Week Two - Neuropsychology Flashcards
How is theory tested in Neuropsychology?
Experiment or accidental injury/incident - testing - theory - application - revision - back to start
Two pathologies of Alzheimer’s Disease?
Amyloid plaques Tau tangles (neurofibrillary)
Early-onset AD vs Late-onset % and reasoning?
1% EO - likely genetic causes, including genes
99% LO - varied reasons and multifactorial (currently unclear)
What is the Amyloid Hypothesis?
What is the general outcome/aim?
The main idea is that AD is caused by the accumulation of amyloid deposits.
If we can stop the production of these in the brain, we can slow/stop people from developing AD and its symptoms.
% of AD research on Amyloid Hypothesis?
70-80% of AD drug research has focused on this reduction of amyloid plaque.
Amyloid Hypothesis drug results?
126 AD drugs (40% were amyloid) - no drugs showed any impact. Some argue that the AH is not right.
Criticisms of Amyloid Hypothesis?
Based on EO AD (only 1%).
High plaques does not equal AD and vice versa.
Cause rather than consequence.
Arguments for Amyloid Hypothesis?
Healthy people can show plaques (i.e., they could be in the early stages of AD)
Amyloid can increase Tau tangles (therefore a causal factor in AD potentially)
Interventions are often given too late so hard to know true effects
What is a Traumatic Brain Injury (TBI)?
An insult to the brain caused by an external force that may result in diminished or altered states of consciousness - resulting in impacted cognitive abilities and physical functioning
2 types of TBI?
Closed head injury
Penetrative head injury
What is a concussion?
Temporary unconsciousness or confusion and other symptoms caused by a blow on the head - This is a mild TBI.
Closed Head Injury?
Non-penetrative blow to the head.
MVA, assaults, falls, sports etc.
Brain damage in TBI typically occurs in what 2 stages?
Primary Injury
Secondary Injury
Primary Injury?
Damage occurring at the time of impact - bleeding, diffuse axonal injury, coup/contrecoup damage
Secondary Injury?
Secondary effects of physiological processes initiated by the primary injury - oedema (fluid), intracranial pressure, necrotic and apoptotic cell death
Three indicators of TBI severity?
- Length of loss of consciousness
- Depth of coma, measured by GCS
- Length of post-traumatic amnesia (PTA)
What is the Glasgow Coma Scale (GCS)?
Assesses the level of consciousness (depth of coma) at a given time following injury
GCS scores?
Mild = 14-15 Moderate = 9-13 Severe = 3-8
What is Post Traumatic Amnesia?
Length of time following TBI in which the person is incapable of learning new information and remains confused/disoriented
PTA Duration times?
<5 mins = Very mild 5-60 mins = Mild 1-24 hr = Moderate 1-7 days = Severe 1-4 weeks = Very severe >4 weeks = Extremely severe
Theoretical debates regarding consciousness?
Consciousness vs Responsiveness (eg locked-in syndrome vs minimally conscious state - veg state). Actually measuring responsiveness when measuring consciousness.
Length vs depth
Second Impact Syndrome?
a 2nd concussion while still experiencing post-concussion symptoms - can lead to a fatal response and increased oedema and intracranial pressure
Criticisms of SIS?
Still a hypothetical diagnosis
Incidence rate is small
Symptoms overlap with other disorders
How can we use theory to predict outcome of concussion/TBI?
Initial severity (eg mild) Performance on neuropsych measures Premorbid characteristics
BUT prediction is still poor
How can we use theory to predict who will recover?
Cognitive/neural reserve theory
Coping theory
Combination of what 3 things to predict outcome and recovery?
Neurological, psychological and sociocultural
e.g., Pleiotropy, Learning Theory and Te Whare Tapa Wha
