Sleep disorders Flashcards

1
Q

Key NTs

A

Sleep: GABA, melatonin
Wakefulness: norepinephrine, histamine, acetylcholine
Across the cycle: serotonin, orexin, hypocretin

hat antihistamines typically cause drowsiness and anticholinesterase inhibitors can cause insomnia or wakefulness.
serotonin, which, which actually modulates the movement through the different sleep stages. There are some hypothalamic neuropeptides, orexin hypocretin, and these help with the regulation of sleep.

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2
Q

What is “normal”?

Sleep architecture in the
context of age

A

Sleep latency - generally < 30 minutes
Sleep quantity - 7-9 hours
Consolidation - uninterrupted sleep
Quality - no daytime impairment

Younger adults - greater difficulty falling
asleep
Older adults - More likely to report middle
of the night or early morning wakening

young adults. And as you can see, they spend more time in stages 3.4. So we’re getting more deeper restorative sleep.

older adults actually lose stages like sleep in stages 3.4. And so stages 3.4 and sleep are associated with deeper or more restorative sleep.

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3
Q

Sleep-Wake Disorders

A

Dysomnias: Problems getting to sleep or staying asleep
Insomnia, RLS, sleep apnea, narcolepsy

Parasomnias: disorders of arousal (sleep-wake transitions)
Night terrors, sleep walking/talking, bruxism

Circadian Rhythm Disorders: a loss of synchronization between internal biological
clock and external environment
Delayed/advanced sleep phase syndrome, jet-lag

So instead of starting to feel tired around 10:00 P.M. you maybe start to feel tired around 02:00 A.M. then of course, this disrupts your entire sleep cycle because now you’re either sleeping in late or having to wake up early to go to school or go to work, and then having disrupted sleep. And then advanced sleep phase is the opposite. You’re falling asleep very early in the evening and then waking up very early in the morning.

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4
Q

Complications
of insomnia

A

Cardiovascular:
High blood pressure
Risk of heart disease

Poor immune system function

Other:
Risk of diabetes
Weight gain, obesity
Low quality of life

Psychological:
Lower daytime performance
Slowed reaction time
Risk of depression/relapse
Risk of anxiety disorde

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5
Q

Insomnia

A

A predominant complaint of dissatisfaction with sleep quantity or quality,
associated with ≥ 1 of:
Difficulty initiating sleep
Difficulty maintaining sleep, characterized by frequent awakenings or
problems returning to sleep after awakenings
Early-morning awakening with inability to return to sleep

Causes clinically significant distress or impairment in important areas of
functioning.
Occurs a least 3x/week for at least 3 months

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6
Q

Stratifying insomnia

A

Acute (<3 months)
Chronic (>3 months)
Primary (10%)
Seconday (90% - 10-15% attributed to substance use)
Sleep-onset
Sleep-maintenance

acute insomnia is mostly the result of a stressful event or environmental disturbances such as noise, extreme temperature, some of those other external factors we’ve talked about like caring for a newborn, jet lag

chronic insomnia is actually likely to be sustained from factors that are different from what initially triggered the sleep difficulty. What we see with chronic insomnia, that it actually becomes a learned behavior and cognitive factors that actually sustain this cycle of inability to sleep.people then fall into this pattern of being so worried about not being able to fall asleep that it actually prevents them from falling asleep

Sleep onset describes people who are having difficulty falling asleep, but then are able to sleep through the night once they do fall asleep
Maintenance involves waking up frequently throughout the night.
Most comon see a mix of these traits

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7
Q

Objectivity - creating a sleep diary

A

Have patient record the following DAILY
Time to bed
Time first tried falling asleep
Time to fall asleep
Nighttime awakenings (quantity, duration)
Time of final awakening (wake up time)
Total duration of sleep
Quality of sleep (feel refreshed upon wakening?)
Daytime fatigue
Daytime napping (frequency, duration)
Alcohol, caffeine, drug use (illicit, prescribed, OTC, CAM)

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8
Q

Rule out
other
causes

A

read slide 16

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9
Q

Clinical Aspects of Insomnia - The 3P Model

A

Precipitating factors
Emotional distress, onset of medical or psychiatric
disorder
Predisposing factors
Factors increasing risk of developing insomnia (e.g., anxious predisposition,
circular thinking, generalized hyperarousal)

Perpetuating factors
Learned negative sleep behaviours and cognitive
distortions

the longer that acute insomnia goes unnoticed, undiagnosed, untreated, or the longer than its mismanaged, the greater the risk is of someone developing really negative cognitive distortions around sleep. And this increases their chances dramatically of converting into chronic insomnia

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10
Q

Insomnia screening questionnaire
Insomnia severity index

A

screening q has not been validated
diagnostic domains:
1. insomnia
2. psych disorders
3. circadian rhythm disorder
4. movement disorders
5. parasomnias

Insomnia Severity Index. So this is something that has been validated in a primary care setting and it can be used to monitor the patient’s progress with their treatment for insomnia, as well as to help make decisions around ongoing care and whether we should consider a referral to a sleep specialist.

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11
Q

When is a sleep study needed?

A

Evaluation of sleep-related systems
Sleep maintenance insomnia
Snoring
Unexplained daytime fatigue or sleepiness

diagnosis of a sleep disorder
Narcolepsy
Parasomnias: formal term for sleep study is polysomnography. And during this process they measure different things so that we can try to identify what the root causes.
So e.g. some of the things that they might measure drain asleep study include how long the person is sleeping for, the number of times they’re waking up during the night, how are their eyes moving while they’re asleep? What is the muscle activity during their sleep? What is their respiratory rate? What is their oxygen saturation, as well as heart rate and rhythm while they’re sleeping
PLMD
REM sleep behavior disorder
Sleep-related breathing disorders (ie. Apnea)
Sleep-related seizure disorders

Treatment of a sleep-related breathing disorders (ie.
using a positive airway pressure titration)

level 1: actually takes place in a lab and they use a lot of fancy equipment to measure, again, brainwave activity, muscle movements, heart rhythms, and the volume of your snoring

level 2: collects the same amount of information, but you can actually do it at home so you don’t need asleep technician to be part of the process.

Level 3: also happens at home and it’s more to collect information around sleep apnea, so it’s less comprehensive than levels 1.2.

Level 4: can be completed at home as well. And this one only measures your oxygen levels while you sleep.

level 1: actually takes place in a lab and they use a lot of fancy equipment to measure, again, brainwave activity, muscle movements, heart rhythms, and the volume of your snoring

level 2: collects the same amount of information, but you can actually do it at home so you don’t need asleep technician to be part of the process.

Level 3: also happens at home and it’s more to collect information around sleep apnea, so it’s less comprehensive than levels 1.2.

Level 4: can be completed at home as well. And this one only measures your oxygen levels while you sleep to identify sleep apnea. Least comprehensive

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12
Q

Goals of
therapy

A

Establish baseline
Establish patient’s perception of sleep and their goals
Reverse sleep disruption to improve daytime functioning
Prevent progression to chronic insomnia
Resolve or mitigate underlying conditions
Prevent dependence on drug therapy
Reinstate normal sleep pattern without need for medication
If required, minimize side effects of pharmacotherapy

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13
Q

Treatment
of acute
insomnia

A

What do the guidelines say?

Treat acute insomnia only if there is a substantial
negative impact on daytime performance.
Intervene early and suggest behavioral therapy such as
cognitive behavioural therapy - insomnia (CBT-I).
Consider using short term (e.g., two weeks)
pharmacotherapy with close follow-up based on the
severity and urgency of the presentation.
Start medication at same time as CBT-I.
Follow-up to monitor progress in two to four weeks. And the typical recommended guideline is anywhere from every two to four weeks. So like pretty frequent follow-up

comprised of weekly sessions that go on for a total of six to eight weeks. Cbt is a very important factor in managing the negative associations that patients can develop around sleep, especially those who are suffering from insomnia. And so again, we want to stop people from falling into these cyclical patterns that then further impair their sleep and further impair their functioning.

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14
Q

5 Components of CBT-I

A
  1. Stimulus Control
    Keep the bedroom for sleep and sex only
    Go to bed only when sleepy
    Get out of bed after 15 min if sleep does not come
    Get out of bed at the same time every morning
    No napping
  2. Sleep Hygiene
    Maintain good sleep habits (environmental factors, routine)
    Limit coffee, nicotine, alcohol, large meals, vigorous exercise before bed
  3. Sleep Restriction
    (paradoxical approach)
    Limit time in bed to actual time asleep
    Increase TIB if SE >90%, or decrease time in bed if SE<80% (~20-30 min/wk)
  4. Relaxation Techniques
    Targets hyperarousal
    Meditation, progressive muscle relaxation, autogenic training
  5. Cognitive Therapy Target and change patient’s dysfunctional beliefs/attitudes about insomnia
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15
Q

NON-PHARMACOLOGIC TREATMEnt

A

Manage chronic insomnia with CBT-I.
If no CBT-I program is available, use CBT-I strategies or
online programs.
Emphasize the synergistic effect of combining CBT-I and
medication for those patients who are using
sedative/hypnotic medication.

, if we’re combining both and offering this dual treatment approach after that initial phase of treatment, it’s really important that if we’re considering tapering or discontinuing pharmacotherapy, that we continue the CBT because we don’t want to push someone to kind of fall back into their sleep-wake disorders who want to remove one agent at a time.

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16
Q

PHARMACOLOGIC TREATMENT

A

Start with a short-term prescription and arrange follow-up
with the patient preferably for 1-2 weeks (but no longer than
2-4 weeks) to assess whether or not there is a need for
continued treatment.

Select an agent according to the type of insomnia and the
presence of comorbidities:
- Consider 1st line pharmacotherapy (those with strongest
evidence for effectiveness, efficacy) or 2nd line
pharmacotherapy (those with moderate/variable
evidence for effectiveness)

Consider off-label medications only in specific clinical
scenarios
NEVER exceed the recommended dose.
DO NOT suggest OTC sleep aids or OTC medication with
drowsiness as a side effect.
Always provide quantity-limited prescriptions and no refills –
this will motivate the patient to return for follow-up.
Arrange follow-up to assess for adverse effects, dependence
and tolerance to sedative/hypnotic medication

17
Q

WHEN to consider long-term therapy:

A

The patient is significantly troubled by inadequate sleep
Concerned about the deleterious impact of inadequate sleep on the
patient’s health, safety and well-being
CBT and/or nonpharmacological options have been tried
Co-morbidities have been ruled out or treated maximally

most people who need long-term therapy for insomnia have not had the root cause identified or resolved. And so this is something that needs to be explored further because without resolving this, We’re gonna end up allowing an environment to persist that creates this like negative cognitive relationship with sleep

keep monitoring q 2-4 wks

18
Q

1st line tx
benzos

A

Benzodiazepines
Decrease sleep latency by 10-19 min
Increase total sleep time by 30-50min
Decrease nocturnal awakenings
BUT…Decrease REM and Delta sleep - Most restorative restful sleep here
Caution in older adults:
Reduced metabolism via oxidation (Phase I) up to 30%
Drugs that only undergo Phase II metabolism less affected
(lorazepam, oxazepam, tempazepam)

cautious when we’re using benzodiazepines for treatment. Especially in some populations who are maybe taking other medications that may have CNS, depression effects.
agent should always be selected based on their half-life and the subsequent risk for next day symptoms like morning sedation or potential for withdrawal side effects.

. If they have a shorter half-life, patients are more inclined to have withdrawal effects in-between doses once they’ve been on medication long-term

19
Q

1st line tx
Zopiclone; Zolpidem

A

Bind to α1 subunit of GABA receptor
α3 may play a role in sleep regulation (eszopiclone)
Decrease sleep latency by 22 minutes (zopiclone)
Similar to BZDs with a slightly improved kinetic profile ( Sleep induction Hangover)
Do not affect sleep architecture
No increase in efficacy over 15mg dose of zopiclone reported
Zopiclone - onset <1hr; t1/2 = 5 hours
Zolpidem - onset 20 minutes; t1/2 = 2.6 hours

zopiclone selective for that Alpha-1 site specifically and does seem to have some binding at the alpha2.

Pharmacologically it actually makes it quite similar to benzodiazepines, but compared to benzos, there’s increased sleep induction and less potential for next day hangover (they still feel really drowsy coming into the next day)

Zolpidem, typically like 5 h in bed is probably enough for that effect to wear off.
- It makes it useful for someone who is suffering with falling asleep or sleep onset.
- But also for someone who may be wakes up in the middle of the night and can’t fall back asleep
- People could maybe use it in the middle of the night, fault, use it to fall back asleep and wake up the next morning and not be like have a lot of next day sedation.

Zopiclone has lone t1/2 - 8 hrs to wear off
Dangeorus to take in middle of the night cuz it could be difficult to wake up in morning and drive to work

20
Q

1st line table

A

Z-drugs complex sleep behaviors that then are present themselves because of the medication. This can include things like sleepwalking, sleep driving, binge, eating while you sleep. So again, can be very dangerous. It’s really important that we talk to patients about this.

doxepin, which is a TCA, and it has some antihistamine properties. This is the main TCA that guidelines suggest or evidence supports use in insomnia. You may see other TCAs being used like amitriptyline nortriptyline. But these TCAs actually typically tend to have more side effects, but can have a role in patients who have co-morbid conditions that are involved in their insomnia patterns. So maybe someone who has pain, they might use a TCA
- Lower dose TCA generally more effective than higher dose
- . Unfortunately, these lower doses can be harder to come by and sometimes require specialty compounding, which can then present barriers to access.s

Temazepam
- quick onset of action and generally has a shorter duration of action. So it reduces the chance of that next day, morning sedation or hangover, especially when we compare it to benzodiazepines
a risk of both physical tolerance and dependence

Trazodone
- shown minimal benefit in non-depressed patients. However, generally these studies were like poor quality. But in practice, it does appear to be like use fairly often because it is relatively effective and it seems to preserve the sleep structure

5-HT to H1 antagonis = mirtazapine
- This is another antidepressant that does have effect in, that does have some effect in patients who are experiencing depression, who are suffering with sleep.
But it is less recommended in patients who are not experiencing depression because it does have some significant side effects, especially as it pertains to weight gain.

21
Q

Second line
pharmacotherapy

A

melatonin
L-Tryptophan
Valerian

melatonin
- hormone that’s naturally secreted by the pineal gland that has sleep inducing properties. It’s best evidence is actually for use in the delayed phase sleep phase syndrome.
- Then in circadian rhythm, circadian schedule or circadian rhythm changes. Again, lower doses tend to be more effective
- we generally recommend taking it like two or less hours before they plan to go to bed.

Valerian,
- product that inhibits the sympathetic nervous system by modifying both the transport and the release of gaba.
Carful with D/I

22
Q

Medications with sedating S/E

A

Sedating antidepressants (trazodone, mirtazapine)
Anticonvulsants (gabapentin, pregabalin)
Antihistamines
Antipsychotics (I.e. quetiapine)
Intermediate and long-acting benzodiazepines (diazepam, clonazepam, etc)
ONLY USE IF INDICATED! Otherwise, re-evaluate cause of insomnia

Quetiapine is seen commonly
- Off-label for treatment resistant cases
- Works really well esp w/ comorbid condtion
- doses under 100 mg are still associated with weight gain, hepatic failure
often very long term. It’s very difficult for patients to stop using it

23
Q

Dependence and misuse

A

Dependence
After 2 wks-1 month of regular use
Z-Drugs: less tolerance and withdrawal due to receptor selectivity; zopiclone causes less
receptor adaptation – STILL A RISK
Minimal with eszopiclone, ramelteon and temazepam (6 months nightly use)

Misuse Potential
Use with caution in patients with substance use disorder
Non-BZDs < BZDs (minimal, but generally less)

these non benzo drugs still, still carry a risk for both dependence and misuse. So for most of these medications, It’s important that when patients decide to stop or our field ready to stop, that they will need to taper.

Some providers feel like a temazepam taper or may not be required. But it’s really important that we assess this on a case-by-case basis.

Zopiclone really hard to taper, pt end up staying on it or going back to original dose

24
Q

So, how do we treat?

A

Can we fix the cause?
Individualize treatment
Type of sleep disorder?
Concurrent mental illness?
Substance abuse risk?
Sleep hygiene/CBT-I should form the initial management strategy
Tolerance/withdrawal is not definitive
Intermittent dosing is recommended to further reduce this risk
Smallest effective dose for the shortest period of time
May require long-term tx!
Use CBT to facilitate discontinuation of medications
Taper dose intermittent use trial d/c q3-6 months