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[Research Paper]
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Delayed Sleep Phase Disorder
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The Research Team are unable to ensure that the information listed below provides an
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Research question: Based on current research, would Delayed Sleep Phase Disorder be
considered permanent? What is the prognosis? What are the most effective treatments and
outcomes of treatment?
Date: 8/7/22
Requestor: s47F - personal privacy
Endorsed by (EL1 or above): s47F - personal privacy
Researcher: s47F - personal privacy
Cleared by: s47F - personal privacy
1. Contents
Delayed Sleep Phase Disorder .................................................................................................. 1
1.
Contents ....................................................................................................................... 1
2.
Summary ...................................................................................................................... 2
3.
Delayed Sleep Phase Disorder ..................................................................................... 2
3.1 Background ............................................................................................................... 2
3.2 Etiology ...................................................................................................................... 3
3.3 Symptoms/functional impact ...................................................................................... 4
3.4 Diagnosis ................................................................................................................... 4
3.5 Treatment .................................................................................................................. 5
3.6 Prognosis ................................................................................................................... 7
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4.
References ................................................................................................................... 8
5.
Version control .............................................................................................................. 8
2. Summary
Delayed Sleep Phase Disorder (DSPD) is the most common circadian rhythm sleep-wake
disorder. DSPD is the inability to initiate sleep at a conventional bedtime and subsequent
difficulty to wake for morning commitments. The prevalence of DSPD is unclear, however is
estimated to be between 0.5-16% of the population with a higher prevalence in adolescents.
True DSPD is an intrinsic sleep disorder affecting the circadian rhythm, however there are
psychological, social and behavioural influences on the natural sleep-wake cycle. These
factors include evening exposure to artificial light and use of electronic devices late at night.
Main symptoms of DSPD include: daytime sleepiness, fatigue, low mood, irritability, poor
concentration, poor memory and decreased attention.
DSPD can be episodic, persistent or recurrent. Most often it follows a
persistent course as
relapse after treatment is common. Left untreated, DSPD can increase the risk of poor life
outcomes such as job loss, truancy, school failure, less participation in sport and social
difficulties. Treatment aims to bring forward the sleep phase to enable early bedtimes and
therefore wake more easily in the morning without experiencing tiredness. Treatments include
exogenous melatonin,
light therapy and
sleep hygiene/behavioural changes. However,
correction of the sleep-wake cycle is rarely permanent. After relapse, individuals should be
encouraged to go back to their original treatment plan.
DSPD is associated with depression, anxiety, OCD, ADHD and ASD. It is important to note
these
comorbidities may impact implementation and/or adherence of the treatment
protocol.
3. Delayed Sleep Phase Disorder
3.1 Background
Delayed Sleep Phase Disorder is the most common of all circadian rhythm sleep-wake
disorders (Nesbitt, 2018; Prihodova et al, 2022). DSPD is defined as difficulty initiating sleep
and an inability to wake for morning commitments as a result of the delayed timing of the major
sleep period (Micic et al, 2016; Richardson et al, 2019). Despite the delay in the onset of sleep
and wake up time, the physiological structure of sleep is preserved (Gomes et al, 2021). That
is, a major sleep episode occurs every 24 hours with usual REM and non-REM sleep, but the
sleep timing is inappropriate to the day-night cycle (Nesbitt, 2018).
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The prevalence of DSPD is difficult to determine due to the blurred boundary between
individuals with an extreme evening chronotype (‘night owls’) and those with DSPD (Nesbitt,
2018). Broad estimates place the prevalence between 0.5-16% of the population (Micic et al,
2016; Nesbit , 2018) with the highest prevalence among adolescents and young adults
(Nesbitt, 2018; Richardson et al, 2017).
DSPD is associated with depression, anxiety, obsessive compulsive disorder, ADHD and ASD
(Nesbitt, 2018; Prihodova et al, 2022; Snitselaar et al, 2019). Research suggests 52% of
patients with DSPD have a comorbid mood disorder, and 45% have a diagnosis of attention
deficit hyperactivity disorder (Prihodova et al, 2022). It is suggested that these comorbid
diagnoses may impact the course of DSPD as they are associated with less motivation to start
and continue treatment (Danielsson et al, 2018).
3.2 Etiology
The pathophysiology of DSPD is multifactorial. True DSPD is a primary intrinsic sleep disorder
where the circadian rhythm and sleep timing are delayed relative to solar cycle (Nesbitt, 2018).
However, a high proportion of people diagnosed with DSPD have delayed sleep episodes with
normally aligned circadian timing (Nesbit , 2018). So while alterations in the natural circadian
rhythm may play a role, there are also psychological, behavioural and social contributors to the
etiology (Prihodova et al, 2022). Highlighting this point, research in a controlled laboratory
environment found the majority of adolescents, all with a diagnosis of DSPD, fell asleep at a
conventional time when they had no access to technology or other distractions (Prihodova et
al, 2022).
In healthy individuals, melatonin levels cycle through the day in response to light intensity –
melatonin levels are negligible in the morning with bright light and rise in the early evening
when light intensity reduces (Micic et al, 2016). The intensity of light is sensed by
photosensitive retinal cells in the eye and conveyed to the natural timekeeper, the
suprachiasmatic nucleus (Micic et al, 2016; Nesbitt, 2018). It is most likely that people with true
DSPD get too much light exposure in the phase delaying portion of the response to light and
too little in the phase advancing portion because they are asleep (Nesbitt, 2018). Alternatively,
some people may have longer biological feedback loops within this neural circuit, meaning it
takes longer for the evening sleep phase to be triggered (Micic et al, 2016; Nesbitt, 2018).
Other influences that can impact the sleep-wake cycle are:
• Onset of puberty, which is typically characterised by a biological delay in the
habitual sleep pattern, tending to reversal to earlier sleep pattern in 20s, however
the delay can be maintained by some individuals into adulthood (Micic et al,
2016)
• Abnormal melatonin secretion (Prihodova et al, 2022)
• Brain injury or head trauma (Snitselaar et al, 2019)
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• Psychological disorders – mood disorders, specific personality traits (such as
neuroticism) (Prihodova et al, 2022)
• Social and behavioural factors – natural evening chronotype, use of electronic
devices, regularly attending late evening events (e.g., classes or sport scheduled
in late evening) (Prihodova et al, 2022) – that increase artificial light exposure in
the evening and decrease it in the morning hours (Micic et al, 2016; Nesbitt,
2018)
• Jet lag (Snitselaar et al, 2019)
3.3 Symptoms/functional impact
Individuals with DSPD demonstrate difficulties initiating sleep, so, when woken at a
conventional time, experience markedly reduced daytime functioning (e.g., excessive daytime
sleepiness, fatigue, low mood, irritability), impaired cognitive performance (e.g., concentration,
memory and attention), and poor social functioning (Gomes et al, 2021; Micic et al, 2016;
Prihodova et al, 2022; Richardson et al, 2017). These symptoms are most notable in the
morning (Richardson et al, 2016), and can impact work capacity and attention due to
decreased cognitive and motor skil s (Gomes et al, 2021).
Over the long term, unmanaged DSPD can cause permanent health and social disruptions,
impacting quality of life. Job loss, truancy, school failure, less participation in sport and social
difficulties are potential risks for people with DSPD (Micic et al, 2016). Some studies suggest
depression, medication use (antacids, hypnotics), tobacco, alcohol and caffeine consumption
are greater for people with DSPD than controls (Micic et al, 2016).
It should be noted, when individuals diagnosed with DSPD are allowed to set their own sleep
schedule – meaning they do not experience forced awakening in the morning and chronic
sleep deprivation – they often experience normal sleep quality and duration for their age and
experience remission of symptoms (American Psychiatric Association, 2013).
3.4 Diagnosis
DSPD is characterised by significantly later sleep onset times compared to social convention
and long sleep latencies when attempting sleep at conventional bedtimes, often between 2-6
hours after the desired sleep time (American Psychiatric Association, 2013; Micic et al, 2016).
DSPD falls under the Circadian Rhythm Sleep-Wake Disorders (CRSWD) in the Diagnostic
and Statistical Manual of Mental Disorders, Fifth Edition (American Psychiatric Association,
2013); the following outlines the criteria for CRSWD and subtype DSPD:
A. A persistent or recurrent pattern of sleep disruption that is primarily due to an
alteration of the circadian system or misalignment between the endogenous
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circadian rhythm and the sleep-wake schedule required by an individual’s
physical environment or social or professional schedule, and
B. The sleep disruption leads to excessive sleepiness, insomnia, or both, and
C. The sleep disturbance causes clinically significant distress or impairment in
social, occupational, and other important areas of functioning
Specify if: Delayed sleep phase type – a pattern of delayed sleep onset and awakening
times with an inability to fall asleep and awaken at a desired or conventionally
acceptable earlier time.
For DSPD, specify if:
episodic – symptoms last at least one month but less than
three;
persistent – symptoms last for 3 months or longer;
recurrent – two or
more episodes are experienced in the space of one year
The clinical diagnostic criteria for DSPD, along with sleep diaries and actigraphy (sleep
monitoring devices), is typically not sufficient to distinguish between DSPD related to
disruption of endogenous sleep-wake regulation and sleep-wake difficulties caused by factors
such as poor sleep hygiene and behavioural delay of sleep onset (Prihodova et al, 2022). A
delay in the dim light melatonin onset (DLMO) – a biological marker in saliva and plasma – can
be used to identify disorders of the endogenous circadian rhythm (Snitselaar et al, 2019).
3.5 Treatment
Current treatments for DSPD aim to advance the natural circadian phase and bring sleep
timing earlier to increase sleep duration and reduce daytime impairments (Gomes et al, 2021;
Micic et al, 2016; Nesbitt, 2018). However as large scale randomised controlled studies in
patient population are lacking there is little supporting clinical evidence how to best manage
the disorder (Nesbit , 2018). Main treatments to regulate the circadian rhythm and induce
earlier sleep phases are chronotherapy or pharmacotherapy, light therapy and behavioural
lifestyle changes (Lu et al, 2022).
Exogenous melatonin supplementation has been a traditional therapy for DSPD, which
provides a sleep time-cue for the body (Nesbitt, 2018). A strategically timed 0.5mg daily dose
taken consistently 10-12 hours prior to the mean mid-point of desired sleep time or 6-8 hours
prior to the desired sleep onset time can be effective in changing sleep phases (Nesbitt, 2018).
Using melatonin in chronotherapy should be closely monitored by a sleep specialist to avoid
desynchronisation to a non-24hr sleep-wake disorder (Nesbitt, 2018).
Light therapy is another treatment that has been used to alter sleep timing to a more desired
schedule as light is the predominant timekeeper of the circadian cycle (Richardson et al,
2017). Morning light is most helpful in phase-advancing, so it should be delivered immediately
on waking. This can be natural light, by going out for a walk or sitting near a window, bright
artificial light, dim light or blue light therapy (Nesbitt, 2018). While there is some mixed data
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regarding the use of artificial light therapy, many studies do show advancement of sleep onset
and sleep offset when artificial light therapy is used consistently in the morning (Danielsson et
al, 2018). Research by Danielsson et al (2018) into the use of artificial light therapy for DSPS
found daily light therapy more predictive of better outcomes than light intensity exposure or
length of time of the exposure. However, a systematic review suggested that while the sleep-
wake cycle may be altered, there was often no corresponding biological change in the
circadian phase as measured by the biomarker DLMO (Gomes et al, 2021).
For optimal effect of morning light therapy, it is suggested it should be combined with
minimising exposure to artificial light from dusk onwards in the evening (Danielsson et al,
2018; Richardson et al, 2017). Sources of artificial light that should be avoided include light
from television screens and handheld devices (Cardinali et al, 2021). Use of blue light filter
goggles or glasses with amber lenses may effectively reduce the stimulation from artificial light
in the evenings (Nesbit , 2018). It is suggested that light therapy, including natural, artificial
bright, dim and blue light, can result in improvements in sleep quality and daytime functioning
(i.e., reductions in daytime sleepiness, fatigue and functional impairment) (Lu et al, 2022;
Richardson et al, 2019), however these improvements are often not sustained long-term
(Gomes et al, 2021).
Another novel technique described in the literature that may manipulate sleep-onset timing is
the use of
exercise to advance the circadian timing. For individuals with DSPD, this may be
undertaking 1 hour of moderate exercise in the subjective “morning” (i.e., soon after waking)
and advancing wake up time and exercise timing by 20-30 minutes earlier each day until
desired sleep timing is achieved (Richardson et al, 2017). This also suggests that people with
DSPD should try to avoid intense exercise late in the day in order to reduce dysregulation of
the circadian rhythm.
Behaviours that promote
good sleep hygiene have also been found to support other DSPD
treatment protocols. Some behaviours include (Mennella & Shiebel, 2018):
• Avoid alcohol, tobacco, and other stimulant prior to bedtime
• Avoid behaviours that require a high level of concentration immediately before bed,
including exciting or emotionally disturbing activities
• Maintain a low-light environment in the evening and avoid using the computer or
watching television
• Invest in good quality bedding and keep the room dark, quiet and cool
• Avoid staying in bed longer than 7.5 hours, use an alarm clock to wake
• Avoid a difference of 2 hours in wake time on weekends
For any DSPD treatment protocol, it is important to consider coexisting conditions that may
either exacerbate DSPD symptoms or make difficult to follow the protocol (Nesbitt, 2018). For
example, patients with comorbid ADHD often show reduced compliance with treatment
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potentially because of the dif iculties these patients have with planning and organisation in
their daily life, which can lead to irregular intake of medication, such as melatonin, and
difficulties following lifestyle guidance such as regular bedtimes and minimising artificial light at
night (Snitselaar et al, 2019).
In general, basic treatment of DSPD involves good sleep hygiene, consistent regular bedtime
with habitual lights off, appropriate light exposure and exogenous melatonin taken at the right
time (Prihodova et al, 2022; Snetselaar et al, 2019). However, implementation of treatment can
be dif icult due to lack of patient motivation and compliance (Prihodova et al, 2022), which may
be secondary to the fatigue and daytime sleepiness experienced by patients with DSPD. It has
been found that psychoeducation can increase adherence to treatment and increase the
chance of successful results (Danielsson et al, 2018). However, with any treatment for DSPD
relapse is common as correction of the circadian delay is rarely permanent (Nesbitt, 2018).
3.6 Prognosis
DSPD can be episodic, persistent or recurrent (see section 3.4 Diagnosis) (American
Psychiatric Association, 2013). While it is more common in adolescents and young adults, it
can continue into adulthood if not managed effectively (Richardson et al, 2017).
DSPD often follows a
persistent course and can be refractory to therapeutic interventions
(Prihodova et al 2022). A
relapse of symptoms is common, and patients should be prepared
for this eventuality and encouraged to go back to their original treatment plan (American
Psychiatric Association, 2013; Nesbitt, 2018).
Exacerbations or relapses are often triggered by a change in schedule that requires an early
awakening time, such as a change in work or school hours (American Psychiatric Association,
2013). Individuals who can manage their schedule to accommodate the delayed sleep phase
timing demonstrate greater resilience to experience remission of symptoms (American
Psychiatric Association, 2013).
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