Dental sleep medicine series 2: What affects normal sleep

Sleep disordered breathing (SDB) is only a small fractions of defined sleep disorders. Many people in today's society are physiologically healthy but have factors such as medications, poor sleep hygiene and other lifestyle factors that can affect their sleep. Often we must rule out or treat SDB to realise an improvement in their condition but the optimisation of sleep quality and quantity only comes with treating the person as a whole and assessing the full range of factors that can affect sleep poorly.

From Sleep medicine 6th edition

Some generalisations about healthy adult sleep

• Sleep is entered through NREM sleep.
• NREM sleep and REM sleep alternate with a period near 90 minutes.
• SWS predominates in the first third of the night and is linked to the initiation of sleep and the length of time awake (i.e., sleep homeostasis). 

• REM sleep predominates in the last third of the night and is linked to the circadian rhythm of body temperature.
• Wakefulness in sleep usually accounts for less than 5% of the night.
• Stage 1 sleep generally constitutes about 2% to 5% of sleep.
• Stage 2 sleep generally constitutes about 45% to 55% of sleep.
• Stage 3 sleep generally constitutes about 3% to 8% of sleep.
• Stage 4 sleep generally constitutes about 10% to 15% of sleep.
• NREM sleep, therefore, is usually 75% to 80% of sleep.
• REM sleep is usually 20% to 25% of sleep, occurring in four to six discrete episodes.  

Factors affecting sleep stage distribution

Age

The largest factor affecting sleep patterns is age. In the first year of life, sleep onset occurs through REM. The NREM-REM cycle is present but occurs in about 50-60 minute cycles. Slow wave sleep is maximal in young children and decreases with age especially in men. It is nearly impossible to wake a young child in SWS of the first cycle of sleep. This often means they skip their first REM cycle until midadolescence. Arousal occurences and length increase with age and often can be reported in the morning whereas short arousals are often forgotten.

Prior sleep history

Previous recent sleep loss encourages the experience of SWS. Recovery sleep is often longer duration and deeper with a higher arousal threshold. SWS is favoured in recovery sleep and once recuperated REM sleep tends to recover. Recovery of sleep tends to have a homeostatic pattern. Deprivation of REM sleep will tend to have more REM sleep and the same is true for NREM sleep. This can have clinical implications if a REM suppressant medication is suddenly withdrawn, the subsequent recovery may exacerbate an underlying sleep disorder (if the condition is worse in REM sleep)

The first night of a laboratory sleep study is associated with more frequent arousals, delayed REM onset/skipping first REM episode, disruption of REM episodes and reduced REM sleep time. 

Circadian rhythms

The circadian phase at the onset of sleep affects sleep staging, therefore when one sleeps helps to determine how long one sleeps. REM sleep occurs in the circadian distribution that tends to peak in the early hours of the morning. Therefore, in delayed sleep onset, REM sleep predominates and may be present at sleep onset. This can occur in a person who has undergone a work shift or in jet lag. Sleep onset is most likely in the cooling area of the temperature circadian rhythm. A secondary peak of sleep onset occurs at the time of the afternoon nap. The cessation of sleep occurs mostly at the circadian increase in body temperature. Patients who wake with events early in the night might have a disorder affecting NREM sleep; patients who wake with events late in the night may have a disorder affecting REM sleep. 

When using sleep restriction to build sleep pressure, treatment will be more effective if sleep is scheduled at the correct circadian phase. The problem of napping in patients with insomnia is that naps diminish the homeostatic drive to sleep.

Temperature

Extremes of temperature tend to disrupt sleep. REM sleep is more sensitive to disturbance which suggests that animals have poorer ability to thermoregulate during REM sleep. As well, responses to temperature extremes such as shivering or sweating are predominantly in NREM sleep and are limited in REM sleep

Drug ingestion

• Benzodiazepines tend to suppress SWS and have no consistent effect on REM sleep.
• Tricyclic antidepressants, monoamine oxidase inhibitors, and certain selective serotonin reuptake inhibitors tend to suppress REM sleep. An increased level of motor activity during sleep occurs with certain of these compounds, leading to a pattern of REM sleep without motor inhibition or an increased incidence of PLMS. Fluoxetine is also associated with rapid eye movements across all sleep stages (“Prozac eyes”).  

• Withdrawal from drugs that selectively suppress a stage of sleep tends to be associated with a rebound of that sleep stage. Thus, acute withdrawal from a benzodiazepine compound is likely to produce an increase of SWS; acute withdrawal from a tricyclic antidepressant or monoamine oxidase inhibitor is likely to produce an increase of REM sleep. In the latter case, this REM rebound could result in abnormal SOREMPs in the absence of an organic sleep disorder, perhaps leading to an incorrect diagnosis of narcolepsy.
• Acute presleep alcohol intake can produce an increase in SWS and suppression of REM sleep early in the night, which can be followed by REM sleep rebound in the latter portion of the night as the alcohol is metabolized. Low doses of alcohol have minimal effects on sleep stages, but they can increase sleepiness in the late evening.
• Acute effects of marijuana (tetrahydrocannabinol [THC]) include minimal sleep disruption, characterized by a slight reduction of REM sleep. Chronic ingestion of THC produces a long-term suppression of SWS.  

Pathology

A number of sleep stage anomolies are associated with sleep disorders

Narcolepsy

Characterised by short delay to REM sleep marked by SOREMPS (Sleep onset REM periods). The dissociation of REM components into wakefulness can cause hypnagogic hallucinations, sleep paralysis and most dramatically cataplexy. However, short latency to REM sleep can be present in infancy, jet lag, acute withdrawal from REM suppressant drugs, chronic restriction or disruption from sleep and endogenous depression. 

Sleep apnoea syndromes

May be associated with supression of SWS or REM sleep. Successful treatment of the disorder can cause large rebounds of SWS or REM sleep when first implemented.

Sleep fragmentation

Sleep fragmentation and increased arousals are associated with sleep and medical disorders involving psysical pain or discomfort including PLMS, sleep apnoea syndromes, chronic fibrositis which can be associated with hundreds of arousals per night. Allergic rhinitis, juvenille rheumatoid arthritis and parkinson disease have brief arousals. In Upper airway resistance syndrome (UARS) EEG arousals are important markers because the respiratory signs are less obvious than OSAS. In specific situations, autonomic changes such as transient changes of BP can be used to signify arousals as they are highly correlated with EEG arousals.