Help me doc, I can't sleep: An Introduction to Insomnia.
- ZZZPack
- Jul 6, 2019
- 8 min read
Hey guys! This is the first of what I hope are many posts related to content of the sleep boards. Insomnia comprises 17% of the exam, and the ICSD-3 (citation below) is one of the most high-yield sources of content. Check out this post for a summary of what the ICSD-3 has to say about insomnia. Let’s get started. 💁♀️
What is Insomnia?
It is a condition with 3 components defined as 1) persistent sleep difficulty + 2) adequate sleep opportunity + 3) associated daytime impairment.
So, if there is no daytime impairment, don’t pursue treatment.
Note: it can be co-morbid with other medical conditions (e.g. medical, psychiatric illness, other sleep disorders, drug use), and still have it’s own separate diagnosis.
This is not in the ICSD-3, but is a great way to understand insomnia. In a way, this is pretty applicable to behavioral insomnia of childhood too. This is the Spielman/ ‘3P’/ Behavioral Model of Insomnia.
Basically, a person is predisposed to insomnia for some reason (e.g. medical condition, anxiety). Then something precipitates the insomnia (an acute event, e.g. death in the family, trauma, financial problem). Then the person develops an insomnia phenotype which may perpetuate for an acute amount of time (<3 months) or longer (>=3 months).
Differences to know about the ICSD-2 vs ICSD-3 definitions
ICSD-2: Insomnia could be primary or secondary (e.g. secondary to underlying medical, psychiatric, substance abuse disorder).
What’s the problem with this? There are a lot of overlapping features, so it is hard to tell what is primary and what is secondary. Also—even if the insomnia is a ‘secondary’ problem, it could remain a problem well after the ‘primary’ condition has resolved.
There used to be multiple categories of insomnia in the ICSD-2, but now there are 3 main categories.
Things to Note:
Hypnotics: If a patient sleeps well on hypnotic medications, they do not meet criteria for chronic insomnia. If they get off the medication and have difficulty, they have insomnia. If they voice a concern about needing medications to sleep, they have insomnia.
Co-morbidities: If the symptom is only due to the co-morbidity (e.g. GERD) then you don’t need a separate diagnosis. If there are other factors that are independent of the co-morbidity, or perpetuating factors have developed from the initial insomnia, then consider a diagnosis of insomnia.
How long is too long to fall asleep?
Sleep onset latency (SOL) >20 minutes in children and young adults can be clinically significant
SOL > 30 minutes in middle aged and older adults
How early is waking up too early?
Waking up at least 30 minutes before desired wake time resulting in reduced total sleep time.
My two cents: Make sure you watch out for advanced sleep phase disorder, more common in the elderly.
What about napping?
Oftentimes people with insomnia are very sleepy during the daytime, but usually do not fall asleep unintentionally. They usually don’t take naps even though they want to. Frequent unintentional napping is usually due to other sleep disorders like untreated sleep disordered breathing, insufficient sleep, a central disorder of hypersomnolence (e.g. narcolepsy), etc.
Behavioral Insomnia of Childhood
This is a topic which should really get it’s own dedicated post, and probably will 😱. To summarize:
Kids (especially younger ones) naturally wake up 4-6 x/night and go back to sleep on their own. But if there are inappropriate associations at sleep onset, that can become a problem with the other awakenings.
1) Sleep onset association: child needs specific stimulation (e.g. parent in room, car ride, object) to fall asleep, otherwise SOL significantly is prolonged. This can be related to fears and anxiety about sleeping alone.
With nighttime arousal, if the initial condition is absent, the child will seek out that condition (e.g. going back to their parents’ room). Remember, sleep like many behaviors is a conditioned behavior (key concept!!). If they needed the condition to fall asleep initially, they will need it in the middle of the night too.
This is a disorder if a) the behavior is problematic/demanding, b) sleep onset is significantly delayed and sleep is disrupted, and c) caregiver intervention is frequently required
2) Limit Setting: bedtime stalling, bedtime refusal that is reinforced by inadequate limit setting by the caregiver. Can result in prolonged nocturnal awakenings.
3) Mixed type: combination of sleep onset and limit setting. When the child seeks out the initial association to go back to sleep but there are inadequate limits enforced thereby causing bedtime resistance, this is mixed type.
Clinically significant when sleep difficulties happen 3x/week and persist for 3 months.
Clinical and Pathophysiological Subtypes
Even though these ICSD-2 subtypes are not formal diagnoses as there can be considerable overlap and clinically difficult to distinguish, they can be helpful in managing your patient.
Demographics
Prevalence of chronic Insomnia is 10% of population. Transient Insomnia prevalence is 30-35% of population. More common in: women, people with medical/psychiatric/substance abuse issues, lower SES. It's more likely to be diagnosed in elderly. It occurs in 10-30% of children, especially those with chronic illness or neurodevelopmental disorders. Prevalence is 3-12% in adolescents. Prevalence in girls is higher than in boys after puberty.
When is it reasonable to start diagnosing Insomnia?
6 months of age. Children should generally sleep through the night by this time.
Familial Patterns
Prevalence of insomnia is higher in monozygotic twins vs dizygotic twins and in first-degree relatives compared to the general population.
Association is higher among mothers and daughters.
What are some developmental issues to consider?
Here are a few:
A child’s stage of development will inform the type of sleep disorder the child will likely have. E.g. limit setting more likely when the child can get out of crib or bed.
If an infant has persistent sleep difficulties, consider underlying medical causes.
Precipitating and perpetuating factors will vary with age group.
Hypnotic medications are disproportionately prescribed to older adults, often with limited benefit.
Pathology and Pathophysiology
This section is dry, but actually really interesting🤓. Here's a summary.
Some changes include:
- Increased heart rate - Altered heart rate variability - Increased whole-body metabolic rate - Elevated cortisol - Elevated ACTH - Elevated CRF (corticotropin releasing hormone), particularly around sleep-onset - Increased body temperature - Increased high-frequency EEG activity during NREM sleep
Some studies suggest heightened activity of the sympathetic nervous system and hypothalamic-pituitary-adrenal axis across sleep and wakefulness (!) which perpetuates sleep-wake dysfunction.
Some people with insomnia may have physiologic dysregulation in general.
Some psychiatric conditions have a stronger relationship with insomnia.
Note: no discrete brain lesion or pathology has been found that is the cause of insomnia. There are some studies suggesting a discrete region responsible, but they are conflicting (e.g. possibly there is reduced hippocampal or anterior cingulate volume?).
What are some Objective Findings?
In the spirit of being high-yield, I'm not sure how important this section is 🤷♀️. The repeated advice I've heard is to know the ICSD-3, and this is a section of the chapter so...
In the spirit of being interesting and possibly esoteric, this does fit the bill. So use your own judgement if you want to read this part or not.
PSG: PSG is not indicated in the routine evaluation of insomnia; but you can use it to rule out other conditions (e.g. SDB) that could cause insomnia.
There is usually more night-to-night variability in PSG findings of people with insomnia vs. good sleepers.
MSLT: MSLT shows normal daytime alertness, and in fact, some studies suggest hyperarousal with prolonged mean sleep onset latency. Decreased mean sleep onset latency should prompt investigation for other sleep disorders.
fMRI: There have been a small number of studies in people with insomnia and controls. The studies show smaller wake to NREM decreases of relative glucose metabolism in sleep/wake-regulating regions such as the thalamus, upper brainstem, anterior cingulate, and limbic cortex. There is increased relative metabolism in these regions relative to self-reported and objective sleep disruption.
Nuclear magnetic resonance spectroscopy: Some studies show reduced GABA signaling in sleep-regulating regions in insomnia.
BOLD fMRI: Reduced activation (this measures blood flow) has been shown relative to baseline levels in people with insomnia during task-related changes. This becomes more ‘normal’ after CBT.
What else should we be thinking about in people with insomnia? What's on the differential diagnosis?
Delayed Sleep-Wake Phase Disorder (DSWPD)
**Dedicated posts on circadian rhythm disorders are coming down the pipeline.
If the presentation is difficulty with sleep initiation, consider DSWPD. In DSWPD, people can fall asleep without difficulty if they can sleep at the time of their choosing in phase with their circadian rhythm.
People with chronic insomnia can’t fall asleep regardless of their bedtime. Consider this especially in young adults.
Advanced Sleep-Wake Phase Disorder (ASWPD)
Consider this in people with difficulty maintaining sleep, or those who wake up earlier than their desired wake time. Sleep initiation is earlier than the desired bedtime as well, consistent with the person’s advanced endogenous circadian rhythm.
This is more common in older adults.
Total sleep time is adequate if their sleep schedule coincides with their circadian rhythm.
Note: there can be an overlap with DSWPD/ASWPD and chronic insomnia if an individual gets frustrated or anxious about not being able to sleep. Maladaptive behaviors may develop.
Poor Sleep Hygiene
If environmental circumstances are a primary cause of the sleep disorder, consider the diagnosis of other sleep disorder.
Insufficient Sleep Syndrome (aka Chronic Volitional Sleep Restriction)
This one is all too common. Can be really frustrating when someone comes in looking for an alternative diagnosis!
These people for a multitude of reasons (e.g. work schedule, social obligations) just don’t sleep enough. People with insomnia can’t sleep but allow themselves sufficient opportunity to sleep.
Insufficient sleep is associated more with EDS, more so than insomnia.
Untreated sleep apnea, untreated RLS , other sleep disorders
A person can still have a diagnosis of chronic insomnia if 1) the insomnia symptoms have independence in onset and variation from co-occurring sleep disorder or 2) when the insomnia symptoms persist despite treatment of the concurrent sleep disorder.
Okay, now we're at the home stretch. Let's go through Short-Term and Other Insomnia.
What about Short-Term Insomnia?
Basically the features are the same as chronic insomnia, but have been occurring for less than 3 months.
There are no clinical or pathophysiological subtypes.
Regarding demographics, Short-Term Insomnia can happen at any age, but it is difficult to establish in infants. Prevalence is unknown, but among adults could be 15-20%.
Predisposing and precipitating factors include being a light sleeper, psychiatric co-morbidity, lack of parental reinforcement of sleep habits (for kids), and acute life stressors.
Familial patterns are less well-documented.
Short-Term Insomnia can develop into Chronic Insomnia like we've discussed above.
Differential diagnosis should include circadian rhythm disorders, shift work disorder, and jet-lag.
Okay, what about Other Insomnia?
There is nothing to add here, except that if there is clinical insomnia not meeting the other two definitions, use this one, but use it sparingly or provisionally.
Everyone is special. Let's talk about some Isolated Symptoms and Normal Variants.
Excessive Time in Bed
Sounds great, right? Sometimes this can be confused for insomnia if there are unrealistic expectations of total sleep time requirements. Common in kids and retired people.
Short sleeper
Some people don't seem to need more than 6 hours of sleep, and have no daytime concerns. Lot's of studies are being done about the clinical significance of this. This is not a sleep disorder.
That's a wrap! You have successfully read through the high-yield parts of the ICSD-3 Insomnia section!
References:
1. American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.
2. '3 P' model image accessed from: https://www.medscape.com/answers/1187829-70509/what-is-the-spielman-model-of-chronic-insomnia
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