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Neuropsychology > Traumatic Head Injury > Flashcards

Traumatic Head Injury Flashcards

1
Q

Pathophysiology of traumatic brain injuries

A

Often no visible scars, it is the physical force placed on the neuron.

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2
Q

Axonal tensile strength

A

The extent to which a neuron can take stress before the axon is damaged

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3
Q

What is resprouting?

A

The healing process of the brain

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4
Q

Epidemiology: technology

A
  • rise of technology has led to an increase in brain injuries
  • cars put us at greater risk and the extent of the injuries are worse
  • there is an improved understanding of TBIs due to rise in technology
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5
Q

Ratio of mild/moderate/severe TBIs

A

70/20/5

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6
Q

Three domains of the Glasgow Coma Scale

A
  1. Language
  2. Consciousness
  3. Motor functioning

(Mild deficits: greater than 13. Severe: less than 5)
Also you can get a score of 3 if you’re dead.

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7
Q

Pros and Cons of the GCS

A

+ it’s universal, which is very useful

- it’s hugely time sensitive, you can have a change in score within five minutes

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8
Q

6 main complications with TBIs

A
  1. Edema
  2. Brain herniation
  3. Extradural and subdural hemorrhaging
  4. Intracranial bleeding
  5. Skull fractures
  6. Post traumatic epilepsy
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9
Q

Edema

A

The swelling of the brain, which can be dangerous due to the fixed nature of the skull

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10
Q

Brain herniation

A

Shift of the brain, movement into a smaller space or a different orientation

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11
Q

Extradural and subdural hemorrhaging

A

A loss of blood or added intercranial pressure

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12
Q

Intracranial bleeding

A

Particularly difficult to stop if the arteries are deep within the brain

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13
Q

Post traumatic epilepsy

A

Could be caused by the addd pressure on the brain or the brain trying to autocorrect for the damages caused.

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14
Q

Neuropsychological outcomes (6 prominent areas of deficits)

A
  1. Amnesia
  2. Memory
  3. Attention
  4. Inhibition
  5. Vision
  6. Motor
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15
Q

Coup counter coup effect

A

Nature of most TBIs, it refers to the way in which the brain hits the front of the skull and then naturally bounces and hits the back of the skull

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16
Q

Education and recovery

A

Individuals who have had an education have more built in adaptive responses, which allows for improved recovery

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17
Q

Considerations for recovery of TBIs (10)

A
  1. Location and extent of damage
  2. Time since injury
  3. Age (plasticity)
  4. Premorbid intelligence
  5. Premorbid personality
  6. Premorbid functioning
  7. Medical health
  8. Emotional health
  9. Support system
  10. Type of treatment
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18
Q

Natural recovery

A
  • Diaschisis

- Plasticity

19
Q

Diaschisis

A

Synaptic pruning of the damaged cells

20
Q

Plasticity

A
  • Axonal sprouting

- Denervation super-sensitivity (the neurons compensate for the damage by becoming super sensitive)

21
Q

Three main methods of recovery

A

Natural, cognitive training and psychotherapy

22
Q

Cognitive training for TBIs

A

Managing and compensating for new deficits

23
Q

Psychotherapy for TBIs

A

Helping people to understand and accept their deficits

24
Q

Concussions vs mild TBIs

A

Concussions are not mild, they can cause a great deal of damage
Also, mild TBIs damage structure and function, concussions affect function only.

25
Q

Five core properties of concussions

A
  1. Caused by a knock to the head or body
  2. Swift onset of short term impairment
  3. Functional injury
  4. Clinical symptoms (cognitive, emotional, physical and sleep)
  5. Normal gross imaging reports
26
Q

Epidemiology of concussions in sports

A

6,2% of all sport injuries in the US.

27
Q

Collision vs contact sport

A

Collision: actively running into other players
Contact: potential to make contact

28
Q

Pathophysiology of concussions

A

Transmission of biomedical forces to the brain

29
Q

Physical symptoms of concussion: (6)

A
  • Nausea
  • Headache
  • Balance
  • Photosensitivity
  • Loss of consciousness
  • Blurred vision
30
Q

Outcomes of concussion: sleep (4)

A
  • Insomnia
  • Excessive fatigue
  • Restless sleep
  • Difficulty waking up
31
Q

Outcomes of concussion: emotional (3)

A
  • Depression
  • Anger/irritability
  • Anxiety
    (But it can be difficult to determine if this is as a result of the concussion or it is because athletes cannot play)
32
Q

Outcome of concussion: cognitive (3)

A
  • Executive functioning
  • Verbal memory
  • Visuospatial
33
Q

Role of impact location on outcomes

A

None!

34
Q

Three step assessment process for concussions

A
  1. Side line evaluation
  2. Medical evaluation
  3. Neuropsychological testing
35
Q

Side line evaluation

A

Usually the SCAT-3, which must be administered by a medical professional

36
Q

Medical evaluation

A

Generally a scan, if the scan comes back clear then it’s usually a concussion

37
Q

Neuropsychological testing

A

Pen and paper tests OR
the ImPACT: immediate post concussion assessment and cognitive test. You need to score at least two standard deviations below your baseline score to fail. (Often athletes bomb their baseline test so that they can keep playing when injured)

38
Q

Rest treatment

A

Physical: no activity that increases your heartbeat
Cognitive: minimal phone, tv, reading etc

39
Q

Problems with rest treatment (concerning BDNF)

A

Rest treatment may cause atrophy, bc the brain isn’t being used. BDNF is a hormone that promotes neuronal activity but is only released when people exercise.

40
Q

Chronic outcomes of concussions

A
  1. Post-concussion syndrome

2. Chronic traumatic encephalopathy

41
Q

Post concussion syndrome description

A
  • Delayed recovery, symptoms usually last between 10 days and 3 weeks (athletes vs normies)
42
Q

Chronic traumatic encephalopathy

A
  • “Punch drunk”
  • Associated with repeated trauma to the brain
  • Requires one perivascular ptau lesion
43
Q

Four stages of CTE

A
  1. 1-2 tangles in sulci in the frontal, temporal or parietal lobes
  2. 3 or more tangles in multiple lobes
  3. Tangles in the subsections
  4. Tangles everywhere
    (Its neurodegenerative, it will worsen)
44
Q

Debate around CTE

A

There are no set diagnostic criteria, so it’s not clear if it is a distinct pathology or just the early onset of already existing neurodegenerative diseases that are exacerbated by the repeated trauma. Also, why doesn’t it affect all sports players? Does it have a genetic component?

Neuropsychology (17 decks)

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