Sleep Disorders Flashcards

1
Q

Insomnia: epidemiology

A

o Prevalence: 10-15% population
• ~10% cases = primary
• ~90% = comorbid (associated with co-occurring medical, psychiatric, or sleep disorders)

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2
Q

Insomnia: pathophysiology

A

Biological factors
• CNS hyperarousal
• Higher proportions of short allele of 5-HTTPR gene

Psychological factors
• More reactive to stressors
• Worries and intrusive thoughts prior to sleep
• Over time may develop negative associations with bedtime/environment
• Maladaptive responses may perpetuuate insomnia

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3
Q

Insomnia: Risk factors

A
o	Age (greater prevalence in older individuals)
o	Female gender (especially post- and perimenopausal)
o	Divorce/separation/widowhood
o	Psychiatric illness
o	Medical conditions
o	Cigarette smoking
o	Alcohol and coffee consumption
o	Certain prescription drugs
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4
Q

Insomnia: common causes/comorbidities

A
Medical
•	Cardiac, pulmonary, rheumatologic, neurologic, endocrine, gastrointestinal, renal, pain syndromes 
•	Medication effects:
Stimulants (modafinil, amphetamine, methylphenidate)
Antidepressants (SSRIs, bupropion)
Theophylline and caffeine
Decongestants (pseudoephedrine)
Diuretics
Corticosteroids
Antihypertensives
Alcohol (esp in 2nd half of night)
Withdrawal from sedative-hypnotics 

Psychiatric
• Mood disorders, anxiety disorders, substance abuse
• Most psychiatric disorders are associated with insomnia
• Chronic insomnia = 2x risk of developing depression

Sleep
• Circadian rhythm disorders
• Sleep-disordered breathing
• Restless legs syndrome (Willis-Ekbom Disease)

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5
Q

Parasomnias: pathophysiology

A

Definition:
o Undesirable physical, experiential or behavior phenomena that occur during sleep or are exacerbated by sleeping

Pathophysiology:
o	Typically arise from Short wave sleep (SWS) = First 1-2 hrs of sleep period
o	Behaviors and mood states
•	Not under conscious control
•	Not remembered on awakening

Arise when elements of specific brain states occur simultaneously:
NREM sleep
REM sleep
Wake

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6
Q

REM vs NREM sleep

A

NREM Sleep
• Increased parasympathetic activity
• Decreased HR, CO, BP
• Decreased EMG activity (but not as great as REM)

REM Sleep 
•	Increased sympathetic activity
•	Dreaming
•	Paralysis of skeletal muscle 
•	Rapid eye movements
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7
Q

Parasomnias: types

A
o	Confusional arousals
o	Sleepwalking 
o	Sleep terrors 
o	REM behavior disorder
o	Variants: Sleep-related violence, sexual activity, eating disorder
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8
Q

Parasomnias: prognosis

A

Often common in children and most tend to grow out of them

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9
Q

Parasomnias: evaluation

A
For NON-REM parasomnias:
PSG not routinely indicated
•	Unless co-morbid sleep disorder suspected 
•	Dangerous or atypical parsomnia
Differential diagnosis
•	Nocturnal panic attacks
•	Nocturnal frontal lobe seizures 
•	Delirium
•	Nocturnal dissociative episodes 
•	REM Sleep Behavior Disorder
Treatment Risk-Benefit analysis for each person

For REM Behavior disorder:
• PSG needed to confirm diagnosis:
• Elevated muscle tone
• Increased submental or ant tibialis EMG

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10
Q

Parasomnias: treatment

A
For NON-REM parasomnias:
Three-Step Model
•	Modify predisposing/precipitating factors 
•	Avoid sleep deprivation, stress
•	Improve safety of sleeping environment 
Pharmacotherapy
•	No controlled trials 
•	Benzodiazepines typically used

For REM Behaviro disorder:
• Treat co-morbid sleep disorders
• Remove iatrogenic causes of RBD (ex: antidepressants)
• Behavioral management = Optimize safety of sleeping environment
Pharmacologic management:
• Benzodiazepines
• Alternatives melatonin, pramipexole

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11
Q

Sleepwalking

A
  • Common in children (10-20%)
  • Ususally resolves by adolescence
  • 1-4% of adults (80% had behaviors in childhood)
  • Strong genetic component:
  • Twin studies, HLA-DQB1*0501
  • Higher risk with family history
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12
Q

Sleep terrors

A

Motoric behavior with affective discharge
• In children = piercing scream, followed by fear, crying and inconsolability
• Increased autonomic activity (HR, Resp rate, sweating)

Prevalence: 5% of children, 1-2% of adults

Amnesia is rule
• But simple mentation may be recalled
• Caution confronting = can morph into sleep-related violence

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13
Q

REM behavior disorder

A

Features:
• Loss of paralysis during REM sleep → Individuals act out their dreams
• Eyes closed; unresponsive to environment
• On awakening = rapid alertness with dream recall
• (Self)-injury often prompts evaluation

Prevalence ~ 0.4-0.5% in elderly
• 70-80% are men
• ~5 years from onset to diagnosis

Risks:
• Associated with narcolepsy in young
• In older men, higher risk of developing Parkinson’s Disease or dementia

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14
Q

Circadian rhythm disorders: pathophysiology

A

o Misalignment of internal clock with environment

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15
Q

Circadian rhythm disorders: clinical presentation

A

Combination of difficulty initiating sleep and daytime sleepiness

Types:
Exogenous
• Chronic misalignment between the body’s natural circadian rhythms and environment
• Ex: Shift work sleep disorder

Endogenous 
•	Delayed sleep phase syndrome 
o	Most common = adolescents
o	Initial insomnia and difficulty waking in morning
o	Daytime sleepiness 
•	Advanced sleep phase syndrome 
o	Most common = elderly
o	Early morning waking
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16
Q

Circadian rhythm disorders: evaluation

A

o Clinical history = key
o Supplemental data:
• Sleep logs
• Actigraphy (wrist-worn accelerometer that measures rest-activity patterns

17
Q

Circadian rhythm disorders: treatment

A
Exogenous
Increase sleep duration 
•	Sleep hygiene education 
•	Hypnotic medication
Increase alertness
•	Prophylactic naps
•	Caffeine
•	Wake-promoting drugs
Re-align circadian rhythm 
•	Adjusting light exposure
•	Melatonin

Endogenous
• Appropriately timed light exposure
• Regularizing sleep-wake patterns
• Appropriately timed melatonin

18
Q

Narcolepsy: epidemiology

A

o Onset = children, teens, young adults

o Prevalence ~0.05%

19
Q

Narcolepsy: clinical presentation

A
Features:
•	Excessive daytime sleepiness
•	Sleep paralysis
•	Hypnagogic/hypnopomic imagery (hallucinations at sleep onset and/or offset)
•	Cataplexy
•	Loss of muscle tone in response to emotional stimuli 
•	Highly specific for narcolepsy
•	Automatic behaviors 
2 types:
1) Narcolepsy with cataplexy
•	Loss of hypocretin/orexin neurons in lateral hypothalamus
o	Normally serve as “finger on switch” to maintain sleep vs. wake state
•	Likely autoimmune reaction
•	Associated with HLA DGB1*0602
2) Narcolepsy without cataplexy
•	Less clear causes
20
Q

Narcolepsy: evaluation

A

o PSG test

o Multiple sleep latency test (MSLT)
• Typically shows mean sleep latency <8 min
• Greater than 2 sleep onset REM episodes

21
Q

Narcolepsy: treatment

A

o Avoid sleep deprivation
o Scheduled naps
o Stimulants = promote wakefulness (Modafinil, methylhenidate, amphetamines)
o Antidepressants = reduce cataplexy
o Sodium Oxybate = treats excessive daytime sleepiness and cataplexy
• Highly controlled drug

22
Q

Restless legs syndrome: epidemiology

A

o Prevalence ~3-5%

23
Q

Restless legs syndrome: pathophysiology

A

Primary
• Thought to be from dysfunction of CNS iron metabolism
• However = most present with normal iron levels in periphery

Secondary
•	Iron deficiency anemia
•	Renal failure
•	Pregnancy
•	Medication induced: antidepressants, antiemetics, antipsychotics, antihistamines
24
Q

Restless legs syndrome: risk factors

A

o Female
o Elderly
o Northern European descent

25
Q

Restless legs syndrome: clinical presentation

A

o Sensorimotor disorder that disrupts sleep initiation, maintenance, and or causes excessive daytime sleepiness

26
Q

Restless legs syndrome: diagnosis

A

o Made clinically
o Associated with periodic limb movements of sleep during PSG (but not specific)

Minimal Criteria:
(URGE)
Urge to move legs
Rest-induced (onset or worsening of symptoms at rest)
Gets better with movement 
Evening predominance
Other features:
Sleep disturbance
Involuntary leg movements
Positive RLS family history
Response to dopaminergic therapy
27
Q

Restless legs syndrome: treatment

A

Non-pharmacologic
• Abstinence from caffeine, nicotine, alchohol
• Evaluate medications that may worsen RLS
• Iron replacement if ferritin <50 ng/mL

Pharmacologic
• 1st line: dopamine agonists (pramipexole, ropinirole)
• 2nd/3rd line: Gabapentin, Low-potency opioids

28
Q

List the pharmacologic treatments available for sleep disorders (insomnia treatment)

A
Benzodiazepine receptor agonists
•	Agonist on GABAA receptor 
Adverse effects:
•	Daytime sedation
•	Cognitive impairment
•	Anterograde amnesia
•	Motor impairment
•	Rebound insomnia upon discontinuation 
•	Parasomnias = Somnambulism, sleep-eating, sleep-driving 
•	Tolerance/dependence/abuse
•	Other: headache, GI (nausea, diarrhea)

Melatonin agonists (Rameleon)
• MT1/2 receptor agonist
• Approved for insomnia treatment
• No cognitive impairment or abuse liability
• Rapid absorption and short ½ life = better for sleep initiation than maintenance

Sedating antidepressants (mirtazapine, trazodone, nefazodone, amitriptyline, doxepin, trimipramine)
• Cholinergic, histaminergic, adrenergic, and serotonergic antagonism
• Little abuse liability
• Probably not as effective as benzodiazepines
Adverse effects:
• Daytime sedation
• Weight gain
• Anticholinergic side effects
• Switch into mania in bipolar disorder

Anticonvulsants (gabapentin, tiagabine, pregabalin)
• Good: little abuse liability, may be helpful with co-morbid RLS
• Probably not as effective as benzodiazepines
Adverse effects:
• Cognitive impairment
• Daytime sedation
• Weight gain
• Edema

Atypical antipsychotics (olanzapine, quetiapine, risperidone, ziprasidone)
•	Dopaminergic, cholinergic, histaminergic, and serotonergic antagonism
•	Used off-label to treat insomnia 
Advantages:
•	Anxiolytic
•	Mood stabilizing in bipolar disorder
•	Little abuse liability 
Disadvantages 
•	Less effective than benzodiazepines 
•	Daytime sedation 
•	Weight gain
•	Risks of extrapyramidal symptoms 
•	Glucose + lipid abnormalities