Sleep Flashcards
Describe the behavioural criteria of sleep
Stereotypic or species-specific posture- but atonia is also important
• Minimal movement- although some people do sleep walk, but some clinical conditions present with movements in sleep
• Reduced responsiveness to external stimuli
• Reversible with stimulation(large stimulus often) – unlike coma, anaesthesia or death
Define sleep- and how much of our lives do we spend sleep
Sleep is defined as a readily reversible state of decreased responsiveness to, and interaction with, the environment. We spend approximately one-third of our lives sleeping. Of that time, one-quarter is spent actively dreaming. The observation that lesions in the brainstem of humans can cause sleep and coma suggests that the brainstem contains neurons whose activity is essential to remaining awake.
What 3 techniques are used to monitor brain activity during sleep
Use all in conjunction in any sleep investigation:
Electroencephalography (EEG)- measures brain waves
Electromyography (EMG)- muscle activity - insert around jaw- facial muscle activity/contraction
Electrooculography (EOG)- eye activity (muscle activity related to eye movements)
Describe the EEG, EMG and EOG in the awake state
EEG – fast brain rhythm – beta waves (~30 Hz)
EMG – reasonable amount of muscle tone because you are maintaining posture and ready for action
EOG- evidence of quite fast activity- you will be looking around
- Describe the EEG, EMG and EOG activity in non-REM sleep.
Stage 1+2 • Light sleep • EEG – theta (4-8 Hz) waves – gradually becoming more and more drowsy • EOG – NO eye movements • EMG – muscle activity reduced considerably Stage 3+4 • Very deep sleep • EEG - Delta activity (< 4 Hz) • EOG – minimal eye movement • EMG – continued relaxation of muscles
- Describe the EEG, EMG and EOG activity in REM sleep.
EEG – brain shifts abruptly back to fast rhythm (similar to wakefulness)- some state of consciousnesss- why we are likely to dream during this state
EOG – rapid eye movement
EMG – muscle activity at its lowest – subject is basically paralysed
What is important to remember about dreaming
It isn’t dichotomous
Not everyone dreams in REM sleep, and some people will report dreaming after sleeping in other stages
Dreams may occur during any stage of sleep but are most prominent in REM sleep, and most easily recalled.
During dreams the limbic system is more active and the frontal cortex less active.
What happens to the EEG as we go through the stages of sleep
The brain waves get larger in amplitude and lower in frequency from the awake state to stage 4
Decreases in amplitude and increases in frequency (becomes more like the awake state in REM/stage 5 sleep)
What is important to remember about the sleep stages
Happen periodically throughout the night- not just activity- sequence of structured events both inside and out the brain
Can see sleep spindles in stage 2 sleep on the EEG- signature of stage 2 sleep
HR and RR decrease like the EEG in NREM sleep, but increase again in REM sleep- could be a physiological response to dreaming
Describe NREM sleep
Non-rapid eye movement (NREM) sleep has high-voltage, low-frequency EEG and is characterized by decreased cerebral blood flow and brain glucose utilization, with maintenance of muscle tone. As an individual falls asleep they pass through four stages of NREM sleep
Describe REM sleep
Subsequently, REM sleep begins after about 90 minutes with the EEG exhibiting a waveform similar to that seen in the awake state. During REM sleep muscle tone is absent (apart from brief twitches of limb muscles and rapid eye movements), autonomic functions become irregular and dreaming occurs.
At what stage do we tend to wake up after
During sleep, we cycle through the different stages tending to awaken just after an REM phase.
What are sleep spindles
Intermittent high frequency spike clusters
Periodic bursts of activity at about 10-12Hz that last about 1-2 and arise as a result of interaction between thalamic and cortical neurones
What is the reticular activating system
The reticular activating system (RAS) maintains arousal.
It consists of nuclei in the brainstem, such as the Raphe nuclei, nucleus coeruleus and cholinergic nuclei, which project directly or indirectly via the thalamus to all areas of the cerebral cortex.
This system controls consciousness- it is the thing that switches the light on- it’s not where consciousness if found or where your inner monologue lies
- How long is a normal sleep cycle?
1-1.5 hours
- How does the reticular activating system control the activity of the cortex?
Either via direct connections
Or via indirect connections through the intralaminar nuclei of the thalamus
Describe the role of the intralmainar nuclei in sleep
Lateral Hypothalamus promotes wakefulness (orexin/hypocretin)- positive effect on RAS
Ventrolateral preoptic nucleus (anterior hypothalamus) promotes sleep- inhibits RAS
Relationship: antagonistic, so activation of one inhibits the other (LH active at start of day and VLP at end)
What happens in narcolepsy
Reduced orexin- cells faulty in lateral hypothalamus- why you may fall asleep easily.
Describe the role of the Suprachiasmatic nucleus in the hypothalamus
Suprachiasmatic nucleus
synchronises sleep with falling light level
Essentially, synchronises the sleep-wake cycle with falling light level.
Describe how the Suprachiasmatic nucleus performs its function
It receives an input from the retina (not from the usual photogenic cells) and as light level falls the suprachiasmatic nucleus becomes more active
Falling light level leads to increased activity of suprachiasmatic nucleus
This leads to activation of ventrolateral preoptic nucleus and inhibition of lateral hypothalamus so you become sleepier
Projection to the pineal gland
Increase in suprachiasmatic nucleus activity leads to activation of pineal gland so that it releases melatonin
Melatonin adjusts various physiological processes in the body that fit with sleep
When is the caudal pontine reticular activating system active
The caudal pontine reticular formation is active during REM sleep. It suppresses general muscle tone and activates rapid eye movements
Where is the pineal gland found
At the back of the third ventricle
Describe the importance of melatonin
We have a profile of melatonin during the day- which tracks the sun- during jet lag- it can take a while for the sleep-wake cycle to readjust with the sun- we can take melatonin- good sleep drug- naturally made by the body- can help to re-calibrate
Summarise how we know that sleep is important
• Most/all animals sleep
• Sleep deprivation is detrimental • Sleep is regulated accurately
§ Sleep is obviously needed as – all/most animals sleep, sleep deprivation is detrimental and sleep is regulated accurately so the body knows of its need.
What is sleep deprivation a key risk factor for
Seizures (especially for epileptics)
Also neurodegenerative diseases and dementia
Describe the psychiatric and neurological effects of sleep deprivation
Sleepiness, irritability, stress, mood fluctuations, depression, impulsivity, hallucinations
Describe the neurological effects of sleep deprivation
Impaired attention, memory, executive function – Risk of errors and accidents
– Neurodegeneration (?)
Describe the somatic effects of sleep deprivation
Glucose intolerance- risk of diabetes – Reduced leptin/increased appetite – Impaired immunity – Increased risk of cardiovascular disease and cancer – Death Hallucinations Sleepiness/irritability Performance decrements Concentration difficulties Sleep is not just a brain thing- systemic
Describe the study which showed the effects of sleep deprivation on mathematical performance
fMRI showed that different parts of the brain where activated when performing the same tasks
Sleep is protective for cognitive faculties- memory and consolidation of tasks
Describe how we know that sleep is regulated accurately
Appears that the brain is taking an audit of our sleeping pattern- and we have to make it up- increasing proportions of REM sleep if necessary- shows that the stages are crucial to normal sleep and that it is not just an on/off activity
- Reduced latency to sleep onset- if you lose a night’s sleep you go to bed earlier the next day
- Increase of slow wave sleep (NREM)- so you sleep for longer if sleep deprived
- Increase of REM sleep (after selective REM sleep deprivation)
Summarise the functions of sleep
Restoration and recovery – but active individuals do not sleep more
• Energy conservation – 10% drop in BMR – but lying still is just as effective
• Predator avoidance – but why is sleep so complex?
• Specific brain functions – memory consolidation, …
What are the 3 differing hypotheses regarding the purpose of sleep
An ecological hypothesis suggests that sleep allows animals to remain quiet and hidden during periods of highest risk of predation.
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A metabolic hypothesis argues that sleep enables correction of chemical imbalances that accrue during the awake state.
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A learning hypothesis suggests that sleep is needed either to unlearn false memories (and so prevent neural networks from becoming saturated) or to consolidate true memories.
Summarise the key features of dreams
Can occur in REM and NREM sleep
• Most frequent in REM sleep
• More easily recalled in REM sleep
• Contents of dreams are more emotional than ‘real life’
• Brain activity in limbic system (important for conscious experience and emotion regulation) higher than in frontal lobe during dreams
Lack of critical processes in dream- you don’t question what you are doing in the dream
What are the functions of dreams
- Safety valve for antisocial emotions
- Disposal of unwanted memories
- Memory consolidation
How can we test whether if someone is having a lucid dream
Ask the subject to moves their eyes left and right- will pick up signal on EOG
Compare the roles of the limbic system and the frontal lobe
o Limbic system = emotions.
o Frontal lobe = logical thought and informed decision making.
How do NREM and REM sleep differ in terms of the memories that they consolidate
NREM sleep – declarative memory – facts and events.
REM sleep – procedural memory – learning skills.
What is a good measure of insomnia
Whether it is having a functional impact on their work or lifestyle- i.e are they performing worse or falling asleep during the day
Summarise the epidemiology of insomnia
Highprevalence
• Most cases transient
This is the most prevalent sleep condition in the population and is defined as an inability to sleep sufficiently long enough or have a satisfying sleep.
Describe the causes of chronic insomnia
– physiological e.g. sleep apnea, chronic pain
– Brain dysfunction eg. depression, fatal familial insomnia, night working
Describe fatal familial insomnia
Progressive insomnia- neurogenerative disease- gets progressively worse- eventually need analgesics to sleep and you will soon die
FFI is caused by an abnormal variant in the prion-related protein (PRPN) gene
How should we think of treatment for sleep disorders
think stepwise
start with lifestyle interventions, before moving onto hypnotics and pharmacological interventions- unrational to become dependent on these and there are issues regarding intolerance
Start with sleep hygiene measures
Summarise the treatment steps for insomnia
• Treatment
– sleep hygiene
– hypnotics (most enhance GABAergic circuits) – sleep CBT
Describe the medications available for insomnia
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Medication – including low-dose benzodiazepines; this must be carefully monitored because of risks of dependency. Melatonin is a night-hormone which may be used in a subpopulation of melatonin-deficient elderly people with insomnia. Melatonin-agonists are being investigated as potential treatment options.
Describe some applications of sleep hygiene
- establishing fixed times for going to bed/waking up
- creating a relaxing bedtime routine
- only going to bed when you feel tired
- maintaining a comfortable sleeping environment
- not napping during the day
- avoiding caffeine, nicotine and alcohol late at night
- avoiding eating a heavy meal late at night
- don’t use back-lit devices shortly before going to bed
What is untreated insomnia a major risk factor for
Untreated insomnia is a major risk factor for the development of psychiatric problems (including depression and substance misuse) and a risk factor for road traffic accidents. It is important to remember that insomnia may be a presenting symptom of psychiatric illness (e.g. depression
What do insomniacs show
Insomniacs show increased adrenocorticotropic hormone (ACTH) and cortisol levels and increased arousal patterns on sleep electroencephalograms (EEGs), suggesting that insomnia may just represent a disorder of hyperarousal.
What are the primary causes of hypersomnia (excessive daytime sleepiness)
Narcolepsy
Post-traumatic brain injury
Idiopathic hypersolmnolence-
What are secondary causes of hypersomnia
Common- Obstructive sleep apnoea Nocturnal pain - diabetic nephropathy or arthritis Anxiety Medication (hypnotic misuse) Restless legs syndrome Neurodegenerative disease- Parkinson's Noise
Rare- Oesophageal acid reflux, severe bruxism
Describe the Hepworth sleepiness scale
Subjective scale for diagnosing insomnia - likelihood of falling asleep during different situations i.e reading, watching T.V
Scale of 0-24
Higher score = more sleepy
Describe OSA
This is the most common medical disorder causing hypersomnia. It is characterized by the collapse of the upper airway during sleep (believed to be due to obesity). This collapse results in a fall in blood oxygenation causing repetitive arousals (up to 100 per hour of sleep), disrupting the quality of the sleep. This disruption is not noted by the patient during sleep, but manifests as daytime tiredness.
What is OSA a risk factor for
Obstructive sleep apnoea (OSA) is a risk factor for hypertension (during night-time wakening sympathetic activation occurs, constricting blood vessels increasing vascular resistance) and is associated with heart disease and type 2 diabetes mellitus (presumably due to obesity).
Describe narcolepsy
Falling asleep repeatedly during the day and disturbed sleep during the night
This is a rare neurological condition that is characterized by the tendency for patients to fall asleep during the day, especially if they are not active or are engaging in non-stimulating activities.
Describe the symptoms of narcolepsy
Other symptoms include cataplexy (paralysis following emotional arousal, e.g. laughing or being scared), hypnagogic (occurring at sleep onset) or hypnopompic (occurring at awakening) hallucinations, sleep paralysis (one wakes to find they cannot move their body, but can breathe and move the eyes), automatic behaviours and disrupted night-time sleep.
What goes wrong in the sleep cycle in patients with narcolepsy
Dysfunction of control of REM sleep
It tends to be due to a dysfunction of control of REM sleep
Patients go straight to REM sleep without going through NREM sleep so they become paralysed
REM sleep = atonia!
Describe the pathophysiology of narcolepsy
o Orexin deficiency – orexin is a neuropeptide which is the transmitter used by the lateral hypothalamus.
Cause could be genetic or autoimmune.
Normally treatment is a strict regimen of sleeping routines.
Narcoleptics have been found to lack hypocretin-1 (also known as orexin) in their hypothalamus, perhaps through an immune-mediated mechanism (90% of patients carry either the HLA-DR15 or HLA-DQ6 gene).
Describe the treatment options for narcolepsy
Treatment options usually include stimulant medicines (e.g. amfetamines). Animal studies have found that systemic administration of hypocretin-1 reduces narcolepsy and could, therefore, suggest a future development in treatment.
Describe the potential dangers of sleep work
- Night working causes physiological processes to become desynchronised
- This can lead to sleep disorders, fatigue and an increased risk for some conditions such as obesity, diabetes and cancer
Describe the feedback process between sleep and diseases
Problems with sleep may be causally related to neurodegenerative diseases, but neurodegenerative diseases may also cause problems with sleep
So sleep may precipitate or perpetuate N.D such as Parkinson’s or dementia
Either way improving sleep may improve quality of life in patients with these conditions and help to manage symptoms
Describe the relationship between sleep and neurodegnerative disease
Addiction or substance abuse can be due to or caused by neuropathology
medication can be due to or lead to neuropatholog
medication may also cause abnormal NT release, activate the stress axis or disrupt the sleep/circadian rhythm
Substance abuse can cause all of these and together with medication can result in co-morbid pathologies, disrupted social behaviour and abnormal light-dark exposure
These can disrupt the sleep/circadian rhthym which can lead to abnormal NT release and thus neuropathology
What are parasomnias
Parasomnias are defined as unpleasant or undesirable behavioural or experiential phenomena that occur predominantly during sleep. Most parasomnias represent the simultaneous combination of wakefulness
Describe the parasomnias associated with non-REM sleep
Non-REM sleep: presenting with disorders of arousal such as sleep-walking, sleep terrors and confusional arousals. They usually arise from slow-wave sleep, therefore presenting in the first third of the sleep cycle. Aetiological factors are those that disrupt the normal sleep neural patterns in already susceptible patients (e.g. febrile illness, alcohol, emotional stress or medication).
Describe the parasomnias associated with REM sleep
Atonia doesn’t happen
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REM sleep: presenting with sleep behaviour phenomena usually in men aged 50 or older. This results in the failure of muscle paralysis during sleep, allowing patients to ‘act out’ their dreams (e.g. punching out) with sometimes violent or injurious results.
What can cause parasomnias
Acute behaviours can be secondary to medication especially serotonin selective reuptake inhibitors (SSRIs). Chronic behaviours can be idiopathic or associated with neurodegenerative disorders, especially the synucleinopathies (e.g. Parkinson’s disease, Lewy body dementia).
When are parasomnias likely to occur
These conditions are likely to occur when the brain crosses from one state to another during the wake–sleep cycle. The primary dysfunction here is believed to be a breakdown in the synchronous neural network activity and neurotransmitter system activity needed for either wakefulness or sleep.
Describe Lewy body dementia
REM sleep behaviour disorder
Acting out dreams, don’t get atonia
Classic precursor for Lewy-body dementia
Therefore correcting sleep problems may improve outcomes for dementia
