Brain injury

Question 1

define tbi

Answer 1

insult to the brain involving an external force that leads to an impairment in functioning for brief or sustained period

Question 2

2 main types of injury

Answer 2

open head & closed head

Question 3

2 brain injury mechanisms

Answer 3

1) cerebral contusions

2) diffuse axonal injury

Question 4

cerebral contusions

Answer 4

bruising found at SITE of impact

on gyri

Question 5

Diffuse axonal injury

Answer 5

when forces are great enough - shearing force
severing of axons - disables communication
death & swelling
herniation

Question 6

recovery from TBI (2)

Answer 6

reorganisation of neural structures

restoration of function

Question 7

Reorganisation of neural structure

Answer 7

plasticity –> reorganisation can occor within remaining circuits
constant competition of cortical space allows for plasticity

Question 8

mechanisms of neural reorganisation

Answer 8

a) strengthening of existing neural connections due to lack of inhibition
b) establishment of new connections by collateral sprouting

Question 9

behavioural compensation

Answer 9

Improved ability on a task does not necessarily reflect reorganisation of the brain — individuals may develop new strategies to perform the task i.e., they adapt

Question 10

Potential motor deficits after TBI

Answer 10

• Weakness or paralysis
  
  • Ataxia (uncoordinated body movements)
  • Balance problems
  • Dysarthria (slurred speech)
  • Dysphagia (swallowing problems)

Question 11

Potential sensory deficits after tbi

Answer 11

blindness

eye movement

Question 12

prospopagnosia

Answer 12

inability to recognise familiar faces

separate neural mech compared with object recognition

Question 13

Alzheimers - what?

Answer 13

most common cause of dementia

Question 14

early stages of alzheimers (3)

Answer 14

selective decline in memory
personality changes
lack of energy

Question 15

mid stages of alzheimers (3)

Answer 15

confusion
anxiety
deterioration of speech

Question 16

latter stages of alzheimers (3)

Answer 16

dependent
no longer recognise family/friends
occasionally hallucinations

Question 17

pathological features (3)

Answer 17

1) shrinkage of the brain
2) senile plaques (out on the neuron & made of lumps of protein - beta amyloid)
3) Neurofibrillary tangles (in the neuron)

Question 18

What protein constitutes to senile plaques?

Answer 18

beta amyloid

Question 19

amyloid cascade theory

Answer 19

beta amyloid precursor protein extends outside cell
secretase cute the app
product = beta amyloid
(40 amino acids = not a prob
42 amino acids = cluster to form toxic plaques)

Question 20

neurofibrillary tangles theory

Answer 20

Tau normally stabilises internal tubes for nutrients to pass through
In alz Tau separates from these tubes causing degen
stands combine to form tangles
As neurons disconnect & die - memory loss

Question 21

5 risk factors for AD

Answer 21

1) being female (hormones)
2) being older
3) having fewer years of education (cognitive reserve)
4) trauma
5) Family history (genetics)

Question 22

what gene is associated with developing LATE onset AD?

Answer 22

Apolipoprotein E Gene

Question 23

How many forms of ApoE is there & what are they involved with

Answer 23

ApoE -2: rare allele involved w protection against AD
ApoE - 3: Common allele - plays neutral role
ApoE-4: INCREASES RISK OF LATE AD

Question 24

The allele which increases risk of AD, how?

Answer 24

less efficient elimination of Beta Amyloid

Question 25

MCI

Answer 25

Mild cognitive impairment: occurs before dementia

Those with ApoE-4 show poorer performance than carriers & non carriers

Question 26

Evaluation of ApoE-4

Answer 26

NOT A NECESSARY GENE FOR DEVELOPMENT
May be mediated by other genetics/enviro
African americans arent affected by it

Question 27

Bennett et al 2003

Answer 27

no correlation between education & number of plaques & tangles
BUT there is between education & their performance on cog tests EVEN IN PRESENCE OF PLAQUES
(in long term educated) 5 x more plaques & tangles needed to show same amount of degeneration