7: Aquired brain injury and neurodegenerative diseases Flashcards

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1
Q

In animal studies, what was the result of leisons on the hippocampus?

A

Mild memory problems

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2
Q

In animal studies, what was the result of leisons on the hippocampus and amygdala?

A

Mild memory problems

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3
Q

In animal studies, what was the result of leisons on the hippocampus and rhinal cortex?

A

Severe memory problems

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4
Q

What is the main function of the rhinal cortex?

A

Combining sensory input from cortical association areas and inputting them into the hippocampus

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5
Q

How is the hippocampus linked to spatial memory?

A

Neurons can be specific to places in space. When participants were asked to recall an area, the corresponding neurons were activated which shows the hippocampus provides spatial context

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6
Q

What is Korsakoff’s syndrome?

A

Caused by a thymine deficiency due to alcohol. Results in cortical atrophy and damage to the diensephalon so the hippocampus can’t communicate with other areas of the brain

Severe reterograde and anterograde amnesia

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7
Q

How is the consolidation of memories linked to the hippocampus?

A

Memories first rely completely on the hippocampus and are eventually consolidated into the wider cortex each time the memory is recalled

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8
Q

What causes strokes generally?

A

A disruption of blood supply to the brain

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9
Q

What is an ischemic stroke?

A

Oxygen supply to the brain is affected.
Can be either embolic or thrombotic

To do with clots

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10
Q

What is a thrombotic stroke?

A

Caused by a clot in the brain’s blood vessels

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11
Q

What is an embolic stroke?

A

Caused by a clot somewhere in the body disrupting oxygen to the brain

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12
Q

What is a hemorrhagic stroke?

A

The rupture of blood vessels in the brain

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13
Q

In what timeframe can motor skills be recovered after a stroke?

A

3 months

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14
Q

In what timeframe can cognitive skills be recovered after a stroke?

A

6 months

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15
Q

What are the language defects resulting from a stroke?

A

Aphasia
Agraphia
Alexia

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16
Q

What is aphasia?

A

Problems producing speech

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17
Q

How is aphasia caused?

A

Damage to the left hemisphere in the frontal and temporal areas

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18
Q

What is agraphia?

A

Problems with spelling and writing

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19
Q

How is agraphia caused?

A

Damage to the left hemisphere visual areas involved in writing

20
Q

What is alexia?

A

Problems with reading

21
Q

How is alexia caused?

A

Damage to the visual and temporal areas of the left hemisphere

22
Q

What is the dual route theory of reading? (Alexia)

A

Dorsal route decodes words and maps them onto sounds

Ventral route directly mapps words to their meaning

23
Q

What is dementia?

A

The loss of cognitive functioning that affects daily life and activities

24
Q

How does Alzheimer’s progress?

A

Over around 10 years it progresses from mild to severe

First issues in memory but later mood disturbances and a loss of independence

25
Q

What is the prevelence for Alzheimer’s?

A

0.5% at 55 years old and the risk doubles every 5 years

At 80 years old, prevelence is at 15-20%

26
Q

What parts of the working memory model are affected by Alzheimer’s?

A

Visuospatial sketchpad and central executive

27
Q

What is the main Alzheimer’s treatment?

A

cholinesterase inhibitors which increase acetylcholine in the brain as it has a role in learning and memory

28
Q

What is the cholinergic hypothesis of Alzheimer’s?

A

There are reduced levels of acetylcholine in the brain of patients and it can be seen in the early stages of Alzheimer’s as well.

29
Q

How effective are cholinesterase inhibitors as treatment for Alzheimer’s?

A

Effective in half of patients for 2 years before becoming ineffective

When they’re taken off the drug, they deline to where they would have been if the drug had never been given - it doesn’t slow the disease

30
Q

What is the role of amyloid plaques in Alzheimer’s?

A

Build up makes learning more difficult and affects the transmission of neurons

31
Q

What two amyloid plaques are involved in Alzheimer’s?

A

Amyloid Beta 40 and 42 - both of which are toxic

32
Q

What are amyloid plaques?

A

Fragments of a larger APP protein

33
Q

What are neurofibrillary tangles?

A

Tangled microtubules that become hyperphosphorelated and impair the function of the neuron

34
Q

What causes neurofibrillary tangles?

A

Abnormal Tau protein

35
Q

How do anti-amyloid drugs work to treat Alzheimer’s?

A

They inhibit the enzymes that break APP down into amyloid beta

All treatments have so far failed

36
Q

What is vascular (Multi-infarct) dementia?

A

Loss of cognitive functioning due to a series of small strokes
There is some recovery between strokes
progressive cognitive impairment with each stroke

37
Q

What is Lewy-Bodies dementia?

A

Shares symptoms of Parkinson’s and Alzheimer’s

Ambormal clumps of proteins leading to cell death

38
Q

What is frontaltemporal dementia?

A

Caused by clumps of Tau protein causing impaired planning, judgemnt and language

39
Q

What are the symptoms of posterior cortical atrophy?

A

Blurred vision
Light sensativity
progressive inability to recognise faces and objects
problems with spatial skills such as driving or dressing
Impaired reading and writing

40
Q

What is parkinson’s disease?

A

Affects motor behaviour and sometimes cognitive skills

41
Q

What are the main symptoms of Parkinson’s?

A

Hypokinesia
Brandykinesia
Akinesia

42
Q

What is hypokinesia?

A

Loss of muscle movement due to disruption of the basal ganglia

43
Q

What is brandykinesia?

A

Slowness when carrying out movements but not when initiating them

44
Q

What is akinesia?

A

Lack of voluntary movement

45
Q

What happens biologically with Parkinson’s?

A

reduction of dopamine in the basal ganglia, substantia nigra and striatum

DOPA and tyrosine hydroxlase is limited which reduces the synthesis of dopamine

46
Q

At what point do the symptoms of Parkinson’s become apparent?

A

When dopamine is reduced by more than 70% as before then, the neurons still functioning are able to compensate