Sleep& sleep deprivation Flashcards
What are the functions of sleep?
- Conservation of effort& energy
- Production of hormones
- Augmentation of immune system
- Memory consolidation
- Mood regulation
- Promotion of optimal performance
- Cleans the brain of toxins (mainly beta amyloid, cleared on a higher rate during sleep)
Outline the REM stage of sleep
- Occurs 90mins after being awake
- Your body goes through several REM stages, first one is the shortest
- Your brain& body are energized and dreaming occurs
- Thought to be involved in the process of storing memories, learning and balancing your mood
- Muscle tone declines during REM sleep
How do we enter sleep and why?
- Sleep is entered through NREM.
- If it is entered through REM, the person is either depressed, sleep deprived or has narcolepsy
Outline the basics of sleep
- SWS (slow wave sleep/deep sleep) dominates in the first third of the night
- REM predominates in the last third of the night
- Wakefulness in sleep is usually less than 5% of the night
- stage 2= the majority of sleep
- NREM= 75-80% of sleep
- REM=20-25% of sleep
Describe HR in NREM vs REM sleep
- NREM= regular
- REM=irregular
Describe BP in NREM vs REM sleep
- NREM=regular
- REM=variable
Describe RR in NREM vs REM sleep
NREM= regular REM= irregular
Describe responses to o2& co2 changes in NREM vs REM sleep
NREM= decreased
REM=significantly depressed
Describe skeletal muscle tone in NREM vs REM sleep
NREM= preserved REM= absent
Describe brain o2 consumption & CBF in NREM vs REM sleep
NREM= reduced REM= increased
Describe thermoregulation in NREM vs REM sleep
NREM= Homeothermic
REM=poikilothermic
Describe penile tumescence/vaginal engorgement in NREM vs REM sleep
NREM= infrequent
REM= frequent
All men without physiological erectile dysfunction experience nocturnal penile tumescence, usually three to five times during the night, typically during REM sleep
Describe how sleep architecture changes with age.
- SWS decreases by 2% per decade until age 60
- loss of 30 mins per decade in TST(total sleep time) from 16-83 years
- Reduced time in N3, with corresponding increases in N1& N2
- REM sleep shifts to slightly earlier at night
- All non-pathological changes
What is the deepest stage of sleep
- REM
- but N3 is the deepest stage of NREM sleep
Describe the changes in sleep as part of the ageing process
- Decrease in TST, less SWS (loss of synaptic density), advanced sleep-wake phase, less homeostatic drive, napping returns
- Co-morbidities associated with ageing apart from age-related changes
- Medical, psychiatric, social, environmental factors & polypharmacy may have an impact on sleep.
Outline what Circadian rhythm sleep disorders are
- Mismatch between endogenous biological rhythms& required social time
- This results in an impairment in sleep& wake functioning
- Sleep is normal when patients can sleep at their desired time
- Divided into intrinsic( primary) and extrinsic (secondary)
Describe Intrinsic (primary) Circadian rhythm sleep disorders.
- Alterations of the circadian timekeeping system
- May result from:
- DSPD(delayed sleep phase disorder)=a sleep disorder that occurs when a person’s circadian ryhthm (sleep/wake cycle) is delayed from the typical day/night cycle
- ASPD(advanced sleep phase disorder)=characterized by a recurrent pattern of early evening (e.g. 7-9 pm) sleepiness and early morning awakening.
- Non-24h e.g in blindness
- Irregular e.g dementia
Describe Extrinsic (secondary) Circadian rhythm sleep disorders.
-Misalignment between intrinsic& extrinsic signals
May result from:
-Shift work disorder
-Jet lag disorder
What is delayed sleep phase?
- Sleep is out of phase with socially acceptable sleep-wake times
- Evening chronotype preference
- About 9.25 hours of sleep required
- Sleep deprivation may lead to worse academic performance, health & well-being
What are the clinical features of DSPD?
- Unable to sleep advance onset
- Restriction to conventional bedtimes results in sleep deprivation
- Insomnia &/or excessive sleepiness
- Sleep is normal when they can sleep at their desired times
- Symptoms are chronic
- History of hypnotic use, alcohol at bed time, psychiatric interventions( e.g antidepressants, psychotherapy)
- 70% will have a comorbid psychological/ psychiatric disorder
What is the treatment of DSPD?
combination of:
- Phototherapy
- Melatonin
- CBT-I
- examine for psychiatric co-morbidity
Outline shift work disorder(SWD)
- Insomnia/excessive sleepiness with a recurring work schedule that overlaps the usual time for sleep
- Symptoms are associated with work schedule for 1 month
- Sleep disturbance is not otherwise explained by another sleep disorder, medication or substance misuse
- Supported by sleep log or actigraphy
What are some short-term consequences of SWD?
- sleepiness at night
- Mood disturbances
- short day time sleep
- Higher risks at night( e.g accidents)
- GI problems
What are some long-term consequences of SWD?
- Sleep disorder
- Mood disorder
- Cardiovascular risk
- Alcohol/drug abuse
- Cancer(breast- circadian disruption appears to be carcinogenic
Define sleep deprivation
-A sufficient lack of restorative sleep over a cumulative period so as to cause physical or psychiatric symptoms and affect daily performance
What are some effects of sleep deprivation
- irritability
- Cognitive impairment
- Memory lapses/loss
- Impaired moral judgement
- Severe yawning
- Hallucinations
- Symptoms similar to ADHD
- Impaired immune system
- Risk of diabetes type 2
- Increased HR variability
- Decreased reaction time& accuracy
- Tremors
- Aches
- Growth suppression
- risk of obesity
- Decreased temp.
Outline hallucinations in sleep deprivation
- Occur at the sleep/wake transition
- Hypnagogic hallucinations= occur on going to sleep
- Hypnopompic hallucinations= occur on waking from sleep
- May occur with isolated sleep paralysis
- Simple visual or auditory hallucinations
- Can be frightening, but insight is retained, and there’s no delusional expansion vs those hallucinations occurring in psychotic illnesses
Are visual hallucinations in psychotic illnesses common?
NO!
What are parasomnias?
- Abnormal behaviours that occur in association with sleep
- occur during NREM & REM sleep
- Diagnostically challenging due to: poor patient recall; limited history if no witness account; routine investigations are often normal
Outline NREM parasomnias
- occur in the first 1/3rd of the night
- frequency varies
- Onset in childhood
- Confusional arousal
- Sleep walking (somnabulism)
- Night terrors (pavor nocturnus)
- Sleep-related eating disorders
- Sexsomnia
How can we treat night terrors?
-Education. CBT-I to stabilise sleep-wake patterns
-scheduled awakening
-keep the room safe; be aware of new environments
-Only wake fully if the episode lasts>45 mins
Pregablin, Clonazepam
How can we distinguish night terrors from nocturnal panic attacks
With nocturnal panic attacks there is…
- Physiologic warning (HR or breathing changes)
- Daytime symptoms of anxiety, panic or agoraphobia
How can we distinguish night terrors from nightmares
- Usual recollection
- Often during REM sleep
What are some of the characteristics of NREM parasomnias?
- Family history
- Exacerbated by sleep deprivation, stress, alcohol, OSA(obstructive sleep apnea), fever
- Patient is often amnesic for the event, but may have partial recollection
- partner may describe tearfulness or confusion
How can we treat NREM parasomnias?
- Reassurance (benign)
- Education-CBT-I to improve sleep pattern
- avoid triggers
- safety
- anti-depressants(e.g Fluoxetine, Trazadone)
- Clonazepam
- Melatonin
Outline REM parasomnias
- Second half of the night
- 1-2 episodes per night
- Frequency varies
- REM sleep behavior disorder
- Nightmares-Rx: stop causative meds( e.g Beta-blockers,L-Dopa), CBT, Prazosin
- Catathrenia-nocturnal groaning
What are the characteristics of REM sleep behaviour disorder?
- 2nd half of the night
- Usually a single episode per night
- frequency varies
- Mean age of onset 50-65 years
- Loss of muscle atonia during REM sleep and a history of abnormal behaviours during sleep
- Often correlate with recalled vivid dreams- usually aggressive
- May injure bed partner
What can contribute to REM sleep behavior disorder?
- Male gender predilection
- Mean onset age range is 50-65years
- unknown prevalence
- Post-mortem studies suggest Lewy body pathology
- A significant proportion of patients with idiopathic RBD( IRBD) may have mild cognitive impairment at diagnosis
- Anti-depressants can induce RBD or make it worse
- Appears that the anti-depressants unmask a subclinical RBD (except buproprion)
What is the association between RBD and Parkinson’s disease?
- RBD is the most robost non-motor predictor of developing Parkinson’s disease, and it is a predictor of early cognitive impairment
- Present in other neurodegenerative conditions(mainly synucleopathies) such as MSA &DLB
- IRBD could convert to a neurodegenerative disease- risk increases as time since diagnosis increases
- Coexistence of mild cognitive impairment indicates the progression to dementia in less than 5 years
How can RBD be diagnoses?
-Clinical history may be highly suggestive but a v-PSG (visual polysomnography) would confirm the diagnosis ( catching an episode or REM without atonia)
List some RBD mimics
- Severe OSA
- severe PLMS, RMD
- Sleep talking, confusional arousals, night terrors(possible overlap disorders
- Nocturnal seizures
- Nocturnal dissociative episodes
How can we treat RBD?
- Patient education
- If possible, discontinue meds which may be contributing
- Safety e.g separate beds
- Simple home oximetry in the sleep
- medication if necessary…
- Clonazepam (cons= daytime sedation possible, worsens OSA and symptoms return on stopping)
- Melatonin ( typical doses=2-8mg, long lasting symptom relief, better tolerated, restores atonia)
Why may melatonin be used to treat a pt with DSPD?
- Hormone made naturally by your body
- Lets your body know it’s night time so that you can relax and fall asleep easier
