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Neuro > Neuro 15: Consciousness and sleep > Flashcards

Neuro 15: Consciousness and sleep Flashcards

1
Q

Define sleep

A

Stereotypic or species-specific posture

Minimal movement

Reduced responsiveness to external stimuli

Reversible with stimulation – unlike coma, anaesthesia or death

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2
Q

What tells you about sleep

A

EEG, EOG and EMG (muscle tone)

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3
Q

How does EEG, EOG and EMG change in stage 1&2 NREM, stage 3&4 NREM and stage 5 (REM)

A

EEG slows in stage 1&2 but increases a lot in 3&4, and is slow in REM

EOG is much slower in NREM 1&2, but like awake in 3&4 and very high peaks in stage 5 (rapid eye movement so EOG is going to be high!)

EMG reduces 1-4 and is almost nothing in REM… stops you acting out your dream

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4
Q

T/F REM is only time you dream

A

F… also during other stages but maybe less

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5
Q

How long is the sleep cycle and what is it made up of

A

Takes 90 minutes, goes through stage 1-5…. earlier on in sleep, NREM stages take up more time in the cycle

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6
Q

What is like EEG like in REM sleep

A

More like awake compared to stage 3/4

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7
Q

As well as EEG/muscular change, what other phsyioligcalt changes occur in sleep

A

Heart rate and respiratory changes— both reduce from stage 1-4, but increase into REM sleep and fluctuate a lot in REM

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8
Q

What controls sleep

A

Reticular activating system (brainstem systems which project fibres onto cortex, hypothalamus and thalamus)

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9
Q

t/f RAS allows for consciousness

A

True… kind of…. it’s necessary for consciousness but alone is not sufficient…. it’s like a dial, but it gates the activity of the cortex

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10
Q

Which brain areas promote wakefullness and sleep

A

wakefulness: lateral hypothalamus (orexin)
sleep: ventrolateral preoptic nucleus (in anterior hypothalamus)

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11
Q

Interaction of hypothalamus with the RAS

A

Orexin based lateral hypothalamus activates the recticular activating system

but the ventrolateral preoptic nucleus inhibits it (GABA)

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12
Q

How does the suprachiasmatic nucleus impact on sleep

A

It synchronises sleep with falling light levels….

CIRCADIAN SYNCHRONISATION of sleep/wake cycle.

It interacts with the hypothalamus (both the lateral nucleus, and the ventrolateral preoptic nucleus) and the RAS and with the pineal gland to release melatonin….

Linked to retina

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13
Q

Effects of sleep deprivation

A

Psychiatric and neurological together- Sleepiness, irritability, stress, mood fluctuations, depression, impulsivity, hallucinations

Neurological- Impaired attention, memory, executive function
Risk of errors and accidents
Neurodegeneration (?)

Somatic-Glucose intolerance
Reduced leptin/increased appetite
Impaired immunity
Increased risk of cardiovascular disease and cancer
Death
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14
Q

t/f sleep loss affects brain activation on fMRI

A

T

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15
Q

How can is sleep regulated (i.e. what can change if you have sleep loss)

A

Reduced latency to sleep onset

Increase slow wave (NREM) sleep as a proportion of sleep if you missed this

Or increase REM sleep after selective REM sleep deprivation

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16
Q

Function of sleep

A

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, …

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17
Q

When do dreams most often occur

A

REM sleep (but can be both), and more easily recalled then

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18
Q

What area of brain active in dreaming

A

Limbic system>frontal lobe

More about emotion than reality

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19
Q

Function of dreaming

A

Safety valve for antisocial emotions
Disposal of unwanted memories
Memory consolidation

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20
Q

Outline insomnia causes

A

Most transient cases

physiological: sleep apnea, chronic pain

brain dysfunction: depression, fatal familial insomnia (caused by pryon protein like CJD) or night working

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21
Q

Outline treatment of inoomnia

A

sleep hygiene, hypnotics (most enhance GABAergic circuits e.g. tamazepam or zopiclone) and sleep CBT

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22
Q

What is narcolepsy

A

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

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23
Q

What is hypersomnia

A

Too sleepy in the day…
due to arousal in the night disrupting sleep wake cycle:

  • sleep apnea
  • anxiety
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24
Q

Differentiate the type of disease of narcolepsy compared to insmnia

A

narcolepsy is a disease of the actual sleep/wake pathways (primary), whereas insomnia the pathway is probably fine and it’s other factors affecting this pathway

25
Q

What is cataplexy and when does it occur

A

In narcolepsy

sudden, brief loss of voluntary muscle tone, often triggered by strong emotions e.g. laughter

26
Q

T/F in narcolepsy because of the disturbed sleep, REM and NREM sleep are comensated depending on which you have less of

A

F: there is Dysfunction of control of REM sleep

27
Q

Narolepsy is caused by what

A

Deficiency of orexin (=hypocretin)

28
Q

What can shift work lead to

A

physiological processes to become desynchronised

sleep disorders, fatigue and an increased risk for some conditions such as obesity, diabetes and cancer

29
Q

Is sleep a consequence or cause of neurological disease

A

Could be either realy

30
Q

Definiton of consciousness

A

the state of being aware of and responsive to one’s surroundings

31
Q

Elements of conscioussness

A

Level, content, self

32
Q

Classify following in terms of VIGILANCE (awake behaviour, eyes open) and AWARENESS (level/content of consciousness…. richness of experience):

Coma
General anaesthetic
Locked in syndrome 
Veg state 
Dementia
A

Coma, very low for both

General anaesthesia similar to coma but could have tiny bit more awareness

Locked in high awareness and high vigilance (just under conscios)

Veg state- high vigilance but very low awareness

Dementia/minimally conscious state= fairly normal vigilance, but reduced awareness

33
Q

Why does RF project to cortex

A

allowing that sensory signals to reach cortical sites of conscious awareness such frontoparietal cortex

34
Q

Types of neurotransmitters in the RAS

A

RF projects to the hypothalamus, thalamus and the cortex

Ventral tegmental Area (dopaminergic neurones)… this relates to reward pathway mesolimbic…. VTA in midbrain

pons- Locus coeruleus (noradrenergic neurones)… this relates to pain

35
Q

t/f consciousness arises from a partcular part of the brain

A

f.. it emerges as a result of cortico-thalamic transmission

36
Q

What is important for consciousness

A

dynamics of neuronal activity– integrated and differentiated

HIGH INTEGRATION, LOW DIFFERENTIATION= generalised seizure (all areas of the brain doing the same thing)

LOW INTEGRATION, HIGH DIFFERENTIATION= e.g. callosotomy… areas doing different things but none of this linked with each other

37
Q

How can consciousness be measured

A

Give TMS and then meausure activity after with EEG

You can measure how well that induced TMS travels across to other brain regions.

In an awake individual, this signal will spread across brain regions (high integration) but in asleep will not (low integration)

Can also see if the different brain areas to which the signal spreads process the signal differently (i.e. high differentiateion, heterogenous) or in the same way (i.e. low differentiation)

Can quantify this to give PCI…. pertubational complexity index (PCI)

38
Q

What is ‘neural correlates of consciousness’ referring to

A

The minimum neuronal mechanisms jointly sufficient for any one specific conscious experience.
Primarily localized to a posterior cortical hot zone that includes sensory areas (Koch et al., 2016)

i.e. where is the brain region that corresponds to a particular experience of consciousness

39
Q

3 disorders of consciousness

A

Coma- Absent wakefulness and absent awareness,

Vegitative state- Wakefulness but absent awareness

Minimally conscious state- wakefulness with minimal awareness

40
Q

T/F brainstem death is a disorder of consciousness

A

F… neither is locked in syndrome

41
Q

Feedforword processing vs top-down recurrent processing

A

feed forward=subliminal or non sonscious
Top dorwn is conscious access

We can have top-down and bottom-up processes – there are non-conscious processes that bubble up to conscious access.

42
Q

State the components of a coma

A
  • can’t be awakened
  • doesn’t respond norally to painful stimulu, light or sound
  • Lacks normal sleep wake cycle
  • Does not initiate voluntary actiond
43
Q

Which area of brain might be affected in:

vegetative state
locked in syndrome
brainstem death

A

vegetative state=cortex/hemispheres (intact RAS)

locked in syndrome=damage e.g. to ventral pons (motor system)…. intact cortex and intact RAS

brainstem death= irremediable damage to brainstem

44
Q

In which types of strokes may visual neglect occur

A

parietal lobe

45
Q

Differentiate hemianopia from visual neglect

A

Both involve part of the world not being seen

with hemianopia this is a visual pathway problem

with visual neglect this is a higher up cortical deficit

often conflated as both can occur due to stroke

46
Q

Different types of waves on EEG and what EEG monitors

A

Monitors level of arousal

BATD: from awake to sleep

Delta= in sleep. Up to 4Hz

Theta= 4-8 Hz.

Alpha=8-13Hz

Beta=13-30 Hz (normal waking consciousness)

40Hz (gamma range) associated with creation of conscious contents via THALAMO-CORTICAL FEEDBACK LOOPS

47
Q

When might alpha waves occur on ECG

A

When drowsy or relaxed

48
Q

When might theta waves occur

A

Stage N1 sleep

49
Q

When might delta waves occur

A

Stage N3 sleep

50
Q

When might you get sleep spindle waves on EEG

Sumarise the EEG seen during different levels of conscioussness

A

stage N2 sleep

B: Awake
A: drowsy, relaxed
T: N1 sleep
Spindles: N2 sleep
D: N3 sleep

REM sleep is fast and random EEG.

51
Q

What are the components of the glasgow coma scale

A

1-4 for eyes
1-5 for verbal
1-6 for motor

52
Q

Minimum GCS score and max

A

min is 3

max is 15

53
Q

Causes of coma

A 
Metabolic:
Drug overdose
hypoglycaemia
diabetes
"the failures"
hypercalcaemia
Diffuse intracranial:
head injury
meningitis
SAH
encephalitis
epilepsy
hypoxic brain injury
Hemisphere lesion:
cerebral infarct
cerebral haemorrhage
subdural
extradural
abscess
tumour
Brain stem:
brainstem infarct
tumour
abscess
cerebellar haemorrhage
cerebellar infarct
54
Q

What is coma

A

Unrousable unresponsiveness

55
Q

What is diffuse axonal injury

A

Damage to white matter tracts e.g. corpus callosum…. higher order cognitive problems due to poor integration…..

can follow traumatic brain injury (e.g. after extradural haematoma etc.)

56
Q

Which types of stroke could cause coma

A

Bitemporal medial thalamic infarcts

or strokes to do with posterior ciruclation

57
Q

Which types of lesions are dangerous due to basic functin

A

Posterior fossa lesions

58
Q

Decorticate vs decerebrate posturing

A

Main difference is decorticate involves flexion at the elbow

Whereas decerebrate involves extension at the elbow and pronation

Decerebrate indicated involvement of the red nucleus and indicates event further down in the brainstem

Neuro (16 decks)

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