Week Two - Neuropsychology Flashcards

1
Q

How is theory tested in Neuropsychology?

A

Experiment or accidental injury/incident - testing - theory - application - revision - back to start

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2
Q

Two pathologies of Alzheimer’s Disease?

A
Amyloid plaques
Tau tangles (neurofibrillary)
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3
Q

Early-onset AD vs Late-onset % and reasoning?

A

1% EO - likely genetic causes, including genes

99% LO - varied reasons and multifactorial (currently unclear)

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4
Q

What is the Amyloid Hypothesis?

What is the general outcome/aim?

A

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.

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5
Q

% of AD research on Amyloid Hypothesis?

A

70-80% of AD drug research has focused on this reduction of amyloid plaque.

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6
Q

Amyloid Hypothesis drug results?

A

126 AD drugs (40% were amyloid) - no drugs showed any impact. Some argue that the AH is not right.

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7
Q

Criticisms of Amyloid Hypothesis?

A

Based on EO AD (only 1%).
High plaques does not equal AD and vice versa.
Cause rather than consequence.

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8
Q

Arguments for Amyloid Hypothesis?

A

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

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9
Q

What is a Traumatic Brain Injury (TBI)?

A

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

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10
Q

2 types of TBI?

A

Closed head injury

Penetrative head injury

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11
Q

What is a concussion?

A

Temporary unconsciousness or confusion and other symptoms caused by a blow on the head - This is a mild TBI.

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12
Q

Closed Head Injury?

A

Non-penetrative blow to the head.

MVA, assaults, falls, sports etc.

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13
Q

Brain damage in TBI typically occurs in what 2 stages?

A

Primary Injury

Secondary Injury

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14
Q

Primary Injury?

A

Damage occurring at the time of impact - bleeding, diffuse axonal injury, coup/contrecoup damage

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15
Q

Secondary Injury?

A

Secondary effects of physiological processes initiated by the primary injury - oedema (fluid), intracranial pressure, necrotic and apoptotic cell death

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16
Q

Three indicators of TBI severity?

A
  1. Length of loss of consciousness
  2. Depth of coma, measured by GCS
  3. Length of post-traumatic amnesia (PTA)
17
Q

What is the Glasgow Coma Scale (GCS)?

A

Assesses the level of consciousness (depth of coma) at a given time following injury

18
Q

GCS scores?

A
Mild = 14-15
Moderate = 9-13
Severe = 3-8
19
Q

What is Post Traumatic Amnesia?

A

Length of time following TBI in which the person is incapable of learning new information and remains confused/disoriented

20
Q

PTA Duration times?

A
<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
21
Q

Theoretical debates regarding consciousness?

A

Consciousness vs Responsiveness (eg locked-in syndrome vs minimally conscious state - veg state). Actually measuring responsiveness when measuring consciousness.

Length vs depth

22
Q

Second Impact Syndrome?

A

a 2nd concussion while still experiencing post-concussion symptoms - can lead to a fatal response and increased oedema and intracranial pressure

23
Q

Criticisms of SIS?

A

Still a hypothetical diagnosis
Incidence rate is small
Symptoms overlap with other disorders

24
Q

How can we use theory to predict outcome of concussion/TBI?

A
Initial severity (eg mild)
Performance on neuropsych measures
Premorbid characteristics

BUT prediction is still poor

25
Q

How can we use theory to predict who will recover?

A

Cognitive/neural reserve theory

Coping theory

26
Q

Combination of what 3 things to predict outcome and recovery?

A

Neurological, psychological and sociocultural

e.g., Pleiotropy, Learning Theory and Te Whare Tapa Wha