week 8 - sleeep Flashcards
What is sleep?
“A periodic state of muscular relaxation, reduced metabolic rate, and suspended consciousness in which a person is largely unresponsive to events in the environment.” (Oxford Dictionary of Psychology)
Sleep is reversible
Five sleep stages: Wake, non-rapid eye movement sleep (Stages N1, N2, N3), and rapid eye movement sleep (REM).
What are the 5 stages?
Wake,
non-rapid eye movement sleep (Stages N1, N2, N3), and rapid eye movement sleep (REM).
How much sleep do we need?
Age Group sleep duration recommended New borns: 0 – 3 months: 14-17hrs Infants: 4 – 11 months: 12-15 hrs Toddlers: 1 – 2 years : 11-14hrs Preschoolers: 3 – 5: 10-13hrs School age children: 6 – 13: 9-11hrs Teenagers: 14 – 17 : 8-10 hours Young adults and adults: 18 – 64: 7-9 hours Older adults: 65+ - 7-8
What drives us to sleep?
The two-process model
Process S – homeostatic drive (Sleep pressure). The longer we stay awake, the greater the need for sleep (purple)
Process C – circadian wake drive. Internal body clock (green)
What drives us to sleep? Process S (Sleep Pressure)
Adenosine builds as a function of sleep pressure.
Caffeine – adenosine receptor antagonist (ARA)
Concept of a coffee-nap (sleep + ARA interaction)
Even during wakefulness, sleep pressure is demonstrated through increased power of slow EEG frequencies
Once asleep, amount of deep sleep (N3) correlates with the sleep drive (e.g., how much sleep deprivation has occurred)
What drives us to sleep? Process C (Circadian Rhythm/Body Clock)
Main biological clock – suprachiasmatic nucleus (SCN) of the hypothalamus
Body clock synchronised by many biological and social stimuli, most importantly light (particularly blue light)
Melatonin – a hypnogenic hormone released in the evening assisting us to sleep
Retina contains photosensitive melanopsin receptors with pathway to the SCN via the retinohypothalamic tract
What drives us to sleep? Process C (Circadian Rhythm/Body Clock) continued…
Blue light suppresses melatonin production, increases alertness, increases cognitive performance
Mobile devices including phones, tablets etc. output blue light extensively
Acute blue light exposure in the evening reduces frontal slow-wave power in the EEG
melatonin
Melatonin is a naturally occurring hormone
Declining melatonin with age can present a challenge to sleep
Prescription melatonin available in Aus
Indicated for short term insomnia in adults aged > 55 years
Brain processes behind sleep
Many brain regions involved in switching sleep on and off: particularly the brainstem, diencephalon, telencephalon
Arousal and waking: midbrain, posterior and lateral hypothalamus, basal forebrain
Pre-optic anterior hypothalamus: GABA-ergic neurons with increased activity in sleep. Responds to sleep promoting signals such as sleep pressure and body temperature increases
Measurement of Sleep – Polysomnography (PSG)
Poly (multiple) somno (sleep) graph (traced measurements)
The ‘gold standard’ for measuring sleep. Common signals acquired include EEG, EMG (chin, diaphragm, and leg), EOG, nasal pressure, thermo-oral flow, ECG, snoring, and respiratory effort.
Can be conducted in a sleep laboratory (best option, and essential for complex cases), or at home (acceptable for simple cases).
EEG allows for the quantification of sleep stages W, N1, N2, N3, REM
https://youtu.be/B2ozqK9T5Bw?t=3m10s
Measurement of Sleep – Polysomnography (PSG)
Alpha (8 – 13Hz) – wake
LAMF (Theta) - (Low Amplitude Mixed Frequency, 4 – 7Hz) – N1
LAMF with Spindles/K Complexes – N2
Delta (0.5 – 2Hz, 75µV amplitude) – N3
LAMF with Rapid Eye Movements and low EMG tone – REM
Measurement of Sleep – Polysomnography (PSG) (stage wake/eyes open, closed, eeg,
Stage Wake
Eyes open – fast beta waves
Eyes closed – slow alpha waves
EEG pattern appears in the eye trace
Alpha waves
8-12hz - eyes closed and awake
Measurement of Sleep – Polysomnography (PSG)
Stage N1
Stage N1
Shallow sleep – a transition between wake and sleep
Look for: EEG pattern no longer reflected in the eye trace, slow rolling eye movements, vertex sharp waves
At least 50% of the epoch is no longer ‘wake’
Measurement of Sleep – Polysomnography (PSG)
Stage N2
Stage N2
Theta/LAMF with spindles and K-complexes
Both spindles and K-complexes are normal phenomena, K-complex also a response to external stimuli
Measurement of Sleep – Polysomnography (PSG)
stage N3
Stage N3
Scored when 20% epoch is in slow, high amplitude delta waveforms
The deepest sleep stage, after waking from N3 a subject can be very drowsy (sleep inertia)
Measurement of Sleep – Polysomnography (PSG)
stage - rem
Stage REM
LAMF, low muscle tone, Rapid Eye Movements
Hypnogram
Hypnogram – shows the distribution of sleep stages
Normal values: N1: 5%, N2: 50%, N3: 20%, REM: 25%
Measurement of Sleep – Actigraphy
Wrist actigraphy uses watch-like devices that measure movement and light to determine sleep/wake
Cannot determine sleep stage
Useful for assessing sleep patterns over a period of time, rather than PSG which is generally used on a single night
Consumer grade devices (such as Fitbit) are implementing Actigraphy features, including attempts to stage sleep from cardiophotoplethysmography
Measurement of Sleep – Actigraphy
Actogram – like the hypnogram, displays sleep/wake/light information across the time the device was worn
Measurement of Sleep – Sleep diary
Sleep diary shows subjective sleep wake patterns, whilst giving insights into daily factors affecting sleep.
E.g., are they drinking 3 cups of coffee in the evening before bed? Are they taking medications that may affect sleep in the evening or alertness the next day?
Measurement of Sleep – Psychometric Tools
Epworth Sleepiness Scale (ESS): Score from 0 - 24 measuring subjective propensity for daytime sleepiness
Pittsburgh Sleep Quality Index (PSQI): Subjective sleep disturbance, scores > 5 indicate poor sleep quality
Dysfunctional Beliefs about Sleep (DBAS-16): Measures agreement with maladaptive statements about sleep that may be perpetuating insomnia
Why is sleep important? 1. Memory
REM and N2 sleep implicated in semantic memory processing – however direct auditory stimulation during sleep does not work!
Increase in number of sleep spindles in sleep after declarative memory training
Memory enhanced by deep sleep (N3), and shortened sleep duration with age may be a factor in memory loss in aging
Sleep enhances consolidation of non-declarative memories (such as piano playing, bicycle riding etc.)
Why is sleep important? 2. Immune Function
Immune functions of the body can trigger an inflammatory state (via pro-inflammatory cytokines etc.) – better to confine this to rest period than when energy is needed during the day
Melatonin and other chemicals whose levels are elevated during sleep counter the oxidative stress (and cell injury) caused by inflammation
Sleep after Hep. A vaccine increases antibody levels substantially
Insomnia may be a risk factor for poor influenza vaccine response
Why is sleep important? 3. Attention and alertness
Child and adolescent learning, school performance, and day time functioning compromised with poor sleep quality, short sleep duration and early waking times.
Severe sleep deprivation in medical interns associated with 35.9% increase in serious medical errors (136 vs 100 errors per 1000 patient days).
Patients with sleep disorders causing excessive sleepiness are 1.5–4x more likely to be involved in a motor vehicle accident.
Why is sleep important? 4. Morbidity and Mortality
Risk of diabetes associated with both reduced and increased sleep duration
Excessive sleep duration associated with increased mortality, decreased sleep more debatable
Likely many confounding health and individual factors
Why is sleep important? 4. Morbidity and Mortality
It can be necessary to re-assure patients with Insomnia, that their sleep problem is not going to kill them!
When sleep goes wrong: Obstructive Sleep Apnoea
In OSA soft-tissue in the upper-airway collapses periodically throughout the night, fragmenting sleep, and causing oxygen desaturations.
Particularly associated with high BMI, older age, and male gender.
OSA Symptomatology
Patients presenting for sleep study for OSA will generally have bed-partners who report snoring, and possibly gasps during the night (as the patient wakes and opens the airway)
Other presenting features include: dry mouth upon waking (mouth opens when snoring), morning headache, feeling unrefreshed upon waking, nocturia, hypertension
https://youtu.be/TgC_S09Xea4
OSA Prognosis
If untreated, OSA increases risk for heart attack, stroke, hypertension, diabetes, depression
Sleep is fragmented with arousals and O2 desaturations – may lead to excessive daytime sleepiness
Daytime sleepiness presents a hazard in safety-critical occupations (commercial drivers etc.)
Tx includes modifying reversal risk factors (obesity, nocturnal alcohol consumption etc), exclusively lateral sleep where OSA is confined to supine sleep, and
Continuous Positive Airway Pressure where necessary.
When sleep goes wrong: Insomnia
Insomnia is a disorder of excessive sleep latency (time to fall asleep) or waking during the evening and being unable to fall back asleep. Referred to as sleep onset, or sleep maintenance insomnia, respectively.
Difficulty sleeping is a common and often normal response to stress in life, situational anxiety, grief etc.
Chronic insomnia is a clinical problem when insomnia occurs at for at least 3 nights per week across a 3 month period.
Common features include worries or pre-occupations about sleep and perceived next-day dysfunction, and safety behaviours to ‘cope.’
When sleep goes wrong: Insomnia
beliefs example from dBAS
Do you agree or disagree with the following statements?
When I sleep poorly one night, I know it will disturb my sleep schedule for the whole week
Without an adequate night’s sleep, I can hardly function the next day
Medication is probably the only solution to sleeplessness
When sleep goes wrong: Insomnia
DBAS
Those questions are items on the Dysfunctional Beliefs about Sleep (DBAS-16) questionnaire.
Measures 4 domains of insomnia cognition Perceived consequences of insomnia Worry or helpless about insomnia Expectations about sleep Beliefs about medication and sleep
Common cognition example: “I have to fall asleep in 10 mins to have 7 hours sleep before work”
When sleep goes wrong: Insomnia
common insomnia behaviours
Clock watching – sleep latency and calculate sleep time upon waking – anxious appraisal
Going to bed early to allow plenty of time to fall asleep - worry, conditioning effects (bed = awake)
Napping or sleeping in – may reduce sleep drive, making next night’s sleep more difficult
Selective attention: monitoring for sleep related threats
When sleep goes wrong: Insomnia
counselling and therapies
Counselling for good sleep practice (sleep hygiene)
Go to bed only when tired
The bedroom and bed is for sleep and sex only!
A ‘wind-down’ period before bed without electronics (blue light = melatonin suppression, increased alertness etc)
Other behavioural therapies in insomnia:
Sleep-restriction therapy (or better labelled ‘bed restriction’) - limit time in bed to calculated actual sleep time
Paradoxical intention – instruct patient to attempt to stay awake
When sleep goes wrong: Insomnia
cognitive approaches
Cognitive approaches
Identify maladaptive beliefs about sleep – challenge these beliefs
E.g., Pt fears next-day consequences of insomnia at work
“You’ve mentioned that your work suffers when you have a bad night’s sleep. What makes you say that? Have your supervisors had issues with your work after a bad night?”
Treating insomnia involves convincing people to ‘let go’ – patients will often try very hard to control their sleep, but this tends to fuel the problem
When sleep goes wrong: Circadian Rhythm Disorders
Circadian rhythm disorders (such as advanced or delayed phase disorder) are problems with initiating or maintaining sleep occur as a result of the body clock being too far advanced or delayed relative to environmental or social cues
Circadian timing will vary over the lifespan: body clocks become slightly delayed in teenagers, and slightly advanced in old-age
Sleep hygiene important, particularly getting morning sunlight. Light therapy devices may be used.
When sleep goes wrong: REM behaviour disorder
Failure of usual muscle atonia in REM sleep
Upsetting, scary, traumatic dreams occur, and lack of muscle paralysis allows Pt to act out these dreams
Can present risk for inadvertent injury to self or others
RBD is highly predictive of future Dementia
Tx is supportive, remove objects that could cause injury
Rx clonazepam may be necessary
Medication and Drug Effects on Sleep
Prescription, over-the-counter, dietary (e.g., caffeine, alcohol), and illicit drugs can all affect sleep, even where the drug does not target sleep
Hypnotics (“sleeping pills”)
- -Benzodiazepines: Valium (Diazepam), Temazepam,
- —–Oxazepam, Lorazepam etc. Agonists at GABA receptors in the brain – central nervous system inhibition, muscle relaxation
Non-Benzodiazepine Benzodiazepine Receptor Agonists – the Z drugs.
Stilnox (Zolpidem), Zopiclone, Zaleplon – work in a similar way to Benzos, more specific for targeting sleep
Medication and Drug Effects on Sleep
concerns
Benzodiazepines reduce sleep latency (time to fall asleep), but also reduce N3 and REM sleep – the resulting sleep is more shallow and less restful
Concerns with side effects, Benzos depress the entire central nervous system, co-administration with other CNS depressants (such as alcohol) could result in respiratory depression
Pt’s will develop tolerance to benzodiazepines
Z drugs have better safety profile and lower risk of tolerance and abuse
Residual (next-day) sedation can be a concern with Benzos and Z class hypnotics, especially where the Pt is prone to falls, or operates a vehicle
Medication and Drug Effects on Sleep
painkillers
Painkillers (Analgesics)
Simple analgesics: Paracetamol and Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) including Nurofen (ibuprofen) and Aspirin
Paracetamol appears to not affect sleep
NSAIDs (via effects on prostaglandin) increase number of awakenings, and time spent awake, also increased latency to deep sleep
Opiates: e.g., Morphine, Endone (Oxycodone), Fentanyl, Codeine
–Decreased N3, increased N2
Medication and Drug Effects on Sleep
antidepressants
caffeien
aclhool
Antidepressants: SSRIs, SNRIs, TCAs In general antidepressants suppress REM sleep. Brainstem control of REM sleep has 'REM-on’ and ‘REM-off’ switches. Increased Serotonin and/or Norepinephrine levels in synapses activate the ‘REM-off’ switch Mirtazapine, a different class of antidepressant NaSSA preserves sleep architecture better than other AD classes
Caffeine
Increases sleep latency, decreases total sleep time, may reduce N3
Alcohol (ethanol)
Reduces sleep latency, increases snoring and apnoea, disrupts sleep architecture in second half of the night
Sleep and other health problems: Headaches
Presence of some shared brain pathways responsible for both sleep and head pain
Reduced or excessive sleep duration, poor sleep quality, social jetlag (circadian misalignment), sleep apnoea are all associated with headaches
Waking in the morning with a headache that resolves after several hours is a ‘soft sign’ of a sleep disorder (J. Rains)
Current research examining how beliefs and behaviours about sleep impact on sleep quality and sensitivity to headaches
Treating Sleep Disorders – Role for Psychologists
OSA – CPAP compliance and acclimation
Insomnia – Cognitive Behaviour Therapy for Insomnia (CBT-i)
Circadian Rhythm Disorders – Sleep hygiene and light therapy
Nightmares associated with PTSD – Psychological Tx for PTSD
Further training in sleep
Australian Psychological Society – online Practice Certificate in Sleep Psychology
Introduction to Sleep Psychology
Insomnia
Circadian Rhythm Disorders
CPAP Compliance
University of Sydney – Online postgrad degrees (Grad Cert, Grad Dip, Masters) in Sleep Medicine
University of Western Australia – Mixed online/intensive clinics postgrad degrees in Sleep Science (Grad Cert, Grad Dip)
