BM - Sleep Flashcards

1
Q

What is sleep?

A

A physical state of:

  • postural recumbency
  • quiescence
  • closed eyes

however 2 separate states of sleep have been identified (through using electrodes in the brain) - REM and non-REM

Sleep isn’t passive - intact very active.

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2
Q

What are the stages of sleep?

A
Relaxed, wakefulness
Stage N1
Stage N2
Stage N3
REM
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3
Q

What is relaxed, wakefulness?

A

Alpha waves are present when one begins a state of relaxation, high frequency.

this is the cosy feeling in bed and is part of the sleep cycle.

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4
Q

What is stage N1?

A

Irregular, jagged, low amplitude waves, brain activity begins to decline, decreases in frequency

The brain is starting to slow down

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5
Q

What is stage N2?

A

Present elf sleep spindles and K-complexes

K complexes and sleep spindles provide vital function to humans

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6
Q

What is stage N3?

A

Low frequency (slow), high amplitude waves (delta waves, slow wave activity - SWA)

Frequency and amplitude have increased

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7
Q

What is REM stage?

A

Irregular, low-amplitude and his frequency (fast) waves; PGO waves; rolling eye movements; loss of muscle tone

REM - tells you about psychopathology, almost a mixture of being awake and being in stage 1 sleep. Just looking at brainwave activity cant actually tell if in REM or just a relaxed state so need to look at muscle tension. Should have no muscle tension during REM. REM behaviour disorder is the acting out of violent or aggressive acts during REM without any knowledge - would have muscle tension. Also might see RBD in Parkinsons and other neurodegenerative disorders. Think something to do with release of acetylcholine

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8
Q

What are the specifics of stage 2 sleep?

A

NREM takes up 75% of the whole night and REM takes up approximately 20-25%

Stage 2 takes up between 45-55% of the whole night.

Have to see a K complex and sleep spindle for someone to be defined as in stage 2 sleep.

Performs several important functions. This is when we review the information form our day and determine what we need to turn into memory later on. Memory filing system. Will get rid of the information that isn’t needed and can consolidate what you do need, and can be turned into long term memory.

See very long stage 2 sleep in fibromyalgia, chronic fatigue syndrome and chronic pain. This is showing the attempt/capacity of the neurological system to mask pain, trying to keep the organism asleep. If there is pain then will automatically evoke a k complex and sleep spindle, stopping focus on the pain and keeping asleep. Also masks anything from the sensory system eg gurgles from digesting food.

Also, when we have a transition in sleep a spindle and k complex will try and cover that distance so that we don’t actually wake up.

A normal healthy adult will wake up 5-6 times at night but wont be remembered because the k-complex and spindle will kick in to put back to sleep until the transition is over.

Don’t see stage 2 in children until they are about 2 years old. Don’t need stage 2 as a small child because don’t need to discard memories, everything needs to be consolidated because everything is new. Sleep stages in children are about 60 minutes alternating between REM and slow wave. Therefore there is no real need, unless the child is in pain, for stage 2 sleep.

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9
Q

What is the hyping jerk?

A

follows stage 1 and is the sign of transition into stage 2 sleep

this is using up the last bits of cortisol in order to sleep. cortisol keeps us unregulated which we don’t want, we want down regulation. the body tenses and released very quickly and resealed this cortisol - completely normal.

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10
Q

What happens in REM sleep?

A

Muscle tension non-existant

body paralysis

eye movements and respiratory system active

dream activity

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11
Q

What is the typical sleep sequence?

A

If prodded in stage 1 likely to say that you were awake because it’s a very light stage of sleep.

You will then have an incident, HYPNIC JERK, this is telling us that it is the transition to stage 2 sleep.

Then into stage 3 - slow wave sleep.

After slow wave sleep we go back up into stage 2 sleep. After another period of stage 2 we will enter into out first REM period.

That should take approximately 90 minutes. Slightly longer for the first sleep cycle and then about 90 minutes.

For the rest of the night we do concentric circles - 2,3,2,REM,2,3,2,REM etc

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12
Q

What happens during stage 3 sleep?

A

This is the only time the immune system is working at its full capacity. If deprived from this then you start to see physical illness. Release growth hormone during this time - growth in young and damage repair in adults. Immuno modulate during this time, produce hormones which will fix the body. Kill caricnoma cells during slow wave sleep. Also fix allergies during this time, body will prodcue immunomodulators to try and fight the allergen. Necrotics - hunt and eat up all the dead things in our bodies during this time. Immense ability to help the physical body during slow wave sleep.

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13
Q

Why do we go back into stage 2 following slow wave sleep?

A

This is assumed to be an evolutionary response - so that we can scan the environment for unusual noises. Make sure that it is safe to continue sleeping. After another period of stage 2 we will enter into our first REM period.

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14
Q

Does all dream activity take place in REM?

A

Not all dream activity takes place during REM. We also dream outside of RME but the dreams are slightly different. If dreaming in colour you are in REM, if in black and white not in REM. You should not hit REM for 90 minutes form falling asleep. This is important in psychopathology. If go into rem quicker than that it is likely that in the next 4-5 weeks you will develop major depressive disorder.

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15
Q

What is the distribution of REM across the night?

A

Over the night the first slow wave block will be about 25 minutes in duration. The first REM cycle will be about 5 minutes in duration. As the night progresses, slow wave sleep decreases and REM increases. By the end of the night likely to have 25mins of rem and less than 5 minutes of slow wave. Makes evolutionary sense as more important to protect the physical body than the mental body, and that is why slow wave first as need to protect and repair physical body first and then if all is well you can then protect the mental body too.

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16
Q

What are the brain mechanics in sleep 1?

A

Prefrontal cortex - inactive

- Memory (STM)
- Attention
- Perception

Limbic cortex - inactive NREM
- Autonomic function

Parietal cortex - less active REM

Frontal cortex - less active NREM

Prefrontal cortex should be inactive throughout the whole process of sleep - not needed any of its functions. No good for us to be creating new knowledge during sleep.

There is a particular issue called cortical arousal which may explain insomnia. This is believed to be because the prefrontal cortex hasn’t become completely inactive.

Limbic cortex should be inactive during nonREM and active during REM.

Parietal less active in REM - parietal cortex for spatial awareness, reasoning, unrational dreams doing weird things show that the parietal cortex is not active, we arent questioning dreams and being rational

Frontal cortex much less active during non REM but more active in REM - personality, emotions etc - shows why have emotions in dreams, still allowing the brian to process emotional information

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17
Q

What are the brain mechanisms in sleep II?

A

Thalamus - bridge between cortex and receptors

Thalamic reticular nucleus

- Excitatory neurons - glutamate
- Inhibitory neurons - GABA --> inhibits arousal in brain centres

Thalamic pacemaker

Thalamic reticular nucleus is the draw bridge of the brain - can be up or down. If up, information travels through, if down, doesn’t pass through. Regulated through excitatory neurones (glutamate) or inhibitory neurones (GABA). Brings up drawbridge between cortex and receptors - this is the thalamic pacemaker.

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18
Q

What is the ascending reticular activating system (ARAS) - reticular formation?

A

A heterogeneous region of several brain areas that runs…
- Through brainstem from the medulla
- To the pons and midbrain
- And into the posterior hypothalamus
Second and third points control wakefulness/sleep

Experimental lesions in animals and clinical observations in patients with strokes/tumours produce hypersomnolence.

Electrical stimulation of this area causes aroused EEG and behavioural activation.

Confirms the reticular formation is necessary for wakefulness.

Monoaminergic – serotonin / histamine / noradrenalin – activity high in wake, reduced in NREM and absent in REM
Cholinergic – acetylcholine – highest in wake and REM and low / absent in NREM
Activation of both systems desynchronises EEG during wake and REM

Monoaminergic – serotonin / histamine / noradrenalin – activity high in wake, reduced in NREM and absent in REM
Cholinergic – acetylcholine – highest in wake and REM and low / absent in NREM
Activation of both systems desynchronises EEG during wake and REM

Neurons of the ARAS produce neurotransmitters
· gamma-aminobutyric acid (GABA)

Inhibitory effects on target neurons promotes sleep by reducing activity of wake-promoting neurons.

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19
Q

What are the neurotransmitters produced by the neutrons of the ARAS?

A
· Acetylcholine (Ach)
	· Norepinephrine (NE)
	· Dopamine (DA)
	· Serotonin (5-HT)
	· Histamine (HA)
Orexin/hypocretin
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20
Q

What happens if there are lesions in any of the ARAS areas?

A

you start to create somulance/hypersomulance - excessive sleepiness. This is the mechanisms by which sleep is turned on or off - the ‘sleep switch’

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21
Q

What does Ach do in ARAS?

A

Keeps us paralysed - parasomnia in non-rem sleep if walking/eating/talking/sex then not producing enough Ach

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22
Q

What is NE doing in ARAS?

A

down regulating

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23
Q

What does DA do in ARAS?

A

also helps to keep us paralysed and from moving too much

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24
Q

What does 5-HT do?

A

high levels indicated in depression and other psychological disorders, in essence it regulates mood

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25
Q

What does HA do in ARAS?

A

is a wakefulness drug. stopping release of histamine makes you drowsy

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26
Q

what does orexin do in ARAS?

A

newest in sleep medicine. During the day if have a huge influx of orexin this is narcolepsy. That suggests to us that orexin puts you to sleep. Does this by inhibiting wakefulness, not a somnogenic. All of the new drugs for sleep in the future will be orexin based - now know it is more important to manage orexin than to manage any of other other elements, such as GABA

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27
Q

What does GABA do in ARAS?

A

reduces wakefulness promoting neurones, but there are some problems with GABA. Associated with dependence, the system likes GABA and so can get addicted and start wanting it. Benzodiazapines has addictive qualities because of this.

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28
Q

What are the sleep mechanisms in sleep III?

A

SCN - regulates circadian rhythm:

  • melatonin
  • BCT
  • cortisol secretion

Circadian rhythm works on basis of cortisol secretion or melatonin. Can buy artifical melatonin from a lot of supermarkets in the US and australia, this is made of dried, ground cow brain. Because of SCM.

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29
Q

What is the suprachiasmic nucleus?

A

when light enters retina will travel via the optic nerve, leading onto SCN. If retina is sensing light will tell SCN to produce cortisol because light is associated with being awake. If there is no light the retina picks that up, goes through optic nerve, tells SCN not to create cortisol, but to inhibit and create melatonin which is the natural sleepiness hormone that we all have. When you start to get tired and yawn, this is proliferation of melatonin. Melatonin also has an age related shift pattern. At puberty we start to produce melatonin slightly differently, on a delayed frame. Prior to puberty produce melatonin quite early. Around 4pm start producing melatonin instead of cortisol, getting you ready for sleep later on. As teenagers, around puberty, this is delayed by a few hours which is why teenagers lose the normal sleep onset time, so go to bed very late and want to wake up later in the day which is why its hard to get people up in the morning. This normally lasts until 21-25.

30
Q

What hormones change during the sleep period?

A
growth hormone (GH) - pituitary gland
Prolactin (PRL) - pituitary gland
ACTH - pituitary gland
Cortisol - adrenal cortex
thyroid stimulating hormone (TSH) - pituitary gland
luteinizing hormone (LH) - pituitary gland
follicle simulating hormone (FSH) - pituitary gland
testosterone - gonads
estradiol - ovaries
insulin - pancreas
melatonin - pineal gland
leptin - adipose tissue
ghrelin - stomach
31
Q

What do leptin and ghrelin do?

A

Leptin tells us when we are full up. Ghrelin tells us when we are hungry. When start to deprive people fo sleep these hormones very quickly become very deregulated. Levels of leptin decrease an ghrelin increase. This leads to eating more and not knowing when you’re full. Depriving sleep down to 4 hours per night then deregulate their sleeping, will crave fat carbs and sugar during the afternoons - want these because want quick energy and the body thinks is under attack. Body automatically goes into a fight or flight response. In longer term with this disregulation is where we start to see a very strong relationship with obesity - more that 9 or less than 6 hours significant association.

32
Q

What does insulin do?

A

nsulin - regulates blood glucose levels from the pancreas. Deprive people of sleep, insulin levels become quickly disregulated. Some tentative suggestion that poor sleep is related to diabetes (Van Cauter).

33
Q

What happens to beta-amyloid in REM sleep?

A

Clear out beta-amyloid from the brain during REM only. This is like ‘brain plaque’. This plaque can build up from neurones firing, this is cleared out during REM. Increased beta amyloid is associated with dementia and alzheimers - link between sleep and neurodegenerative disorders. If not a causal factor then might be useful in treatment - if get people sleeping well might be able to reduce some of the symptoms and the progressive element.

34
Q

What is the cardiovascular physiology during sleep?

A

Changes in autonomic nervous system provide respite to the cardiovascular system.

Sleep provides respite to the CVS. This done in REM and non REm. Non REM best for CVS - relaxes and takes a break. Heart rate and pressure and flow reduces - puts back into a state of homeostasis. All at a reduced level.

In REM have surges in cardiac capacity. Surges in blood flow and acceleration in heart rate. If fragmented sleep then would have problem in cardiovascular homeostasis. Problems at night lead on to problems during the day.

Most people die around 4am, usually stroke or heart attack. This is about the surges in cortisol mathcing in with the surges in cardiac sympathetic and parasymapthetic activity. The switch point at this time is getting ready to wake up. Starts producing cortisol and stopping melatonin. This initial switch point has been associated with nocturnal death.

35
Q

What are the cardiovascular differences between REM and NREM?

A

NREM

  • reduced HR, arterial pressure and blood flow
  • relative autonomic stability and functional coordination between: respiration, pumping action of heart, maintenance of arterial blood pressure

REM

  • surges in cardiac-bound sympathetic and parasympathetic activity
  • accelerations (up to 37% increase in heart rate) and pauses in heart rhythm, fluctuations
  • surges in coronary blood flow
  • alterations in ponto-geniculo-occipital (PGO) activity and theta rhythm - signs on phasic central nervous system activation - correlate with heart rate surges
36
Q

What happens to the respiratory system during sleep?

A

• Loss of voluntary control of breathing
• Increased airflow resistance due to muscle atonia in REM
• Decrease in the usual ventilatory responses to
○ Low oxygen (hypoxia)
○ High carbon dioxide (hypercapnia)
–> most depressed in REM
• Irregular respiration during REM

Although REM exhibits atonia, chest movements from the intercostal muscles to allow breathing are maintained.

Basal level during nonREM and decreases even further during REM. Resp levels fall, but saturation levels remain constant. Will see irregualr respoiration around REM, tied to regualtion and production of acetylcholine.

37
Q

What is sleep paralysis?

A

Sleep paralysis - body has produced too much acetylcholine and kept in paralysis even though woken up. Mythical association to the ‘night hag’ from scotland sweden etc - if you are awake but in full paralysed state, your respiratory system also reduced significantly. The first thing you feel is that you are being suffocated because of this and you will start to hallucinate due to hypoxia - these hallucinations tend to always be an old woman and that is where these cultural versions of the night hag come from.

38
Q

What changes with circadian rhythm?

A
body core temperature
chronobiological changes
endocrine changes
(endogenous)

periods, production of semen, endocrine system, all work around the body clock

39
Q

What is the problem with human circadian rhythm?

A

Problem with human circadian rhythm is that it isn’t 24 hours, it is 24 and a quarter hours on average. This means that the way we regulate ourselves to 24 hours is through SCN, cortisol and melatonin - use light and dark from the environment. At 4am (Nadir) switch point between cortisol and melatonin see a lot of deaths, 4pm (acrophase) switch from cortisol to melatonin makes you feel very sleepy in the afternoon. Circadian rhythm relies on zietgebers (time givers) - main factor is light/dark, but also exercise (change body core temp) and also food (in additon to central pacemake SCN also have peripheral clocks in heart llung liver kidney and pancreas and can offset timing of circadian rhythm with food. If eat at diff time the peripheral oscilators can offset the central regulators by up to three days - can use this when suffering from jet lag, time light food and exercise to offset the main circadian pacemaker. Can only do this for up to three days, after which the main regualtor will take over again.) jet lag is when the circadian rhythm is in the environment you were in, rather than currently in.

40
Q

About the average circadian rhythm…

A

Average circadian rhythm is 24.2 hours.

Used to remove all access to cues for time for people and they start to adopt a circadian rhythm of 24.2 hours.

As we get older our circadian system starts to degenerate, around 60-65, along side this degeneration start to see advanced sleep phase syndrome.

Circadian rhythm moved forward, sleep earlier and wake earlier. Blind people have a longer circadian system at almost 25 hours on average.

There are individual differences but all tend to be around 24 hours. System will reset itself each day, it will never just stop it just continues.

41
Q

What is the two process model of sleep?

A

Model proposed by Borbély (1982) describes 2 drives for sleep:

- Homeostatic (process 'S')
- Circadian ©
- Homeostatic influence results from accumulation of 'some substance (S)' during prolonged wakefulness

During prolonged wakefulness, energy producing brain systems run down.

42
Q

What are the two processes in the two process model of sleep?

A

2 processes: C and S
C: circadian rhythm, proliferation of melatonin. Resets every single day.
S: the homeostat/homeostatic drive. Only will reset after you have slept. Very important. Like regular meals and buffet analogy on hunger. Can offset the drive to sleep. Sleep drive builds from the moment you wake up in the morning. This si the test for all sleep medicine, if don’t feel refreshed in the morning there is a problems with quantity/quality of sleep. Should get more and more tired throughout the day at which point you sleep, wake up in the morning and its started all over again. If take a long nap at 4pm then can delay the sleep onset. If sleep for an hour in the day time it is worth 2 hours in the night. ‘sleep-debt’ - if don’t go to sleep then the body doesn’t reset - 2 things could happen - have a microsleep where body involuntarily goes into sleep mode, or if carry on as the body doesn’t reset eventually will be forcing yourself to sleep.

43
Q

What is extended wakefulness?

A

If you add additional sleep pressure, the first thing the body will do is have big chunks of slow wave sleep (repair the body). Night after that will proliferate with REM - ‘REM rebound’.

Measure sleep using objective measures.

44
Q

How do we measure objective sleep?

A

PSG - polysomnography

A continuous all night recording of
- Electroencephalographic activity (brain waves: EEG)
- Electrooculographic (eye movement: EOG)
- Electromyographic (chin muscle movements: EMG)
Sleep-related breathing, cardiac rhythm and leg muscle movements

45
Q

What is polysomnography?

A

This data is usually examined in 30 second epochs EEG activity to usually divided into 4 categories based upon frequency, slowest to fastest.

(wave cycles per second)

Alpha (8-13 cps)
Theta (4-7 cps)
Delta (0.5-3 cps)
Beta (14-35 cps)

46
Q

What is actigraphy?

A

The use of a wrist - watch devcie which measures movement across the 24-hour cycle
- Clinical effectiveness (Morin and Wiseby, 1994)
Gold Standard (Chesson et al, 2000)

47
Q

What is a brief history of insomnia?

A

Been 4 formats under which we’ve diagnosed insomnia.

First was ICD - generally classifies insomnia as organic or non organic - originating within the body or externally caused?

Second started as DCSAD and has now become the ICSD (international classification of sleep disorders - by american academy…), 16 sleep disoders, research suggeests the majority of these are not valid. ICSD 3 has now been released and is much simpler.

DSM-5 - 2013 created the diagnostics term insomnia disorder. By american psychological and psychiatric association

RDC created by Jack Edinger in 2004, but this has never been updated.

48
Q

What are the three current nosologies of insomnia?

A

The ICD-10 classification of mental and behavioural disorders
International classifcation of sleep disorders
Diagnostic and statistical manual of mental disorders (DSM-5)

Now will have eihter ICD-10 (don’t use for insomnia), ICSD3 and DSM5. ICSD3 and DSM5 are now the same, didn’t used to be.

49
Q

What is insomnia (DSM-5)?

A

DSM-5 insomnia disorder (780.52):
Rejects distinction between Primary and Secondary Insomnia

  • Reported difficulty in getting to sleep, staying asleep, or waking too early
  • Problem exists despite adequate opportunity to sleep
  • Problem exists for at least three nights per week
  • Problem has been evident for at least three months
    The insomnia causes significant daytime impairment

DSM 5 rejects distinction between primary and secondary insomnia. Primary classified as having insomnia and no other health complain, physical or psychiatric, no other sleep disorder, substance use or medication use. This has now been rejected as we now know insomnia is a significant risk factor for a vast amount of diseases ans disorders. Cancer for example, depression - when these conditions are treated the insomnia still stays. This means that insomnia is not a symptom - it is a disorder in its own right and must be treated in this way which is very important. Until 2013 it was generally assumed that insomnia was because of cancer/depression/anxiety/etc but now seen that it probably has more of a causal role than we thought.

50
Q

About diagnosing insomnia…

A

Use 5 main criteria for diagnosis of insomnia (from DSM-5).

Difficulty getting to sleep (early insomnia), staying asleep (middle insomnia) or waking too early (late insomnia) make up three subtypes.

Say three nights a week as research has been done on night to night comparability and seen that there is a pattern in sleep disorders of ‘bad bad bad good bad bad bad good bad bad bad good etc’. This reflects how the homeostat cant go more than 3 days without having to reset.

3 months prevalence has no evidence to show this, looking at the period before the three months is also very important to look at.

If you meet all the criteria irrespective of other problems and disorders, you will still now get an insomnia disorder diagnosis meaning that it has to be treated. GPs are still slightly lagigng behind, and will try and find the reason for the insomnia to treat instead and this is why so much is spent on sleep medication each year.

51
Q

What is the prevalence of acute insomnia?

A

Acute insomnia is before 3 months.

Looked to see the epidemiology of insomnia disorder in the general population. Almost 8% of population will have acute insomnia, making it quite a big disorder.

52
Q

What is the prevalence of chronic insomnia?

A

Chronic when its over 3 months. Around a 3rd of people will have some kind of problems with sleep. Adding on the daytime consequences goes down to 9-15%, dissatisfaction with life down to 8-18%, and diagnosis only around 6%.

The prevalence and how it exists depends solely on how it is defined.

53
Q

What are the costs of insomnia?

A

On average people who don’t have insomnia cost half as much as those who do in health care costs.

These people are less productive and those with no insomnia have much higher costs associated.

£50 billion a year being costed to the government in terms of people not going to work, not being productive, seeing doctors, getting other illnesses and being miserable all due to insomnia.

Insomnia has high prevalence and a high cost in terms of healthcare and productivity.

54
Q

What are the consequences of insomnia?

A
  • CHD
  • Prostate cancer
  • Osteoarthritis
  • Breast cancer
  • Hypotension
  • Type II diabetes
  • Obesity
  • Hypertension
  • Smoking
  • Alcohol abuse
  • Marital satisfaction
  • Presenteeism
  • Absenteeism
  • Sexual risk taking
  • Illicit drug use
  • Accidents
  • Suicide
  • PTSD
  • Major depression
  • Anxiety disorders
  • Falls
  • Hyperlipidaemia
  • Social isolation
  • Academic performance

This is the list of consequences that we have to date. If you have insomnia you are more likely to get all of these things (2x likely to get prostate cancer, breast cancer)

Newest addition is suicide - insomnia is an extremely significant predictor of attempted and completed suicide. Problem solving centres of brain will switch off at night even if awake or not, if very suicidal then the part of brain dealing with rationality, problem solving and impulse control is gone, then you are more likely to attempt suicide.

Most evidence out there related to major depression. If have insomnia are twice as likely to get first onset of major depression.

55
Q

What is an example of research on insomnia?

A

Amazing research out there looking at how research is the link with depression.

Got group of people who had never had health or psychiatric problems or insomnia before and were going through first ever period of insomnia.

Tracked them over 6 months using polysonography.

Put into 3 categories - normal, acute to remission or acute to chronic. In terms of biological signature how long time took to get into REM was same in normal sleepers ad those who recovered around normal.

Those who turned into chronic took on average 65 minutes to get into REM and also reduced slow wave so ability to repair diminished, and REM came in quickly so study showed that those people 2 people at 1 month into chronic and 5 by the time reached 3 months.

Compared to normal and remitting group are seeing very high level of people who go through their first insomnia and end up with major depression.

56
Q

What is direct and indirect insomnia?

A

Direct

- Pro-inflammatory state
- Insulin dysregualtion

Indirect
- Mood dysregulation
Impaired decision making

How is this caused? Can end up in one of two camps… direct or indirect

Direct - is innate immune response damaged directly, is it about insulin dysregulation

Indirect - problem with mood, mood might influence decisions (eg drinking, drugs)

Likelihood is that its going to be a bit of both. We don’t know what the direct and indirects are at this time.

Indirect routes are very hard to test ethically.

57
Q

What is the 3P model of insomnia?

A

Predisposing factors:

  • biologic traits
  • psychological traits
  • social factors

Precipitating factors:

  • medical illness
  • psychiatric illness
  • stressful life events

Perpetuating factors:

  • excessive time in bed
  • napping
  • conditioning
58
Q

How do we conceptualise insomnia?

A

he 3 P model of insomnia. Most well known and most used. Developed in 1987 by Arte Spielman

Have the 4 stages shown and within have the 3 p models.

Fist is predisposing factors making it more likely for you to be vulnerable to insomnia. Looking for genes, psychological traits (perfectionism, neuroticism, impulsivity), biological traits (nothing concrete), social factors.

Precipitating factors - medical illness, psychiatric illness, stressful life events. This pushes us into the fight or flight response. The precipitant has pushed us over the threshold into insomnia and as a result will have reduced sleep. Stress makes you sleep less as need more time and energy to deal with the things.

The fight or flight repsonse has to reduce, cant keep producing cortisol for that long and so the biological factor starts to reduce…

Third P is perpetuating factors - coffee, naps, early nights - downregualting in day and upregulating at night. These things destroy the homeostat. These perpetuating factors, including conditioned arousal, perpetuate the insomnia. In treating chornic insomnia should be trying to manage the perpetuating factors. This is done in CBT-I.

59
Q

About CBT for insomnia (CBT-I)…

A

Sleep history / medical history / psychiatric history

Basic package of six weeks (1 hour sessions)

1. Sleep education
2. Sleep hygeine and begin sleep restriction
3. Stimulus control and cognitive control
4. Paradoxical intention and thoght control/distraction
5. Dealing with dysfunctional beliefs
6. Review (possible extensions mindfulness/relaxation techniques)

Always review at beginning of next session and look at sleep diary to determine any changes in sleep titration.

this is a variant on CBT. framework specifically for people with insomnia.

60
Q

What is the role of sleep hygiene in CBT-I?

A

Sleep hygeine - doesn’t work. Doesn’t cause insomnia or fix insomnia. It helps with sleep health. Included in therapy because results are seen better if they have good sleep health - the spit and polish.

61
Q

What is the role of sleep restriction in CBT-I?

A

Misnamed, should be restriction of time in bed.

People spend too much time in bed awake. If spend a lot of time trying to sleep and not being able to then start to get frustrated and angry and will associate bedroom with these things and with anxiety.

Restricting time in bed will increase the homeostat and eventually will sleep, done by giving a small dosage of sleep deprivation.

62
Q

What is the role of stimulus control in CBT-I?

A

Dealing with the negative lying in bed situations and association with the bedroom being a bad space.

People often say they can fall asleep in front of TV, wake up to go upstairs to bed and when they get into bedroom they suddenly feel awake and this is conditioned arousal to see the bed and become awake because you have conditioned yourself to the room being a place where you are awake.

Stimulus control is the 15 minute rule - if youre in bed for more than 15 minutes without being asleep you have to leave the room so that you don’t start associating the room with being awake.

63
Q

What is the role of cognitive therapy in CBT-I?

A

Dealing with the anxiety and worry

64
Q

What is the role of paradoxical intention in CBT-I?

A

Humans by their very nature are paradoxical - asked not to do something and you will do it - patients are trying so hard to go to sleep that they can’t.

If want to elicit a behaviour of going to sleep and if you are a paradoxical person then you need to be told to get into bed and stay awake.

65
Q

What is the role of thought control/distraction in CBT-I?

A

Give them something to think about and they’ll start doing it. Counting sheep eg is too simple, can think about the sheep and also your other problems at the same time. Have to create something that is all consuming eg counting backwards in 7s. Eventually the brain will send you to sleep.

66
Q

What is the role of dealing with dysfunctional beliefs in CBT-I?

A

Dealing with beliefs such as how many hours you believe you need - not clean cut but people don’t know that

67
Q

About the meta-analyses on CBT-I…

A

This is the 11 meta analyses that have been done on CBT-I (analyses of all the studies that have bene done beforehand). There are now 16. these show that CBT-I work and is better and longer lasting than sleep medication and doesn’t cause problems.

68
Q

Is CBT-I effective in co-morbid populations?

A

Can be used with other health problems too etc.

Bipolar not so good, doesn’t work and can set it off.

69
Q

What are the differing delivery methods of CBT-I?

A

Get reduction in 50% of depression, anxiety and suicide ideation symptoms. British pharmacological society even said to use CBT-I instead of medication.

However - there are only 8 trained people in the UK who can deliver this treatment. There is a high prevalence of insomnia and so how do these people get treated??

Group therapy? Online therapy - 4 online therapies for CBT-I (sleepio, sleepful, sleepstation, shuti)

70
Q

What are the pros and cons of non-direct delivery methods of CBT-i?

A

Pros
- Accessibility (increase i great as such few people are available to give treatment - group/online/etc)

Cons
- Limited assessment of comorbidities
- Reduced efficacy (SOL)
- Extreme variability
High attrition levels (52%)
- don’t really assess comorbidity, got to be careful with other conditions. Online as delivered autonomously don’t assess comorbidity very well. Sleep onset insomnia not as efficient, variability between courses and also a lot of people don’t like online therapy, want to be seen by a real person, about half will drop out of online therapy.
71
Q

What are the new approaches to address attrition in CBT-I?

A

Combining CBT-I with a stimulant
Combining CBT-I with a hypnotic
Including partners in CBT-I

Combine with a stimulant - put to sleep at night with CBT-I and stimulants to keep them up in the day - didn’t work.give a hypnotic at night and CBT-I - didn’t work

Start finding out the barriers, why do people drop out? Because of their partners who don’t like what we do as it disrupts the household so we should include partners in CBT-I and it does have an impact. Need to look beyond the physical into the social-emotional.