Week 2 - Neuropsychology Flashcards

1
Q

What is the process of utilising accidental injuries/insults for neuropsychological research?

A

Experimental or accidental injury/insult

Testing

Theory

Application/further evidence

Revision

Repeat

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2
Q

What are the two pathological signs of alzheimers?

A

Amyloid (A-Beta) Plaques

Tau (neurofibrillary) tangles

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3
Q

What causes early onset Alzheimer’s?

A

Largely genetic causes

Genes associated with increased plaque deposits

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4
Q

What causes late onset alzheimers?

A

Cause likely to be varied and multifactorial, but currently unclear

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5
Q

What is the amyloid hypothesis?

A

AD is caused by a build up of amyloid deposits

If we can stop the brain from producing as many plaques, we can stop people developing AD or at least reduce/slow symptoms

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6
Q

How much drug research has been dedicated to amyloid plaque reduction?

A

70-80%

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7
Q

What are the criticisms of the amyloid hypothesis?

A

Some people with high plaque loads don’t get AD, and some people with AD don’t have high plaque loads

Preclinical testing (eg animal and cell studies) create high amyloid deposits, then presume that is a good model of AD

Cause vs consequence - does cough mixture cure a cold? amyloid plaques could just be part of a protective response the brain is having

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8
Q

Amyloid can increase…

A

Tau tangles

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9
Q

What are the arguments for the amyloid hypothesis?

A

Identification of gene variants that have been demonstrated to cause amyloid build-up in all the early onset AD cases

While some healthy people have plaques, they could be in the prodromal stages of AD

Amyloid can increase tau tangles

Some drugs have been shown to not do what we thought it did… so not actually impacting on amyloid plaques

Interventions have been given too late - people already have the disease after years of being in pre-clinical/prodromal phase

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10
Q

What factors may cause us to keep researching a questionable theory, especially when no other theory is available?

A

Social and financial factors

Lack of research into new theories

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11
Q

What is a closed head injury?

A

Non-penetrative blow to the head. Common causes include MVA, assaults, falls and sports. Can also be percussive (eg blast injuries)

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12
Q

What are the two stages that occur when somebody gets brain damage in TBI?

A

Primary injury

Secondary injury

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13
Q

What is a primary injury?

A

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

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14
Q

What is a secondary injury?

A

Secondary effects the physiological processes initiated by the primary injury - oedema, intracranial pressure, necrotic and apoptotic cell death etc

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15
Q

What are the three key indicators that are used to determine how severe a TBI is?

A

Length of Loss of consciousness (LOC

Depth of coma, measured by the Glasgow Coma Scale (GCS)

Length of post traumatic amnesia (PTA)

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16
Q

What is the Glasgow Coma Scale?

A

Assesses level of consciousness (or depth of coma) at a given time following injury out of 15

17
Q

What classifies mild, moderate and severe scores on the Glasgow Coma Scale (GCS)?

A

Mild: 15-15

Moderate: 9 - 13

Severe: 3-8

18
Q

What is considered to be the “gold standard” for measuring consciousness in medical settings?

A

Glasgow Coma Scale

19
Q

How does post-traumatic amnesia help determine TBI severity?

A

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

20
Q

What is second impact syndrome?

A

When someone receives a second concussion while their brain is still healing from a first concussion

21
Q

What is the death and disability rate of second impact syndrome?

A

Death: 50%

Disability: 100%

22
Q

What makes second impact syndrome a “hypothetical” diagnosis?

A

Currently not a recognised diagnosis with the World Health Organisation (WHO)

Signs and symptoms vary (eg. presence of haematoma)

Incidence rate is very small

Symptoms overlap with other disorders

23
Q

What did Elder (2013) discover when they explored paediatric TBI in a Maori population?

A

Recovery is improved by considering the Te Whare Tapa Wha (the four-walled house) model of wellbeing

Whanau (extended family)

Tinana (physical)

Hinengaro (mind)

Wairua (connectedness with the universe)