Ch 18: What alcohol-related cognitive impairments occur Flashcards

1
Q

Alcohol related disorders: 3 simultaneous processes

A
  1. direct neurotoxic effects
  2. indirect neurotoxic effects
  3. irreversible influence on physiological processes (B1 deficit)
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2
Q

Alcohol: acute effects

A
prospective memory
explicit memory
reduced ability to perceive emotions
less response inhibition
loss of control
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3
Q

Alcohol: neurotoxicity

A

stimulating GABA system –> neurotransmission slowed down –> disorders
inhibition of NMDA receptors (glutamate) –> memory disorders
counter reaction: NMDA receptors become more sensitive

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3
Q

Alcohol: neurotoxicity

A

stimulating GABA system –> neurotransmission slowed down –> disorders
inhibition of NMDA receptors (glutamate) –> memory disorders
counter reaction: NMDA receptors become more sensitive

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4
Q

Brain areas most sensitive to alcohol

A

neocortex (frontal lobes)
hippocampus
cerebellum
limbic system (hypothalamus)

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5
Q

What if patient completely stops using alcohol?

A

brain volume loss is partially reversible

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6
Q

Alcohol: four patterns of cognitive impairment

A
  1. impaired executive functions with spared intelligence and memory
  2. combined executive impairments and memory deficits with spared intelligence
  3. global cognitive deterioration
  4. unimpaired cognitive capabilities
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7
Q

Korsakoff’s syndrome

A

amnestic syndrome

  • difficulty learning new info
  • difficulty digging up present info

cause: long term poor diet
- -> indirect effect of alcohol abuse (deficiency in B1)

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8
Q

Korsakoff’s syndrome: confabulations

A

disturbances in anterograde+retrograde memory and executive functions
implicit memory is intact
unable to live independently
spontaneous confabulations are caused by:
1. decreased executive control –> incorrect memories retrieved
2. temporal confusion –> memories associated with the wrong time
3. impaired reality monitoring
4. spontaneous confabulations are mainly present in the acute phase and gradually decrease

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9
Q

alcohol related dementia

A

expressed by memory deficits
different from other dementia’s because:
1. there is no clear pathophysiological process or underlying neuroanatomical substrate
2. there is no further progression of cognitive functioning in abstinence
3. the dementia must still be present sixty days after the last drop of alcohol has been consumed, preceded by at least 5 years of excessive alcohol use

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