Sleep and consciousness Flashcards

1
Q

What three techniques are used to monitor activity during sleep?

A

Electroencephalography (EEG)
Electromyography (EMG)
Electrooculography (EOG) = eye movements

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2
Q

Describe the EEG and EMG activity in wakefulness.

A

EEG – fast brain rhythm

EMG – reasonable amount of muscle tone because you are maintaining posture and ready for action

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3
Q

Describe the EEG, EMG and EOG activity in non-REM sleep. What stages of sleep do they correspond to?

A

Stage 1 and 2:
= Light sleep
EEG - theta waves (gradually becoming more and more drowsy)
EOG - NO eye movements
EMG - muscle activity reduced considerably

Stage 3 and 4: 
= Very deep sleep 
EEG - Delta activity  
EOG - minimal eye movement 
EMG - continued relaxation of muscles
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4
Q

Describe the EEG, EMG and EOG activity in REM sleep (i.e. stage 5)

A

EEG – brain shifts abruptly back to fast rhythm (similar to wakefulness)
EOG – rapid eye movement
EMG – muscle activity at its lowest

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5
Q

How long is a normal sleep cycle (incorporating stages 1-5)?

A

~90 minutes

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6
Q

Compare the relative amounts of NREM and REM sleep in a sleep cycle at the start of a night’s sleep and at the end.

A

Start of the night – more NREM sleep

End of the night – more REM sleep

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7
Q

Describe how heart rate and respiratory rate change during sleep.

A

SLOW during NREM

FAST during REM sleep

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8
Q

Which system is responsible for the control of consciousness?

A

Reticular activating system

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9
Q

How does the reticular activating system control the activity of the cortex?

A

Either via direct connections

Or via indirect connections through the intralaminar nuclei of the thalamus

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10
Q

What are the two important nuclei in the hypothalamus that are responsible for influencing the reticular activating system and, hence, regulating the sleep-wake cycle?

A

Lateral Hypothalamus – excitatory (promotes wakefulness via orexin neurotransmitter)
Ventrolateral Preoptic Nucleus – promotes sleep

NOTE: they have an antagonistic relationship

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11
Q

Describe the circadian synchronisation of the sleep-wake cycle.

A
  • The suprachiasmatic nucleus is responsible for synchronising the sleep-wake cycle with falling light level
  • It receives an input from the retina (not from the usual photogenic cells) and as light level falls the suprachiasmatic nucleus becomes more active
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12
Q

Describe the effect of the increased activity of the suprachiasmatic nucleus on the nuclei within the hypothalamus.

A

This leads to activation of ventrolateral preoptic nucleus and inhibition of lateral hypothalamus so you become sleepier

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13
Q

What other important projection does the suprachiasmatic nucleus have and what is the importance of this projection?

A

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 associated with sleeping

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14
Q

List some consequences of sleep deprivation?

A
Sleepiness/irritability 
Performance decrements 
Concentration difficulties 
Glucose intolerance – risk of diabetes 
Reduced leptin 
Hallucinations
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15
Q

Describe three ways in which sleep is regulated after sleep deprivation.

A
  1. Reduced latency of sleep onset (i.e. able to fall asleep faster)
  2. Increased NREM sleep (sleep for longer)
  3. Increased REM sleep (after selective REM sleep deprivation)
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16
Q

During what stages of sleep can you dream?

A

Both NREM and REM but you tend to dream more and are able to recall dreams better during REM sleep

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17
Q

Describe the brain activity of the limbic system compared to the frontal lobe in sleep.

A

Brain activity in the limbic system is higher than in the frontal lobe
This is because the content of dreams tends to be more emotional than in real life

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18
Q

Summarise the functions of sleep

A
  • Restoration and recovery
  • Energy conservation
  • Predator avoidance
  • Memory consolidation
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19
Q

State some causes of insomnia that are physiological, and due to brain dysfunction.

A

Physiological – sleep apnoea, chronic pain

Brain Dysfunction – depression, fatal familial insomnia

20
Q

What are some potential treatment options of sleep disorders?

A
  • Improve sleep hygiene
  • Hypnotics (most enhance GABAergic circuits)
  • Sleep cognitive behavioural therapy (CBT)
21
Q

State a common primary and secondary cause of hypersomnia (excessive daytime sleepiness)

A

Primary = narcolepsy

Secondary (due to poor quality overnight sleep) = obstructive sleep apnoea, neurodegenerative diseases

22
Q

What scale can be used to measure daytime sleepiness?

A

Epworth sleepiness scale

23
Q

What is narcolepsy characterised by?

A

Falling asleep repeatedly during the day and disturbed sleep during the night

24
Q

Narcolepsy can also come with cataplexy. What is cataplexy?

A

Sudden, brief loss of voluntary muscle tone, often triggered by strong emotions

25
Q

Explain narcolepsy with regards to the sleep cycle.

A

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

26
Q

What is narcolepsy caused by?

A
  • Orexin deficiency

- Orexin deficiency could be autoimmune or genetic

27
Q

Define consciousness

A

The subjective experience of the mind and the world around us.
The state of being aware of and responsive to one’s surroundings

28
Q

What structure within the brain is heavily involved in regulating alertness and level of consciousness?

A

Reticular Activating System

29
Q

What is the reticular formation?

A

Polysynaptic network in core of midbrain, pons and upper medulla

30
Q

What are the sensory inputs to the reticular formation?

A

Sensory and pain from ascending pathways
Vestibular information from medial vestibular nucleus
Visual from superior colliculus
Auditory from inferior colliculus
Olfactory via the median forebrain bundle

31
Q

The RF modulates cerebral activity via various projections. What are these projections?

A
  • Noradrenergic projections from the nucleus coeruleus to the cerebral cortex
  • Dopaminergic projections from the ventral tegmental area to the cerebral cortex
  • Cholinergic projections to the thalamus
  • Raphe nuclei in the midline which are the main source of serotoninergic projections to the brain and spinal cord
32
Q

Which of these projections is most important in regulating the level of arousal?

A

Cholinergic projections

33
Q

What are the three mechanisms by which the cholinergic projections regulate the level of arousal?

A
  1. Excite individual thalamic relay nuclei leading to activation of cortex
  2. Projections to intralaminar nuclei, which in turn project to all areas of cortex
  3. Projections to reticular nucleus, which regulates flow of information through other thalamic nuclei to cortex
34
Q

How is the hypothalamus also involved in maintaining awake state?

A

Tuberomammillary nucleus (histaminergic) in hypothalamus projects widely to cortex and is involved in maintaining awake state

35
Q

Different levels of arousal can be seen as a change of waveform in EEG, which records activity from the cerebral cortex. What are the four basic rhythms and what levels of arousal do they represent?

A

Delta (0.5-4 Hz) present during sleep
Theta (4-8 Hz) associated with drowsiness
Alpha (8-13 Hz) subject relaxed with eyes closed
Beta (13-30Hz) indicates mental activity and attention

Gamma range (~40 Hz) – creation of conscious contents in the focus of the mind’s eye, via the recurrent thalamo-cortical feedback

36
Q

Define confusion/delirium and stupor?

A

Confusion and delirium = sustained disturbance of consciousness where mental processes are slowed. Subject may be inattentive, disorientated and having difficulty carrying out simple commands or speaking

Stupor = (more profound) lack of critical cognitive function and consciousness – only responsive to pain

37
Q

Damage to the reticular formation can lead to coma. What is a coma? Why is it different from sleep?

A

State of unconsciousness in which the subject cannot be roused even by strong sensory stimuli
Different from sleep – metabolic activity of the brain is depressed and there is total amnesia for this period

38
Q

Identify causes of coma

A

Metabolic alteration e.g. hypoglycaemia, hypoxia, intoxication
Bilateral lesions in the cerebral hemispheres - only if massive and bilateral (flat EEG)
Lesions in the thalamus or brainstem eg. due to raised intracranial pressure

39
Q

What is the Glasgow Coma Scale? How is the Glasgow Coma Scale is structured?

A

International standard measure of level of consciousness

Eye opening; max 4
Verbal responses; max 5
Motor responses; max 6

40
Q

What causes a persistent vegetative state?

A
  • Disconnection of the brainstem from the cortex or widespread cortical damage
  • Brainstem is still functioning so reflexes, postural movements and sleep-wake cycle may still be present
41
Q

What is brain death?

A
  • Irreversible coma due to brainstem death, but body kept alive artificially
  • Decision to cease treatment depends on demonstration of absence of brainstem reflexes & response to hypercapnia
  • EEG not diagnostic
    NOTE: spinal reflexes and some postural movements may be present
42
Q

What imaging technique can be used to study consciousness in health and disease?

A

Functional MRI

43
Q

Define the concept of neural correlate of consciousness

A

The minimum neuronal mechanisms jointly sufficient for any one specific conscious experience

44
Q

What would the consequences of a right parietal lesion be?

A

Hemispatial neglect – the patient will not pay attention to the left visual field
Information from the left visual field is reaching the primary visual cortex but because of the parietal damage, the patient is not conscious of this visual field

45
Q

Explain the phenomenon known as ‘blindsight’?

A

Brain-damaged (occipito-visual cortex) patients who are perceptually blind of their visual field can demonstrate some responses to visual stimuli e.g. manually interacting with ‘unseen’ objects and avoiding ‘unseen’ objects