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PSY325 - Neuropsychology & Clinical Neuroscience > Week Three - Traumatic Brain Injury & Cerebrovascular Disorders > Flashcards

Week Three - Traumatic Brain Injury & Cerebrovascular Disorders Flashcards

1
Q

The brain represents what % of total body weight?

A

2%

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2
Q

How much % of normal cardiac output does the brain use?

A

15%

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3
Q

How much of the body’s oxygen consumption does the brain need?

A

25%

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4
Q

When oxygen is cut from the brain, how long do we have before irreversible damage occurs?

A

2-3 minutes

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5
Q

Where do arteries carry blood?

A

Away from heart to vital organs

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6
Q

Where do veins carry deoxygenated blood?

A

Back to the heart

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7
Q

What are the two pairs of arterial blood supply?

A

Internal carotid arteries

Vertebral arteries

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8
Q

What is the advantage of the circle of willis?

A

if a given artery is blocked, then other arteries can still supply blood to that area

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9
Q

What are the 3 main cerebral arteries in the brain?

A

Anterior
Posterior
Middle

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10
Q

What does the anterior cerebral artery supply to?

A

the medial, frontal, and parietal lobe

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11
Q

What does the middle cerebral artery supply to?

A

Most of the lateral surface of the cerebral hemisphere

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12
Q

What does the posterior cerebral artery supply to?

A

the medial of the occipital lobe and inferior temporal lobe

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13
Q

What is the circle of willis?

A

A joining area of several arteries at the bottom side of the brain

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14
Q

What do the posterior communication arteries allow? (2)

A

Allow joining of vertebral-basilar and carotid system.

Allows transfer of blood to the other side of brain by acting as a route of transmission

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15
Q

What is CVA?

A

Vascular disorder which results in brain injury

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16
Q

What is Ischaemia

A

Insufficient/lack of blood flow to the brain

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17
Q

What is Infaction?

A

Tissue death due to inadequate blood supply

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18
Q

What is Infarct?

A

Area of damaged or dead tissue from infarction

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19
Q

What is Penumbra?

A

Tissue surrounding infarct which may recover/die

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20
Q

What is Excitotoxicity?

A

Excess activity in glutamate signalling pathways resulting in death

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21
Q

What is Oedema?

A

Swelling of the brain

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22
Q

What are some signs of stroke?

A

weakness, numbness, paralyses
difficulty speaking
dizziness/balance issues
loss of vision

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23
Q

What are 5 factors involved in stroke recovery?

A 
The type of stroke
Size of blood vessel (larger = worse)
Remaining intact vessels (can help with supply)
Premorbid factors
Location of stroke
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24
Q

What are the 2 main types of stroke?

A 
Obstructive Stroke (ischaemic) 
Haemorrhagic Stroke
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25
Q

What is an Obstructive (ischaemic) stroke?

A

Where there is a reduction of blood flow or complete blockage of a blood vessel

Often due to fatty plaques

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26
Q

What is an Hemorrhagic stroke?

A

Results from bleeding into brain tissue (rupture of blood vessel)

Often due to weakening malformation in vessel wall (aneurysm)

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27
Q

What are Obstructive (ischaemic) stroke caused by? (2)

A
  1. Thrombosis (occlusion of blood vessel by a thrombosis)

2. Embolism (occlusion of blood vessel by embolism which has broken off from a thrombosis in a larger blood vessel)

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28
Q

How long does an obstructive stroke take to develop?

A

Can occur suddenly, often taking 30 min to full develop

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29
Q

what % show sig improvement in functioning following an OIS?

A

80%

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30
Q

What % remain significantly disabled?

A

50%

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31
Q

After an OIS, at what point are we unlikely to have further improvement?

A

3 months

32
Q

Where do most Thrombotic strokes occur?

A

In the internal carotid or vertebral-basilar arteries

33
Q

What are the signs of Thrombotic stroke?

A

Lateralised limb weakness and somatosensory changes as well as visuospatial (right) and language deficits (left)

34
Q

What effect do OIS strokes have on cog and behavioural factors?

A

Unilateral effects on function

Prominent acte effects (but become less prominent over time)

Signs of bilateral or diffuse damage in acute stages

35
Q

What are the unilateral effects in OIS?

A

Hemiparesis: weakness in vertical half of body
Hemiplegia: complete paralysis of vertical half of body
Aphasias: language disorder
Unilateral neglect (often right): failure to attend to space at the opposite side of lesions

often transient

36
Q

What is a TIA

A

An episode of temporary obstruction of a blood vessel lasting less than 24 hrs

37
Q

What are the two types of TIAs?

A

Those lasting >45 and show infarction

Those lasting <45 with no evidence of infarction

38
Q

What % of people will develop a full-blown stroke following a TIA?

A

30%

39
Q

What % of people will die following a Hemorrhagic stroke?

A

35-52% within the first 30 days

40
Q

Risk factors for Hemorrhagic stroke?

A

Hypertension/blood pressure (chief risk factor)

Chronic use of oral anticoagulants

Cocaine/alcohol use

41
Q

What are the two primary mechanisms that cause arterial haemorrhage?

A
  1. Weakening of a vessel due to pathological aberrations secondary to hypertension (77-88% of cases)
  2. Rupture associated with a vascular abnormality, such as aneurysm, AVM, tumour etc
42
Q

What is an aneurysm?

A

Weak area in an artery wall, causing it to balloon out

43
Q

Why do aneurysms occur?

A

May be due to:

  • congenital
  • born with it
  • trauma/infection
44
Q

The risk of having a ruptured aneurysm is more dependent on what?

A

The characteristics of the aneurysm as opposed to characteristics of the person

45
Q

Who are some people that have an increases risk of a ruptured artery?

A

Women and older people

46
Q

What two types of aneurysms increase the risk factor of a ruptured artery?

A

symptomatic aneurysm

basilar artery aneurysm

47
Q

Symptoms of ruptured aneurysm?

A

Severe headache (nausea/vomiting)

48
Q

The rupture of an aneurysm can be what?

A

Fatal with a 50% mortality rate in the first month

49
Q

Which blood vessels/brain areas are affected by hypertensive haemorrhages?

A

Blood vessels at the base of the cerebral hemisphere

mostly affect thalamus, BG and brainstem

50
Q

What are AVM’s?

A

Tangled masses of arteries and veins of congenital origin with grow gradually like a tumour - only 1% of strokes

51
Q

What is locked in syndrome?

A

A disorder frequently caused by ischemic or hemorrhagic stroke in the basilar artery

52
Q

What does locked in syndrome result in?

A

Loss of all motor function with the exception of eye movement

53
Q

What are the 2 types of head injury?

A

Closed head

Penetrative head

54
Q

What occurs in a Penetrative head injury

A

The skull is fractured, exposing the brain allowing the entry of foreign matter (eg gun shot)

55
Q

What is a closed head injury?

A

Non-penetrative blow to the head (assaults, falls, sorts)

56
Q

Brain damage in TBI typically occurs in what 2 stages?

A

Primary injury: Damage occurring at the time of impact

Secondary injury: Secondary effects of physiological processes initiated by the primary injury

57
Q

What is a predominant cause of damage in statis injuries?

A

Contact forces (force of impact)

58
Q

What is a static injury?

A

Where the head is still and receives a blow. There is an inward deformation of skull with outward deformation in adjected areas

59
Q

What are inertial forces?

A

Movement of the brain within the head as a result of acceleration or movement

60
Q

What are 3 types of inertial forces?

A

Translational: head moves in straight line with brain centre of gravity

Rotational: Brain rotates around centre of gravity

Angular: combination of translational and rotational forces)

61
Q

What can we categorise primary injuries as? (4)

A

Coup: site of initial impact

Contre-Coup: brain rebounds causing further damage

Diffuse Axonal: deceleration leading to damage (axons get torn, twisted and broken)

Intra-cranial Haemorrhage: torn blood vessels resulting in haematomas (epidural and subdural)

62
Q

What 3 haematomas are caused by intracranial haemorrhages?

A

epidural (EDH): between skull and dura matter, often due to contact injury

subdural (SDH): between dura matter and arachnoid membrane, often due to torn veins

intracerebral (ICH): frontal and temporal lobes (BG and cerebellum, often due to rupture of blood vessel

63
Q

What are some secondary changes following primary injury?

A 
swelling
cell death
ICP
hypoxia
BBB issues
infection
64
Q

Cerebral oedema types (2)

A
  1. Vasogenic: when damage to the brain leads to EXTRACELLULAR fluid
  2. Cytotoxic: when a neuron’s membrane pump fails, leading to increase INTRACELLULAR fluid
65
Q

What 2 processes occur when a cell dies?

A

Necrosis: passive death as a result of damage, within hours of injury. Leading to damage of surrounding cells

Apoptosis: programmed death as a result of damage, may take days. No damage to surrounding cells

66
Q

What are the 3 apoptotic stages?

A
  1. Cell shrinks
  2. Material is divided into vesicles
  3. Scavenger cells cleans up the debris
67
Q

What are the 3 indicators to how severe an injury is?

A

Loss of consciousness

Depth of coma (GCS)

Length of PTA

68
Q

What is post traumatic amnesia (PTA)?

A

A period of time following TBI in which the person is incapable of learning new information (remains confused/disoriented)

69
Q

What are some problems with estimating severity of TBI? (5)

A 
time of assessment
reliability of information
med interventions
drug/alcohol use
elderly
70
Q

Physiological problems following TBI? 5

A 
headaches
fatigue
dizziness
nausea
visual/auditory impairment
71
Q

Cognitive problems following TBI? 4

A

Attention/concentration
Processing speed
Memory
EF

72
Q

Emotional/behavioural problems following TBI? (5 - emotion)

A 
lack of emotional control
emotional lability
emotional blunting
lack of emotional awareness
disinhibition
73
Q

Psychosocial problems following TBI?

A

relationships - increased strain
work - reduced capacity
social activity

74
Q

Clinical problems following TBI?

A

depression
anxiety
PD
PTSD

75
Q

How do we predict outcomes of TBI? 3

A

severity
performance on measures
premorbid characteristics

PSY325 - Neuropsychology & Clinical Neuroscience (12 decks)

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