Brain injury Flashcards
define tbi
insult to the brain involving an external force that leads to an impairment in functioning for brief or sustained period
2 main types of injury
open head & closed head
2 brain injury mechanisms
1) cerebral contusions
2) diffuse axonal injury
cerebral contusions
bruising found at SITE of impact
on gyri
Diffuse axonal injury
when forces are great enough - shearing force
severing of axons - disables communication
death & swelling
herniation
recovery from TBI (2)
reorganisation of neural structures
restoration of function
Reorganisation of neural structure
plasticity –> reorganisation can occor within remaining circuits
constant competition of cortical space allows for plasticity
mechanisms of neural reorganisation
a) strengthening of existing neural connections due to lack of inhibition
b) establishment of new connections by collateral sprouting
behavioural compensation
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
Potential motor deficits after TBI
- Weakness or paralysis
- Ataxia (uncoordinated body movements)
- Balance problems
- Dysarthria (slurred speech)
- Dysphagia (swallowing problems)
Potential sensory deficits after tbi
blindness
eye movement
prospopagnosia
inability to recognise familiar faces
separate neural mech compared with object recognition
Alzheimers - what?
most common cause of dementia
early stages of alzheimers (3)
selective decline in memory
personality changes
lack of energy
mid stages of alzheimers (3)
confusion
anxiety
deterioration of speech
latter stages of alzheimers (3)
dependent
no longer recognise family/friends
occasionally hallucinations
pathological features (3)
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)
What protein constitutes to senile plaques?
beta amyloid
amyloid cascade theory
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)
neurofibrillary tangles theory
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
5 risk factors for AD
1) being female (hormones)
2) being older
3) having fewer years of education (cognitive reserve)
4) trauma
5) Family history (genetics)
what gene is associated with developing LATE onset AD?
Apolipoprotein E Gene
How many forms of ApoE is there & what are they involved with
ApoE -2: rare allele involved w protection against AD
ApoE - 3: Common allele - plays neutral role
ApoE-4: INCREASES RISK OF LATE AD
The allele which increases risk of AD, how?
less efficient elimination of Beta Amyloid
