Acquired brain injury and neurodegenerative disease Flashcards

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1
Q

What effects did HM have after bilateral surgery?

A

Intense anterograde amnesia, but other than this no difference in intelligence or psychological illness. This showed that only his new declarative memory had been affected. This showed that the hippocampus is very important for forming new memories.

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2
Q

What part of the brain contains information on declarative memory?

A

Medial temporal lobe (the hippocampus)

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3
Q

What else was affected in HM’s brain other than the hippocampus?

A

The amygdala and rhinal cortex were also removed

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4
Q

What did a test of recognition memory in monkeys on the same areas of the brain affected in HM show?

A
  • Mild impairment to the hippocampus
  • Mild impairment in a hippocampus and amygdala lesion
  • Severe impairment to a hippocampus and rhinal cortex lesion
  • There was no impairment on a short delay which shows that there is only impairment on memory and not on visual processing or understanding of the task
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5
Q

What is the rhinal cortex?

A

Highly processed sensory data from cortical association areas pass through here to reach the hippocampus. This is therefore the gateway for unimodal and multimodal sensory input to the hippocampus.

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6
Q

How do place cells work in the hippocampus?

A

The place cells tile the environment providing a spatial map, then the place cells fire when the animal is in a specific place.

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7
Q

How have place cells been found in humans?

A

Maguires study into taxi drivers

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8
Q

What does hippocampal damage tell us about memory?

A

There are dissociable systems - if one is affected not necessarily others are. The hippocampus also goes beyond just spatial memories as it has a more general role of linking memories to where and possibly when they happened. The hippocampus is also crucial in forming new memories but it is not important for recall of old memories, this means memories must be consolidated and become hippocampal independent over time.

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9
Q

What causes Korsakoff syndrome?

A

Thiamine deficiency due to alcoholism. This then results in cortical atrophy and major damage to diencephalon which act as a relay between the hippocampus and cortex. This causes severe anterograde but also retrograde amnesia.

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10
Q

How does systems consolidation of memories work?

A
  1. Sensory information is processed in the hippocampal formation and then stored as a memory
  2. Recall involves activation of the cortex by the hippocampus via mamillary bodies and thalamus - the hippocampus teaches the cortex the memory trace.
  3. Over time memories are consolidated and become independent from the thalamus and hippocampus.
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11
Q

What are issues with the systems consolidation of memory theory?

A

Episodic memories become more semantic over time and are represented in the cortex as meaning without the context information provided by the hippocampus.

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12
Q

What did Bayley et al show regarding semantic learning without a hippocampus?

A

Patients can exhibit the ability for limited semantic learning without hippocampus.

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13
Q

What is a stroke?

A

Disruption of blood supply which results in damage to the brain.

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14
Q

What is an ischemic stroke?

A

A clot that affects oxygen supply to the brain:

  • Thrombotic stroke - clot in the brains blood vessels
  • Embolic stroke - clot forms somewhere else
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15
Q

What is a haemorrhagic stroke?

A

A rupture of blood cells which means the blood is toxic for cells.

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16
Q

What are the effects of a stroke?

A
  • Transient symptoms - functional disturbance of surrounding neurons
  • Primary cell death, aptosis
  • Secondary cell death - increased intracranial pressure due to swelling in response to an injury
17
Q

How are brains physically affected after strokes?

A

The lesion will grow but also attempt to restore itself , showing the plasticity of the brain

18
Q

How fast is rehabilitation after a stroke?

A

Most recovery occurs over the first 3 months, this is when rehabilitation is most important. From 6 months onwards there is limited scope for improvement.

19
Q

What language deficits are there after a stroke?

A
  • Aphasia (damage to the left hemisphere and or temporal regions results in problems producing speech)
  • Agraphia (damage to left hemisphere visual areas involved in writing leads to problems with spelling and writing)
  • Alexia (visual aphasia resulting from damage to visual and temporal regions in the left hemisphere causing problems with reading)
20
Q

What is the dual route theory of reading?

A

The dorsal route - used for when phonetically decoding words

The ventral route - direct mapping of words onto their meaning

21
Q

How is alexia explained by the dual route theory of reading?

A

Patients have to read via meaning using the ventral route as dorsal route is impaired so have good reading ability but cannot read non words aloud or recognise rhymes.

22
Q

What is dementia?

A

Loss of cognitive functioning that affects daily life and activities

23
Q

What are the major forms of dementia?

A
  • Alzheimer’s disease
  • Vascular dementia
  • Lewy body dementia
  • Frontotemporal dementia
  • Posterior cortical atrophy
24
Q

What are the symptoms and progression of Alzheimer’s?

A

AD progresses from mild to moderate to severe. It begins with memory problems (Mild cognitive impairment) that then worsen, and in later stages mood, behavioural disturbances, and loss of independence develop.

25
Q

What are the risk factors of Alzheimer’s?

A
  • Age - at 55 years there is a 0.5% prevalence whereas at 80 there is a 15-20% prevalence
  • Early onset familial AD shows a clear inheritance pattern
26
Q

What is the criteria for mild cognitive impairment?

A
  • Evidence of impairment in one or more cognitive domains

- Daily function is not impaired

27
Q

What treatment options are there for AD?

A

All treatment options only treat symptoms but do not prevent or stop AD. Cholinesterase inhibitors increase acetylcholine in the brain (which has a role in learning and memory).

28
Q

What are the 3 major theories of AD that have guided drug development?

A
  • Cholinergic hypothesis
  • Amyloid hypothesis
  • Tau hypothesis
29
Q

Slide 35

A

slide 35