

1. Difficulty initiating sleep.
2. Difficulty maintaining sleep.
3. Waking up earlier than desired.
4. Resistance to going to bed on appropriate 		schedule.
5. Difficulty sleeping without parent or caregiver 	intervention.
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17
Q

Chronic Insomnia Disorder

A

The patient reports, or the patient’s parent or caregiver observes, one or more of the following related to the nighttime sleep difficulty:

1. Fatigue/malaise.
2. Attention, concentration, or memory impairment.
3. Impaired social, family, occupational, or academic 	performance.
4. Mood disturbance/irritability.
5. Daytime sleepiness.
6. Behavioral problems (e.g., hyperactivity, impulsivity, 	aggression).
7. Reduced motivation/energy/initiative.
8. Proneness for errors/accidents.
9. Concerns about or dissatisfaction with sleep.
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18
Q

Comorbid insomnia and psychiatric disorders

A

Insomnia is correlated with the likelihood of having at least 1 psychiatric diagnosis with an odds ratio of 5.0 for severe insomnia
In a large European study, 18% of the population reported insomnia of 6 months duration or longer, and of those 48% had a current psychiatric disorder by DSM-IV
Medications for psychiatric disorders can affect sleep
Medications for sleep disorders can affect psychiatric symptoms

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19
Q

Prevalence of Insomnia in OSA ?

A

A high prevalence (39%-58%) ofinsomniasymptoms have been reported in patients withOSA

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20
Q

Do insomniacs have apnea hypopnea index greater than 5?

A

Between 29% and 67% of patients withinsomniahave an apnea-hypopnea index of greater than 5

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21
Q

Does CBTi work for patients with OSA?

A

Combination therapy, of CBTI and OSA treatment, resulted in greater improvements ininsomniathan did either CBTI orOSAtreatment alon

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22
Q

What is the effect of exercise on sleep?

A

Acute exercise has small self reported benefits on total sleep time, sleep onset latency, sleep efficiency and moderate benefits for wake after sleep onset.
Regular exercise has small self reported benefits on total sleep time, sleep efficiency, sleep latency, and moderate benefits on sleep quality

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23
Q

What are benefits of cognitive therapy ?

A

Address thoughts and beliefs that interfere with sleep.

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24
Q

What are benefits of relaxation training?

A

Reduce arousal & decrease anxiety

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25
Q

How does sleep restriction work?

A

Restrict time in bed to improve sleep depth & consolidation

Determine average time asleep based on baseline sleep diary
Set time in bed = time asleep
Consistent wake-up time
No daytime naps
If time asleep > 85% of time in bed then increase time in bed (15-20 minutes)
If time asleep < 80% of time in bed then decrease time in bed (15-20 minutes)
Time in bed increases continue as long as sleep efficiency > 85% until patient reports optimal daytime functioning

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26
Q

What is stimulus control?

A

Strengthen bed & bedroom as sleep stimulus

Use bed for sleep and sex only
Go to bed only when sleepy
Get out of bed when unable to sleep after approximately 15-20 minutes
Wake up at a consistent time, including weekends
Avoid daytime naps

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27
Q

What is sleep hygiene?

A

Promote habits that help sleep; provide rationale for subsequent instructions.

Regularize sleep / wake schedule
Avoid stimulants and stimulating behavior
Establish relaxing bedtime routine
Provide conducive sleep environment
Limit daytime naps
Reduce or eliminate alcohol and caffeine
Obtain regular exercise
Avoid clock watching
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28
Q

What are most commonly used sleeping pills?

medications commonly used for insomnia (MCUFI)

A

3% on MUCFI and 55% of MCUFI users take at least one other sedating medication and 10% take ≥ 3

High rates of MCUFI among elderly and individuals seeing mental health provider

Most commonly prescribed Trazodone & Zolpidem

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29
Q

Neurotransmitters promoting arousal

A 
Acetylcholine
Dopamine
Glutamate
Histamine
Norepinephrine
Orexin 1 and 2
Serotonin
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30
Q

Neurotransmitters promoting sleep

A 
Adenosine
GABA
Galanin
Glycine
Melatonin
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31
Q

What are the kinetics of Zaleplon®

A

onset 10-20 min half-life 1.0 dose 5-20 mg

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32
Q

What are the kinetics of Zolpidem®

A

onset 10-20 min half-life 1.5-2.4 dose 5-10 mg

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33
Q

What are the kinetics of Zolpidem CR®

A

onset 10-30 min half-life 3-4.5 dose 6.25-12.5 mg

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34
Q

What are the kinetics of Eszopiclone®

A

onset 10 min half-life 5-7 dose 1-3 mg

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35
Q

What are the kinetics of Triazolam®

A

onset 10-20 min half-life 1.5-5 dose 0.125-0.25 mg

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36
Q

What are the kinetics of Temazepam®

A

onset 45-60 min half-life 1 8-20 dose 7.5-30 mg

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37
Q

What are the kinetics of Flurazepam®

A

onset 15-30 min half-life 36-120 dose 15-30 mg

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38
Q

What are the kinetics of Quazepam®

A

onset 15-30 min half-life 15-120 dose 7.5-15 mg

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39
Q

What are Benzodiazepine Receptor Agonists: Effects on Sleep

A 
Sleep continuity
↓ Sleep latency
↓Awakenings
↑ Sleep Duration
 ↓ Slow Wave Sleep (BZs only)
 ↓ REM (BZs only)
↑ Duration and number of sleep spindles
 ↓Periodic limb movements and associated arousals
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40
Q

What are BZA side effects

A 
Daytime Sedation
Cognitive/motor impairment
Anterograde amnesia
Rebound insomnia upon discontinuation
Parasomnia
Tolerance/dependence/abuse/withdrawal (DEA schedule IV)
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41
Q

What zolpidem effects

A 
Associated with 
Longer total sleep time
Fewer awakenings after sleep onset
Shorter sleep latency
Greater ease of falling asleep
Better quality of sleep
Increased sleep efficiency
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42
Q

What are features of melatonin

A

1.3% or 3.1 million US adults use melatonin based on surveys from 2002-2012 per the National Health Statistics Reports, 2015
Melatonin use among adults in the US more than doubled between 2007 and 2012.

Ramelteon, a melatonin receptor agonist, does not affect AHI or oxygenation in mild to moderate OSA

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43
Q

Describe Suvorexant

A

Suvorexant is a dual orexin receptor antagonist, the first in this new class of medications
Half life 12 hours
Recommended dosing: 10mg within 30 minutes before going to bed, in patients who plan to sleep continuously for at least 7 hours, with a maximum dose of 20mg
Dose reduction should be considered in obese females, or patients taking moderate CYP3A4 inhibitors; excreted in feces and renally

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44
Q

What is the effect of SSRI on sleep

A

Decrease REM and sometimes SWS

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45
Q

What is the effect of mirtazepine on sleep

A

Increase sleep continuity

46
Q

What is the effect of trazodone on sleep

A

Increase sleep continuity

47
Q

Describe pharmacotherapy antihistamines on sleep

A

Mechanism of action
H1 receptor antagonism
Variable antagonism of cholinergic, serotonergic, adrenergic receptors

Adverse effects
Sedation, grogginess
Dry mouth
Psychomotor impairment
Delirium
48
Q

What the effects of hormone replacement therapy on sleep.

A

Studies have shown that women on HRT seem to fall asleep faster, have longer periods of REM sleep, have fewer arousals, and sleep longer than those not on HRT. Taking HRT at bedtime seems to be the most helpful timing of drug.

49
Q

What are side effects of high doses, valerian

A

blurred vision, excitability and cardiac arrhythmias.

50
Q

What are side effects of kava

A

The FDA has also warned that kava may be linked to serious liver damage and in addition should not be used by persons with cardiovascular disease.

51
Q

What are the sleep architecture effects of Clomipramine

A

Clomipramine, a tricyclic antidepressant, is one of the most potent REM suppressing drugs available. Other tricyclic drugs and SSRIs tend to cause a more modest suppression of REM sleep.

52
Q

What are the sleep architecture effects of Trazodone and nefazodone

A

Trazodone and nefazodone have fewer effects on REM, and some reports have even shown an increase in REM sleep. In general, antidepressants have few effects on slow wave sleep. However, tertiary tricyclic antidepressants and trazodone have been found to increase slow wave sleep in some studies.

53
Q

Can benzodiazepines help PAP Therapy

A

benzodiazepines may be of benefit in promoting sleep and improving tolerance of PAP. Non-benzodiazepine benzodiazepine receptor agonists such as zolpidem and eszopiclone do not affect obstructive sleep apnea AHI or SpO2. Multiple studies show improved adherence to PAP therapy when the patient is concurrently initiated on a Non-benzodiazepine benzodiazepine receptor agonists.

54
Q

What are the side effects of zolpidem

A

The most common side effects of zolpidem may include nausea, dizziness, malaise, nightmares, agitation, headaches.Do not see rebound insomnia between nights of treatment and drug-free nights. Zolpidem as-needed administration may allow patients to adapt treatment to their needs and to the evolution of their insomnia.

55
Q

Where the effect sizes of benzodiazepines for sleep.

A

The effect of benzodiazepine receptor agonists versus placebo was measured as the effect size d, which is a standardized measure of the difference between active treatment and placebo. By convention, effect sizes below 0.5 are considered small, between 0.5 and 0.8 moderate, and above 0.8 large. On measures of self-reported sleep latency, total sleep time (TST), number of awakenings, and sleep quality, benzodiazepine receptor showed a consistently superior effects to placebo. The effect sizes were moderately large, demonstrating that these drugs are indeed efficacious for short-term treatment.

56
Q

Describe the effects of sleep restriction

A

Sleep Restriction Therapy is designed to consolidate sleep by increasing sleep drive. The technique involves an initial reduction in the time spent in bed followed by a gradual extension of time in bed, The patient is initially prescribed a time-in-bed period that is roughly equal in length to the total amount of sleep reported on baseline sleep diaries. The actual placement of the sleep period should be determined based on the patient’s circadian rhythm preference and specific life constraints. The minimum time in bed recommended is 5 hours nightly. When sleep efficiency is at least 85% on average for approximately 1 week, the time in bed is increased by 15-20 minutes if the patient reports adverse daytime consequences. Increases in time spent in bed continue in 15-20 minute increments per week, as long as the sleep efficiency remains above 85% When sleep efficiency drops below 80%, time-in-bed is decreased by 15-20 minutes until sleep efficiency increases above 85%.

57
Q

Sleep Heart study and insomnia

A

There is a 29% higher risk of cardiovascular disease in the insomnia group

Insomnia or poor sleep was not associated with all cause mortality

58
Q

What neuroanatomic findings occur in insomnia patient’s

A

Insula is a critical region for sleep maintenance

Prefrontal cortex and default mode neck or may play crucial role and cognition dysfunction

Increased Activity between right auditory language comprehension Center in executive control network leads to inability to disengage from external auditory stimulation and leads to hyperarousal

59
Q

Actigraphy versus sleep diaries in insomnia evaluation

A

Compared to sleep diaries actigraphy

Estimated a mean of 38 minutes more sleep in intervention studies and 35 minutes in non-intervention studies

60
Q

How does actigraphy compared to polysomnogram

A

Compared to PSG it estimates 10 extra minutes of sleep

61
Q

How does actigraphy compared to Diary in sleep late

A

Compared to PSG it estimates 8 less minutes of sleep Latency

62
Q

Compare agents regarding sleep latency

A

Lunesta and 14 minute decrease in sleep latency with a moderate to large effect.

Ramelteon had a 9 minute decrease in sleep latency with no improvement in sleep quality

Temazepam had a 37 minute reduction in sleep latency with a small affect and sleep quality. Triazolam had a 9 minute reduction in sleep latency with a moderate improvement in sleep quality zaleplon and a 10 minute decrease in sleep latency with no improvement in sleep quality resulted in had a 5-12 minute decrease in sleep latency with a moderate sleep quality

63
Q

Compare agents regarding sleep maintenance

A

In sleep maintenance

Doxepin 26-32 minutes small to moderate

Lunesta 2857 minutes moderate to large

Restoril 99 minutes small

suvorexant 10 minutes

Zolpidem 29 minutes moderate

64
Q

Compare agents altogether

A

Sleep onset is ramelteon triazolam and zaleplon

Sleep maintenance is doxepin and suverexant

Both is Lunesta zolpidem and temazepam

65
Q

What percentage of people feel medication helps insomnia

A

67% of people using long-term hypnotic medications to help them sleep rated their sleep quality as improved and only 14% reported little or no improvement

66
Q

What are risks of insomnia

A

Insomnia patients have substantially increased risk of future mood and psychiatric disorders higher health care use and costs elevated risk of falling reduced quality of life increased absenteeism and cognitive impairments

67
Q

How long do insomniacs use medication

A

70% of insomniacs use for two weeks or less.

68
Q

What are the PharmaKinetics a melatonin

A

melatonin has a maximum concentration of about .5 hours and elimination half-life of one hour. It is effective for sleep onset. It may be associated with reversible inhibition of spermatogenesis and ovulation

69
Q

What are Pharmacokinetics of ramelteon

A

Ramelteon is a half-life of 1 to 2.5 hours. Therapeutic dose of 8 mg is given 30 minutes before bedtime.

70
Q

When is doxepin effective

A

Doxepin is more effective in the last third of the night.

71
Q

What are the PharmaKinetics of trazodone

A

Trazodone t max of 1 to 2 hours and a half-life of 7 to 15 hours.

72
Q

What are the effects of gabapentin

A

Gabapentin exerts its fact through binding to the alpha-2 Delta subunit of the N type voltage gated calcium channel. T max is 3.5 hours and half-life is 5 to 9 hours. Used in people with restless leg syndrome alcohol dependence and seizure disorder

73
Q

What is the role of sodium oxybate

A

Sodium oxybate has a Tmax of .5 to .8 and a half life of .3 - 1.2 hours. It is dose to bedtime and in the middle of the night is dosed in the range of 2.5 to 4.5 g. Side effects include Parasomnias celebration nausea and vomiting and amnesia. It should not be used in people with respiratory depression including those with sleep disordered breathing and COPD.

74
Q

Exceptions to three month rule for diagnosis of insomnia

A

– Patients with recurrent episodes lasting several weeks at a time over several years, yet not meeting the 3-month duration criterion for any single episode may be diagnosed as chronic
– Patients sleeping well with the use of a hypnotic
medication who would meet the criteria without the
medication - especially when voicing concerns about their inability to sleep without sleep medication

75
Q

Performance issues that must be present to diagnose insomnia

A
  1. Fatigue/malaise
  2. Attention, concentration, or memory impairment
  3. Impaired social, family, occupational, or academic performance
  4. Mood disturbance, irritability
  5. Daytime sleepiness
  6. Behavioral problems (e.g., hyperactivity, impulsivity, aggression)
  7. Reduced motivation/energy/initiative
  8. Proneness for errors/accidents
  9. Concerns about or dissatisfaction with sleep
76
Q

What are Insomnia Treatment Modalities

A 
• Sleep hygiene recommendations
• Psychotherapeutic techniques
• Behavioral strategies
• Cognitive behavioral therapy for insomnia (CBT-I)
• Light/dark exposure
• Schedule manipulations
• Pharmacotherapeutic:
– Substances
– Medications
77
Q

What are the Components of CBT-I

A 
• Cognitive therapy strategies
• Sleep restriction therapy
• Stimulus control therapy
• Relaxation therapy
• Sleep hygiene education and rules
• Paradoxical intention
• Biofeedback
• Multicomponent therapy without cognitive
therapy
78
Q

What cognitive distortions does cognitive psychotherapy attempt to correct

A

• Chronic insomnia patients often:
– Assume daytime problems result from poor sleep
– View transient sleep problems as chronic
– Have unrealistic expectations about their sleep need
– Exhibit cognitive errors: overgeneralization,
rumination, and magnification
– Have high anxiety associated with attempts to fall
asleep

79
Q

What are Sleep Restriction Therapy guidelines

A

• Initial prescribed time in bed (TIB) determined by
average sleep from 2-week sleep log
– Awaken by alarm same time 7 days a week
– Bedtime delayed for restricted schedule
– No napping
– (Do not limit TIB to less than 5 hours)
• TIB bedtime adjustments are made each week
– If sleep efficiency is 90% or greater, bedtime is adjusted 15
to 30 minutes earlier
– If sleep efficiency is 85% or less, bedtime is adjusted 15
minutes later
• Treatment course typically is 6 to 8 weeks

80
Q

What is Stimulus Control Therapy

A

• Developed by Richard Bootzin (1970s)
• Addresses the reinforced association between
the bed, bedroom, and attempts to fall asleep
in relation to excessive arousal, prolonged
wakefulness, and frustration
• Essentially, deconditions while some sleep
deprivation promotes a reassociation of going
to bed with successful sleep onset

81
Q

Trazodone

A 
Biphasic T½ – 3 to 6 hours – 5 to 9 hours
Onset 30 – 120 minutes
Receptor effects
– 5-HT2A,2B receptor antagonist
– 5-HT1A partial agonist
– α1 -receptor antagonist
– α2 -receptor antagonist
– Histamine H1 antagonist
– Serotonin reuptake inhibition
Side effects – Dizziness– Sedation– Hypotension– Headache– Sweating– Arrhythmias– Priapism– Serotonin syndrome
Active metabolite: mCPP
82
Q

What are GABA A Alpha Subunit Subtypes

A

α Subtype % of CNS GABA A receptors Known Action Mediated α1 % of receptors 60 Sedation, amnesia, ataxia (!)
α2 15 - % of receptors 20 Anxiolytic, myorelaxation α3 10 - 15 Myorelaxation (high doses), ataxia
α4 % of receptors < 5 Insensitive to BZRAs
α5 % of receptors < 5 Partial myorelaxation, ataxia
α6 % of receptors < 5 Insensitive to BZRAs

83
Q

Benzodiazepines Immediate Release

A

Estazolam ProSom Dose 1, 2 half-life 10 to 24
Flurazepam Dalmane Dose 15, 30 half-life 2.3 (active metabolite: 48 - 160)
Quazepam Doral Dose 7.5, half-life 15 39 (active metabolite 73)
Temazepam Restoril Dose 7.5, 15, 22.5, 30 half-life 3.5 to 18.4
Triazolam Halcion Dose 0.125, 0.25 half-life 1.5 to 5.5

84
Q

Nonbenzodiazepines Immediate Release

A

Eszopiclone Lunesta dose 1, 2, 3 half-life ~6 (~9 in elderly)
Zaleplon Sonata dose 5, 10 half-life 1
Zolpidem Ambien dose 5, 10 half-life ~2.5

85
Q

Nonbenzodiazepines Alternate Delivery

A

Zolpidem oral spray Zolpimist dose 5, 10 2.7 – half-life 3.0
Zolpidem sublingual Edluar dose 5, 10 half-life ~2.5
Zolpidem sublingual Intermezzo dose 1.75, 3.5 half-life ~2.5

86
Q

Nonbenzodiazepines Extended Release

A

Zolpidem ER Ambien dose CR 6.25, half-life 12.5 2.8 in males (longer in females)

87
Q

What are Discontinuation Effects of sleeping pills

A

• Rebound insomnia: Sleep is worsened relative
to baseline for 1 to 2 nights after
discontinuation. More likely with higher doses
and short/intermediate half-life hypnotics
• Recrudescence: Return of original insomnia
symptoms
• Withdrawal: New cluster of symptoms not
present prior to treatment (e.g., anxiety,
seizures)

88
Q

What was the 2014 Update Drug Safety Communication regarding Eszopiclone

A

FDA Recommends lower initial dose for men and women to be 1 mg at bedtime

89
Q

What are BZRA Hypnotics Possible Adverse Effects

A
  • Residual effects
  • Dizziness
  • Headache
  • Somnolence
  • Blurred vision
  • Nausea/diarrhea
  • Fatigue
  • Ataxia
  • Anterograde amnesia
  • Somnambulism/complex sleep behaviors
90
Q

What are efects of Ramelteon

A 
• FDA approval: Indicated for the treatment of
insomnia characterized by difficulty with sleep
onset
• No limitation on duration of use
• Non-sedating
• Single dose: 8 mg (Flat dose-response
relationship)
• Take about 30 minutes prior to bedtime
• Avoid hazardous activities after dose
• Elimination half-life 1 – 2.6 hours
Adverse events
– Somnolence (5%)
– Dizziness (5%)
– Fatigue (4%)
Avoid with
– Hepatic impairment (moderate to severe)
– Fluvoxamine (Luvox) coadministration
91
Q

What are Doxepin adverse effects

A 
Most common adverse events
– Somnolence/sedation
– Nausea
– Upper respiratory tract infection
Elimination half-life: 15.3 hours
92
Q

How do you use Suvorexant

A

USE:
– 10 mg taken only once
– Within 30 minutes of going to bed
– At least 7 hours remaining before the planned
time of awakening
– Dose may be increased to a maximum of 20 mg
– 5 mg is recommended for people talking a
moderate CYP3A4 inhibitor
– Time to effect may be delayed with food

93
Q

What is pathogenesis of primary insomnia which is a state of physiologic hyperarousal

A

Meeting sleep latencies on an SLT or higher are comparable to those of controls

Increased 24-hour metabolic rate

Increased global cerebral glucose metabolism awake and asleep on PET

Increased beta and decreased data delta EEG activity during sleep

Increased ACTH and cortisol secretion

94
Q

What are Elimination half-lives of hypnotic agents

A 
• Less than 1 hour:
– Ramelteon
– Zaleplon
• 2 to 6 hours:
– Eszopiclone
Triazolam
– Zolpidem
• 6 to 24 hours:
– Doxepin (low-dose)
– Estazolam
– Temazepam
– Suvorexant
Greater than 40 hours:
– Flurazepam
– Quazepam
95
Q

There is insufficient evidence for the effectiveness in insomnia of

A

Cognitive therapy alone
Sleep hygiene education alone
Imagery training alone

96
Q

There is sufficient evidence for effectiveness of

A 
Stimulus control therapy
Relaxation training
Sleep restriction
Multicomponent therapy without cognitive therapy
Paradoxical intention
Biofeedback
97
Q

What characterizes non-benzodiazepine benzodiazepine receptor agonist

A

Similar hypnotic action to benzodiazepines
No muscle relaxant anticonvulsant or anxiolytic properties
Not likely to cause rebound insomnia withdrawal symptoms or tolerance or to alter sleep architecture

98
Q

What are the cardiovascular effects of sleep duration

A

Long and short sleep duration cause all cause mortality hypertension obesity and diabetes

99
Q

What condition is associated with H Per2 gene

A

Advanced phase sleep disorder

100
Q

What effect does evening light have on advanced sleep disorder.

A 
Evening light has a week therapeutic effect on advanced sleep disorder.
4000 lx for 2 hours
Duration 12 days
Increasing total sleep time
Main phase delay is 2.4 hours
101
Q

What is epidemiology of narcolepsy

A

Contrary to widely held views, narcolepsy is not a rare disorder. Well designed studies have shown that the prevalence of narcolepsy with cataplexy in western European countries and North America approaches 0.05% (range 0.02% - 0.06%), or one case for every 2,000 people.1 This figure is not very different from that reported for multiple sclerosis (range 0.06% - 0.14%), another common neurological disorder.2 Some studies have shown that narcolepsy may be more frequent in Japan and rare in Israel.

102
Q

What are essential and associated symptoms of narcolepsy

A

Essential
Excessive daytime sleepiness (EDS)
Cataplexy

Associated
Hypnagogic hallucinations
Sleep paralysis
Disturbed nocturnal sleep

103
Q

Excessive daytime sleepiness

A 
Sleep attacks on a background of chronic sleepiness or fatigue
Frequent napping, usually refreshing
Memory lapses and automatic behaviors
Impaired attention / concentration
Decreased work performance
Increased drowsy driving crashes 
Visual disturbances
104
Q

What is incidence of difficulty falling asleep or staying asleep

A

Insomnia is a common complaint in the population in general. Studies suggest that up to 30-40% of the population complain of difficulty falling or staying asleep, or non-restful sleep.

105
Q

What is the prevalence of insomnia

A

Insomnia that is also associated with daytime impairment or significant distress constitutes the general definition of insomnia as a disorder and is less common than the complaint of sleep disturbance alone (8-19%).

106
Q

What is the differtence in prevalence of insomnia with men compared to women

A

Insomnia is more likely to be reported by A meta-analysis found that women are almost 50% as likely to develop insomnia compared with men (relative risk 1.41).

The difference in insomnia prevalence between men and women increases with age, and reaches greatest significance in the post-menopausal period.

107
Q

Risk factors for insomnia

A

Previous history of insomnia

Increasing age

Female sex

Psychiatric symptoms and disorders

Medical symptoms and disorders

Stress

Lower socioeconomic status

Fewer years of education

108
Q

What factors disrupt sleep in pregnancy:

A

Nocturia
Gastroesophageal reflux
Hormonal changes such as oxytocin release in late pregnancy
Fetal movements & contractions
Musculoskeletal pain
Sleep disorders which develop during pregnancy (OSA and RLS)

109
Q

What factors that impact sleep quality in menopause

A

Reproductive hormone levels
Mood symptoms
Vasomotor symptoms

110
Q

What are risks of insomnia in women

A

Impact on pregnancy and post-partum course
Association with pre-term birth
Association with longer labor and cesarean deliveries
Higher risk of incident and recurrent post-partum depression
Deficits in post-partum neurobehavioral performance
Increased pain in fibromyalgia

111
Q

What are some Class C (potential benefit outweighs risk) drugs to avoid in pregnancy

A

zaleplon, eszopliclone, zolpidem, ramelteon, gabapentin, doxepin and trazodone

112
Q

What is graduated extinction

A

Graduated extinction consisted of the parent putting the child to bed and ignoring the tantrum activity for increasingly longer amounts of time throughout the treatment.

CNS / Insomnia (1 decks)

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