2.5 Consciousness Flashcards

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1
Q

NREM sleep makes up __% of sleep

A

75%

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2
Q

Which arm of the autonomic nervous system is more active during NREM/REM sleep?

A

NREM: Parasympathetic
REM: Sympathetic

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3
Q

REM sleep makes up __% of sleep

A

25%

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4
Q

What happens to sensation during REM/NREM sleep?

A

NREM: Limited/absent
REM: Vivid, internally generated

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5
Q

Describe muscle activity during REM sleep

A

Movements are commanded, but none are carried out

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6
Q

Why is REM sleep called paradoxical sleep?

A

EEG looks more awake than asleep.

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7
Q

Oxygen consumption of brain during REM vs NREM

A

REM: Elevated
NREM: Decreased

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8
Q

How are muscles paralyzed during REM sleep?

A

Glutamatergic neurons in the brainstem activates neurons in the medulla. They release GABA, inhibiting the activity of skeletal muscles.

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9
Q

Describe the four stages of NREM sleep

A

Stage 1: Hypnagogic hallucinations

Stage 2: Harder to awaken

Stage 3: Few eye and body movements

Stage 4: Sleep talking

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10
Q

Describe the sleep cycles

A

Move from stage 1 to stage 4 of NREM. Back up to stage 1 sequentially, and into REM. This is one sleep cycle.

With each cycle, we spend less time in N3 and N4, and longer in REM.

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11
Q

Describe the two mechanisms by which neurons can create synchronous rhythms

A
  1. Central pacemaker (orchestra conductor)
  2. Inhibiting/exciting one another (all playing)
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12
Q

Gamma EEG waves

A

Conscious perception/problem solving

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13
Q

Beta EEG waves

A

Waking state; alertness

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14
Q

Alpha/Mu EEG waves

A

Quiet waking state. Relaxed, lucid, calm.

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15
Q

Theta EEG waves

A

Deep relaxation/light sleep; meditation

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16
Q

Delta EEG waves

A

Deep sleep

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17
Q

What EEG waves can be found in someone who is awake/in REM sleep?

A

Beta waves (gamma can also be found in wakefulness)

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18
Q

What EEG waves can be found in someone who is in Stage 3/Stage 4 NREM sleep?

A

Delta waves

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19
Q

What EEG waves can be found when we are drowsy/relaxed?

A

Alpha waves

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20
Q

What EEG waves are most prominent in Stage 1 NREM sleep?

A

Theta waves

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21
Q

What happens to EEG activity between Stage 1 and Stage 2 sleep?

A
  • More theta
  • Increased amplitude
  • Sleep spindles (inhibit cognitive processes)
  • K complexes (memory consolidation)
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22
Q

This part of the reticular formation is responsible for promoting wakefulness…

A

Ascending reticular activating system (ARAS)

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23
Q

How is the ARAS activated?

A

By the release of a peptide called orexin from the lateral hypothalamus

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24
Q

In order to fall asleep, we need to inhibit ARAS. How is this done, and by what system?

A

VLPO (Ventrolateral preoptic area) releases GABA to inhibit ARAS modulatory neurons

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25
Q

How does adenosine progressively make us sleepier?

A

Takes foot of ARAS accelerator (reduces orexin release).

Puts foot on ARAS brake (increases GABA release from VLPO)

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26
Q

How does caffeine make us less sleepy?

A

Binds to adenosine receptors

27
Q

Give some examples of zeitgebers

A
  • Sunlight
  • Food
  • Exercise
  • Social interactions
28
Q

Describe how the suprachiasmatic nucleus regulates sleep/wake cycles in response to sunlight

A
  • Increases Orexin release from LH
  • Decreases GABA release from VLPO
  • Decreases melatonin release from pineal
29
Q

Why is melatonin called the dracula hormone?

A
  • Released in response to dark
  • Inhibited release in response to light
30
Q

How is it thought that melatonin makes us sleepy?

A
  • Decreases orexin from LH
  • Increases GABA from VLPO
31
Q

Define consciousness

A

Full awareness of the self and one’s relationship to their environment

32
Q

Define coma

A

Patient has closed eyes and is unable to interact with their environment (GCS 8 or less)

33
Q

What are the two main components of consciousness?

A
  • Arousal
  • Awareness
34
Q

Which neuroanatomical areas are responsible for arousal?

A

Thalamic/extrathalamic ascending systems

35
Q

What is the relationship between awareness and arousal in terms of interdependence?

A

Awareness requires arousal, but arousal does not require awareness.

36
Q

Describe the structure of the neuroanatomical regions responsible for awareness

A
  • Distributed neuronal circuits
  • Modular in nature
  • Loop from thalamus and cortex
37
Q

Lesions in which brain areas can lead to coma?

A
  • Cortex
  • Thalamus
  • Brainstem
38
Q

What is brain death? How is it different from death?

A
  • Permanent loss of all brain activity
  • Occurs when a patient dies whilst on life support; if life support is removed, the patient will die.
39
Q

What is a minimally conscious state?

A
  • No ability to follow instruction or communicate
  • Appears to have awareness of surroundings

Minimal = only just passing = can do it, but can’t follow INSTRUCTIONs (maybe better…)

40
Q

What is a vegetative state?

A

Complete unawareness of the self and the environment — but seems to be awake.

Awake but not aware (like the microbiome of on a piece of brocolli)

41
Q

Locked in syndrome

A
  • Alert wakefulness
  • Inability to move or speak
42
Q

What is akinetic mutism?

A
  • Very infrequent movement or speech
  • Well preserved eye movements; can speak or move occasionally if directed
43
Q

What is the role of the hypothalamus in the baroreceptor response to low BP?

A

Stimulates vasopressin release -> fluid retention -> increase BP

44
Q

Define syncope

A

Sudden, transient loss of consciousness due to cerebral hypoperfusion

45
Q

List some different causes of syncope by category

A
  • Reflex (e.g. vasovagal)
  • Cardiac (e.g. structural heart disease, arrhythmia)
  • Neurologic (e.g. CVA)
  • Psychogenic (e.g. anxiety)
  • Other (e.g. anaemia)

PRNC= Prank = Face syncope = first cause in acronym

46
Q

Which type of syncope has the worst prognosis

A

Cardiac origin (e.g. arrhythmia, structural heart disease)

47
Q

Vasovagal syncope mechanism

A
  • Higher cortical sites trigger exaggerated sympathetic activity
  • Followed by increased parasympathetic tone
  • Bradycardia, dilation of blood vessels
  • Cerebral hypoperfusion -> syncope
48
Q

Vasodepressor vs cardioinhibitory vasovagal syncope

A

Vasodepressor: loss of arterial blood pressure

Cardioinhibitory: Bradycardia/asystole

(In most vasovagals, both are involved)

49
Q

Prodromal symptoms of vasovagal syncope

A
  • Sweating
  • Dizziness
  • Epigastric discomfort
  • Nausea
50
Q

Describe the mech of how increased intrathoracic pressure can cause situational syncope

A
  • Increased ITP
  • Vena cava compression
  • Decreased venous return
  • Decreased intra-aoritc pressure (baroreceptors)
  • SNS activation
  • When pressure released: increased PNS activation
  • Bradycardia
  • Cerebral perfusion down
  • Bye bye
51
Q

Is orthostatic hypotension/syncope associated with increased vagal response?

A
  • No
  • Rather, an insufficient baroreceptor-mediated sympathetic response to standing
52
Q

Why are older adults at increased risk of orthostatic syncope?

A
  • Decreased baroreceptor responsiveness
  • Polypharmacy
53
Q

What are some reasons why pregnancy can increase likelihood of syncope?

A
  • Progesterone lowers BP
  • Dehydration (e.g. morning sickness)
  • Iron deficiency anaemia
54
Q

Can hypoglycaemia cause syncope?

A
  • Not often — only in old patients on glucose-lowering drugs for diabetes.
  • It mimics syncope, but does not have to have cerebral hypoperfusion
55
Q

True or false: hyoglycaemic crisis causes no change (or an increase) of postural tone

A

True

56
Q

True or false: syncope in the presence of cardiac cause is more sinister than vasovagal syncope

A

True. Not good.

57
Q

Syncope red flags

A
  • Occurs during exercise
  • Pupils aren’t equal in size
  • Precipitated by severe headache
  • Double vision
  • Back/abdo pain (aortic dissection)
58
Q

Explain how raised ICP can cause a vicious cycle

A

Raised ICP -> Lowered CPP -> Hypoxia -> Oedema -> raised ICP -> death

59
Q

Investigations for a comatose patient

A
  • EUC/LFT, glucose, creatinine
  • ABG, CRX, ECG (if o2 concerns)
  • Lumbar puncture (exclude meningitis)
  • Toxicology (?Alcohol/drugs)
  • CT/MRI
60
Q

Other than brain masses/lesions/infections, what are some other causes of coma?

A
  • Organ failure
  • Epilepsy
  • Psychogenic
  • Metabolic
61
Q

Patient has focal neuro dysfunction, progression, localising deficit, and coma. Is the lesion supra or infratentorial?

A

Supratentorial

62
Q

Patient has immediate coma, pupil/occulomotor/respiratory abnormality. Is the lesion supra or infratentorial?

A

Infra

63
Q

Delirium associated with a coma, and seizures. What is the common cause?

A

Metabolic

64
Q

Describe treatment of patient with coma

A
  • ABC (Airway, breathing, circulation)
  • Get to scanner as fast as possible
  • If structural: neurosurg registrar. If metabolic: medical registrar.

(Basically: keep them alive, work out what’s wrong, then find who can fix it)