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BAB > Arousal, coma and unconsciousness > Flashcards

Arousal, coma and unconsciousness Flashcards

1
Q

What is a focal head injury?

A

Confined to one area of the brain, usually as a result of a severe blow to the head or a fall.
May have damaged skin, bone or brain. Consider the size and any penetration

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2
Q

What is a diffuse head injury?

A

Widespread damage to the white matter of the brain cause by a high acceleration-deceleration injury. It creates a loss of interface between the white and grey matter and vessels. Patient is usually unconscious and there is a high risk of death.

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3
Q

How can a primary injury lead to deterioration?

A

A primary injury may cause subsequent pathological changes, such as swelling, that cause a secondary injury.

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4
Q

How is a secondary injury identified?

A

Deterioration is detected by a falling conscious level, monitored frequently by GCS.

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5
Q

What is a main cause of secondary injury after a head trauma?

A

Ischaemic injury from insufficient blood supply. BP will fall due to bleeding and ICP will rise due to swelling and CPP will fall causing ischaemia.

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6
Q

What is arousal?

A

A state of wakefulness

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7
Q

What is consciousness?

A

Aroused and content, aware of self and environment with motor responses to internal and external stimuli.

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8
Q

What is the definition of a coma?

A

Total absence of awareness of self or environment. Impairment of arousal with the inability to obey commands, speak or open eyes.

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9
Q

How is the level of consciousness or severity of coma measured?

A

GCS

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10
Q

What GCS score defines a coma?

A

<9 out of 15

Lowest score is 3 even if dead

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11
Q

What are three aspects of GCS?

A

Eye opening
Best verbal response
Best motor response

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12
Q

What is the scale of eye opening?

A

Spontaneous - 4
To speech - 3
To pain - 2
None - 1

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13
Q

What is the scale of best verbal response?

A 
Orientated - 5
Confused - 4
Inappropriate - 3
Incomprehensible sounds - 2
None - 1
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14
Q

What is the scale for best motor response?

A 
Obey commands - 6
Localises to pain - 5
Flexion to pain - 4
Abnormal flexion - 3 (distal extension)
Abnormal Extension - 2
None - 1
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15
Q

What determines arousal and awareness?

A

An intact RAS in the brainstem

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16
Q

What determines cogniton and consciousness?

A

Cerebral cortex

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17
Q

What injury will result in a coma?

A

Impairment of both cerebral hemispheres and/or brainstem affecting RAS

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18
Q

How do head injuries usually start and what can this lead to?

A

Usually start at the top and work their way down so there is a risk of herniation or swelling progressing down to the brainstem

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19
Q

Where is RAS located?

A

Pontine-medullary region of the brainstem

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20
Q

How do the neurons from RAS ascend?

A

Ascend towards the cortex to influence cortical activity

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21
Q

When does an event become conscious?

A

Once it reaches the cortex

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22
Q

What is the main component of RAS?

A

The central tegmental tract - It receives information form the surrounding neural structures and conveys through multineuronal, polysynaptic pathways to the hypothalamus and thalamus and onto the cortex

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23
Q

Where does the central tegmental tract extend to?

A

From the caudal medulla to rostral midbrain.

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24
Q

What causes cortical feedback to modulate RAS?

A

Information from brainstem nuclei and descending cortical signals act on reticular neurons.

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25
Q

Which nuclei is involved in providing RAS with input regarding postural status?

A

Vestibular nuclei

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26
Q

Other than postural status, what other factor causes an arousal effect?

A

Ascending pain pathways

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27
Q

What problems may arise alongside a lesion to RAS and what signs are associated with this?

A

Adjacent nuclei may also be affected, impacting respiration, CVS and visceral sensory and motor. A coma is therefor associated with disturbances of respiration, pulse, BP and CN function

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28
Q

What 3 locations does RAS project to?

A
  • To midline nuclei of thalamus an onto cortex
  • To thalamic neurons that have focal projections to the cortex to regulate thalamocortical transmission
  • To thalamic reticular nucleus to regulate thalamocortical relay in a -ve feedback to prevent over excitement.
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29
Q

Where is the thalamic reticular nucleus?

A

A thin sheet of neurons that envelops the thalamus and projects onto thalamic neurons.

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30
Q

Where is a stroke most likely to occur?

A

In the internal capsule.

31
Q

How will symptoms of a stroke present?

A

On the contralateral affecting motor and sensory areas of the homunculus.

32
Q

Which arteries supply the internal capsule and why do they make the area vulnerable to a stroke?

A

Supplied by perforating branches of the middle and anterior cerebral A. The branches are small making them more vulnerable to an ischaemic stroke when blocked by a clot.

33
Q

Why can large areas of the cortex be damaged without causing a coma?

A

The areas involved in alertness and self awareness are widespread in the cortex, unlike motor and sensory which are confined to localised areas. Whilst alertness is impaired, cognitive damage may rise e.g. stroke.

34
Q

Why is the GCS preferred to altered states of consciousness?

A

The descriptions are interpretive where are the GCS is definitive.

35
Q

What is acute clouding of consciousness?

A

Lack of attention, slow thinking, confusion, memory loss and drowsy

36
Q

What is delirium?

A

Disorientation and hallucination

37
Q

What is stupor?

A

Sleep like state that requires vigorous stimulation for arousal

38
Q

What are the effects of dementia?

A

Impaired mental function, memory, comprehension and speech

39
Q

What is hypersomnia?

A

Excessive drowsiness with intermittent waking

40
Q

What is a vegetative state?

A

Awake with no evidence of conscious cognitive ability.

41
Q

What 5 things may cause a coma?

A
  • Diffuse brain dysfunction from lesions
  • Supratentorial mass lesion causing brainstem compression
  • Infratentorial lesion causing brain stem compression
  • Intrinsic lesion of brainstem
  • psychiatric states the mimic comatosed state
42
Q

If a pt presents with pupillary signs, where is the site of lesion?

A

Diffuse brain dysfunction

43
Q

If a pt presents with oculocephalic and oculovestibular signs, where is the site of lesion?

A

Supratentorial lesion (Uncal herniation or lobe displacement)

44
Q

If a pt presents with motor response to painful stimulus, where is the site of lesion?

A

Tentorial herniation

45
Q

If a pt presents with altered respiratory pattern, where is the site of lesion?

A

Infratentorial lesion (brain stem glioma)

46
Q

Why is GCS plotted over time and why is important to know the time of when the injury occured?

A

To detect any deterioration due to a secondary injury. Need a starting point of consciousness as some Pts can be unconscious as time of injury and then have a lucid period.

47
Q

Where do signs present with damage occur with a blow to the motor cortex?

A

On the contralateral side to the brain damage. But there is asymmetry between the effects on the body and eyes.

48
Q

What problem arises from a raised ICP?

A

Herniation through tentorial notch

49
Q

What does a herniation result in?

A

Compresses CN III

50
Q

What sign presents with compression of CN III?

A

Fixed dilated pupils on the ipsilateral side to the compression due to compression of the parasympathetic fibres.

51
Q

Why does compression of CN III result in dilation and not constriction?

A

The occulomotor nerve only carries parasympathetic fibres, so when damaged the sympathetic fibres produce an opposing and dominating effect of dilation

52
Q

When will fixed constriction occur?

A

Caused by damage to the sympathetic supply to the radial muscle, resulting in an opposing and dominating constricting effect from the parasympathetic fibres. The sympathetic fibres run with the opthalamic N (V1)

53
Q

What sign helps to distinguish between a metabolic and structural coma?

A

The light reflex. Only a few metabolic causes result in fixed dilated pupil - anoxic encephalopathy,anticholingerics, botulism.
Apart from these, the pupils will have been affected by a structural damage.

54
Q

What do fixed dilated pupils usually signify?

A

Death

55
Q

What is the function of cortico bulbar fibres and where do they arise?

A

The occipital and parietal lobes give rise to the fibres to the brain stem nuclei II, IV, VI for slow movement to allow locking onto an object without falling over.

56
Q

What allows rapid movements of the eye?

A

Voluntary control of frontal gaze centre allows it to occur alongside cortiobulbar influence for repositioning of body. So the eyes move at the same time as the head.

57
Q

What happens to movement of the eyes if the cortex is damaged?

A

Cortical influence is lost so the eyes don’t move with the head.

58
Q

When cortical influence is lost, how can the integrity of the brainstem be tested?

A

Via the reflexes of the eye movements

59
Q

What are the reflexes of the eye?

A

Oculocephalic reflex - If the head is rotated to one side and the eyes then rotate to the new position slowly, the brainstem is intact.
Oculovestibular reflex - Cooling of the tympanic membrane with saline causes a slow deviation to the cooling side and then a fast response to the opposite if the brainstem is intact. If damage is present there is tonic deviation to the cooled side.

60
Q

What type of damage is signified by abnormal flexion / distal extension?

A

Hemispheric dysfunction

61
Q

What type of damage is signified by abnormal extension?

A

Cerebrum or upper brainstem

62
Q

What damage is signified by no motor response?

A

Pontine medullary

63
Q

What allows override of autonomic respiration for voluntary speaking?

A

Cortiospinal anterior cells

64
Q

What controls autonomic respiration?

A

Blood gas homeostasis via NTS which sends signals via reticulospinal tract to respiratory muscles

65
Q

What is locked-in syndrome?

A

Lesion of corticospinal tract causing the pt to lose voluntary control of breathing

66
Q

What is Ondine’s curse?

A

Can only breathe voluntarily so whilst sleeping they may hypoventilate or stop.

67
Q

What effect on breathing results from damage to forebrain?

A

Increased sensitivity to CO2 with regular waxing and waning of respiration (Cheyne strokes) - inspiration increases and then falls and becomes silent

68
Q

What effect on breathing results from damage to midbrain?

A

Hyperventilation

69
Q

What effect on breathing results from damage to pontine?

A

Prolonged inspiration

70
Q

What effect on breathing results from damage to medulla?

A

Slowing and shallowing respiration due to IX, X, XI nuclei damage

71
Q

How does an extradural haematoma present and why?

A

Fracture of the pterion ruptures middle meningeal A. Unconcious at time of event but then have a lucid period before collapsing again. The bleed compresses the brain and shifts the midline structures.

72
Q

What causes diffuse brain dysfunction?

A

drugs, toxins, epilepsy, subarachnoid haemorrhage, metabolic disorder. Primary injury causes a secondary injury due to increased ICP and herniation

73
Q

What causes a cerebral mass lesion?

A

Vascular infact, infection, tumour, trauma

74
Q

Why does ICP rise?

A

The cerebral blood flow is limited. CPP falls and causes hypertension, bradycardia and respiratory irregularity.

BAB (11 decks)

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