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Brain and Behaviour Year 2 > Sleep and Arousal > Flashcards

Sleep and Arousal Flashcards

1
Q

How is consciousness tested clinically

A

Glasgow coma scale

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2
Q

what is consciousness

A

this is the ability of an individual to react appropriately to stimuli

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3
Q

consciousness is not a….

A

consciousness is not an all-or-nothing state but a continuum, with different stages

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4
Q

Name the different stages of consciousness

A
  • coma
  • unconsciousness
  • sleep
  • drowsy wakefulness
  • normal wakefulness
  • high arousal
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5
Q

Describe the different stages of consciousness

A
  • Coma=unarousable unresponsiveness (with or without reflexes present)
  • Unconsciousness =arousable (but perhaps only temporarily by intense stimuli)
  • Sleep= arousable by normal stimuli
  • Drowsy wakefulness= responding in a non-reflex way
  • Normal wakefulness= responding to spoken or written stimuli
  • High arousal= hyper alert and fast reactivity
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6
Q

What is the maximum points of the GCS

A

15 for being alert and awake

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7
Q

What are the 3 things GCS is measured on

A

Eye opening
verbal response
motor response

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8
Q

Describe the GCS

A 
eye opening 
4 spontaneous 
3 to sound 
2 to pressure 
1 none
verbal response 
5 orientated 
4 confused
3 words 
2 sounds 
1 none 
Motor responses 
6 obey commands 
5 localising 
4 normal flexion 
3 abnormal flexion 
2 extension 
1 none
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9
Q

how can we measure brain arousal

A

EEG

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10
Q

describe how an EEG works

A
  • small voltages that are recored from pairs of scalp electrodes
  • these average the activity of nerve cells
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11
Q

what is the downside of EEG

A
  • can have artefact signals due to muscles in the head such as extra ocular eye muscles
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12
Q

What is an artefact signal

A

signals not due to neuronal activity

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13
Q

what can EEGs be used to measure

A
  • normal sleeping
  • normal walking
  • seizure activity
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14
Q

what does a normal EEG look like and why

A

normal waking EEG is a high frequency low amplitude signal
o Desynchronized appearance: some neurons fire out of phase with others (this is normal): cancel each other out. for example if one cell is being depolarised another is hyper polarising so they cancel out there effect on the brain

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15
Q

what does an EEG look like during a seizure and why

A
  • high amplitude waves and slow waves occur
  • this is because there is synchronised electrical activity and the cells are firing in phase with each other
    = this causes loss of consciousness
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16
Q

synchronised firing ….

A

means that there is something wrong for example a seizure

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17
Q

the more synchronisation of cortical neuronal activity….

A

the less conscious the individual is

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18
Q

consciousness is a …

A

consciousness is a function of desynchronisation

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19
Q

what happens in sleep to consciousness

A
  • sleep is a state of unconsiocuness
  • therefore there is cortical neuronal synchronisation and thus large amplitude (delta) slow waves which can be similar in appearance to seizure activity
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20
Q

Why do we sleep

A

• Maintenance and Repair
• Increased growth/maintenance of immune, nervous, skeletal and muscular systems
- growth hormone is secreted in sleep
- wound repair
- during slow wave sleep the CSF moves between neurones and one of the function is to rinse the debris of neurotransmitter and bits of broken membrane and wash it out of the brain

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21
Q

What are the two types of sleep

A
  • Slow wave sleep (Non-REM sleep)

- REM sleep

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22
Q

What is slow wave sleep/ normal sleep

A
  • this is a state during which the EEG becomes synchronised and produces large amplitude signals
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23
Q

what is the use of melatonin

A
  • it is a free radical scavenger
  • main function is to remove or neutralise the free radicals that accumulate during waking as high levels of aerobic metabolism that occur in the brain during wakefulness produces free radicals
  • has an important role in maintained GABA function and preventing seizures in the brain
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24
Q

what happens to glycogen stores during sleep

A

Glycogen stores in the brain increase during sleep, and are depleted through metabolism during wakefulness.

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25
Q

where is the pineal gland found

A

Found at the posterior border of the third ventricle; not part of the brain but an endocrine organ

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26
Q

what produces melatonin

A

pineal gland

27
Q

name the 4 stages of sleep

A
  • REM
  • NON-REM 1
  • NON-REM 2
  • NON-REM 3
  • NON-REM 4
28
Q

how long to sleep cycles last

A
  • Sleep stages 1-4 repeat in 90 minute cycles through the night
29
Q

what happens in REM sleep

A
  • rapid eye movement

- EEG is now desynchronised time to wake up

30
Q

Where does the control of sleep and wakefulness happen

A
  • controls happens in the reticular formation of the pons

- this is modulated by the hypothalamus which decides when we need to sleep

31
Q

describe how the reticular formation keeps us awake

A
  • there are certain systems of neurones in the pons which project diffusely to the cerebral cortex and this activity keeps us awake
  • when these neurones are switched off we sleep
32
Q

name the 2 stimuli for sleep

A
  • chemicals in the blood

- diurnal rhythms

33
Q

describe how chemicals in the blood can cause us to fall asleep

A
  • in the blood brain barrier there are leaky areas in the medial and ventrolateral preoptic areas of the hypothalamus thus they can detect the blood levels of verious molecules
  • the preoptic nuclei project to the tuberomamillary nucleus which has histaminergic neurones
  • one of the ways that the hypothalamus inhibits sleep is by triggering the tuberomamillary neurones, it can also activate sleep by inhibiting the activity of the tuberomamillary neurones
  • hypothalamic neurones have receptors for various molecules that leak out of the blood these can promote or inhibit sleep
34
Q

name two sleep inhibitors

A
  • Ghrelin.

* Glucose

35
Q

name sleep inducers

A

• Leptin
• Adenosine
• Antihistamines (work on histaminergic neurons).
NOTE: caffeine is an antagonist at A1 adenosine receptors: therefore, caffeine helps keep us awake

36
Q

describe how histaminergic neurones work in terms of sleep and arousal

A

o Active during waking.

o Silent during sleeping.

37
Q

what can be used as a treatment for insomnia

A
  • antihistamines such as diphenhydramine and doxylamine, can be used to treat insomnia.
38
Q

describe how diurnal rhythms can act as a stimuli from sleep

A

• The suprachiasmatic nucleus (SCN) receives input from the retina and is involved in regulation the diurnal rhythm of sleep. It projects to the TMN.
o Neurons of retina fire continuously during daylight. therefore they continuously project to the TMN keeping us awake

39
Q

what happens if you have a lesion in the suprachiasmatic nucleus

A
  • it destroys the diurnal sleep rhythm, they still sleep in irregular patterns
40
Q

what is a cause of narcolepsy

A

• Loss of orexins due to autoimmune attack from T-cell lymphocytes on orexin-containing neurons.
o These are found in the posterior hypothalamus.

41
Q

what do orexin do

A
  • the orexin neurones excite the monamine neurones in the brainstem especially the locus coeruleus and raphe nuclei
  • also have diffuse axonal projections to all areas of the cerebral cortex
42
Q

what do orexin stimulate the release of

A
  • Acetylcholine
  • Noradrenaline
  • Serotonin.
  • Dopamine
43
Q

what neurones is wakefulness maintained by

A

orexin of the posterior thalamus and histaminergic neurones of tuberomamillary nucleus

44
Q

When does sleep onset occur

A
  • Sleep onset occurs when signals from preoptic nuclei and suprachiasmatic nucleus inhibit histamine and orexin neurons.
  • These stop excitatory transmission to the reticular formation of the pons which are necessary for cortical arousal
45
Q

name the monamine systems in the brainstem and what neurones they release
- these are important for maintaining wakefulness

A
  • Ventral tegmental area = dopaminergic cells
  • pedunculopontine = cholinergic cells
  • locus coreuleus = noradrenergic cells
  • raphe nucleus = serotoninergic cells
46
Q

what is dopamine like during sleep

A

low level

47
Q

what do lesions in the reticular formation in pons or midbrain result in

A
  • they result in a coma that may be permanent
48
Q

damage in cholinergic neurone system…

A

Damage to the cholinergic neurone systems occur in early alzheimers disease

49
Q

when are chloinergic systems activated

A

• Activity increased in REM sleep (as well as in waking).

50
Q

describe the correlation between cholinergic activity and desynchronised EEG

A
  • Slow wave (NREM) sleep – all 3 went down (noradrenaline, serotonin and acetylcholine)
  • REM sleep – acetylcholine – active, serotonin and noradrenaline – inactive
  • Thereofre we know that the EEG during REM sleep is like the EEG during sleeping therefore there is a correlation between cholinergic activity and descyrhonises EEG
51
Q

during all forms of sleep the activity …

A
  • During all forms of sleep the activity in the brainstem noradrenergic neurons drops to a low level
52
Q

describe how the locus coeruleus activates the alertness and attention system

A

. The locus coeruleus is a “control centre ’for the sympathetic nervous system, but it also projects rostrally to the cerebral cortex and activates a form of ‘central sympathetic system’
- This central noradrenaline system activates our brain’s ALERTNESS AND ATTENTION systems. With it switched off we are inattentive to the outside world.

53
Q

what does the central sympathetic system activate

A

• CSS: activates our alertness and attention. Allows us to retrieve memory and use this in dreams.

54
Q

what is the theory of serotonin regarding sleep

A

Theory: serotonin maintains connection between UML and LMN. Motor cortex is active in sleep. We don’t move because it is believed that without firing of serotonin this connection not happen (why we don’t move in dreaming)
- our lower motor neurones (except respiratory and extra ocular muscles) are paralysed during REM sleep .

(!) Sleepwalking/nocturnal motion are thought to be a failure of this motor disconnection during rem.

55
Q

what can cause a complete cessation of dreaming

A

lesions in the orbitofrotnal limbic cortex

56
Q

what is dreaming initiated by

A
  • Solms* argues that dreaming is initiated by activity in mesolimbic dopamine neurons stimulating the orbito-frontal cerebral cortex.
  • This dopamine activity occurs intermittently during REM sleep
57
Q

dream sleep v REM sleep

A
  • they are not the same thing
  • dreams have been reported by people woken from non-REM sleep
  • but dream sleep is normally limited to REM sleep because REM is when the muscular paralysis occurs.
  • The paralysis occurring during REM sleep prevents people physically acting out their dreams
58
Q

What is the function of REM sleep

A
  • memory consolidation
  • removing junk and defragmenting memories
  • coping with life stresses
59
Q

what happens between specific serotonin reuptkae inhibitors and sleep

A

• Serotonin ceases during sleep.
• If kept high might interfere with sleep = decrease in sleep efficiency.
- these drugs block the reuptake of serotonin and noradrenaline
-

60
Q

what is the effect of TCAs on sleep

A
  • Tricyclic antidepressants (TCAs) such as amitriptyline promote sleep.
  • They are often used in depressed patients who have prominent insomnia.
  • they work by blocking histamine H1 receptors
61
Q

what TCA is now marketed for primary insomnia

A

Doxepin

62
Q

what do MAOi do to sleep

A
  • they reduce sleep
  • this may be because they increase noradnraline, dopamine, and serotonin levels in the brain that may make it difficult to initiate sleep
63
Q

How do you treat insomnia

A
  • Lifestyle changes
  • CBT
  • Antihistamines
  • Benzodiazepines
  • Zopiclone (increased release of GABA).
64
Q

What is sleep apnea and what can it lead to

A

• Motor disconnection during REM must specifically AVOID the respiratory system.
o Otherwise they would stop breathing.
• If this happens = sleep apnea: muscles of the throat relax too much (obstruct the airway).

Lead to sudden infant death syndrome.

Brain and Behaviour Year 2 (36 decks)

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