FINISH Neurobiology of learning, memory and cognition: memory Flashcards

1
Q

Retrograde amnesia

A

Forgetting of events occurring prior to trauma e.g closed head injury/ electroconvulsive shock therapy

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2
Q

Anterograde amnesia

A

Inability to retain in a permanent form new material: i.e an inability to learn

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3
Q

Causes of amnesia (KAINE)

A

Anoxia, ischaemia, encephalitis, alcoholism & associated dietary insufficiency (Korsakoff’s syndrome), neurosurgery e.g to relieve epilepsy

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4
Q

Alzheimers disease- regions affected

A

Amnesia is a prominent component

Neuropathology strikes especially hippocampus & entorhinal cortex (within parahippocampal gyrus) of temporal lobe

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5
Q

Medial temporal lobe amnesia- patient HM

Unilateral lesions to R or L?

A

Received bilateral resection of his temporal lobes to relieve epilepsy.
Profound, polymodal anterograde amnesia for verbal & non-verbal material. However can hold a conversation, perform mental arithmetic, remember events from more distant past (a few years prior to op)

  • severe recognition memory deficit as shown on performance matching to sample
  • milder retrograde amnesia
  • intact digit & spatial span and short term memory
  • preserved IQ.
  • sparing of procedural memory: can learn to draw in a mirror even though no recollection of daily sessions of testing.

Unilateral lesion limited to right: generally produce nonverbal memory deficits

Unilateral lesion limited to left: generally produce verbal memory deficits.

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6
Q

Diencephalic amnesia: patient NA, Korsakoff’s

A

NA: lesion of mediodorsal nucleus of the thalamus. Developed anterograde amnesia

Korsakoff patients have damage to diencephalic structures, including Papez’s circuit. Show anterograde amnesia (NB but also greater degree of retrograde amnesia than HM)

Sparing of procedural memory: learn perceptual skill of mirror reading as rapidly as controls, but are impaired at remembering what words they read. NB contrast Huntington’s Disease: impaired at developing mirror reading skill but perform better on word recognition.

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7
Q

Papez’s circuit

A

Cortex -> Hippocampus -> via fornix -> Mammillary body -> Thalamus -> Cortex

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8
Q

Damage to the posterior cortex, generally temporal-parietal junction.

A

Selective deficit in intermediate memory, shown by deficient memory span. However are able to consolidate info into LTM- not anterograde amnesiacs
Often conduction aphasiacs.
May involve a specific type of STM that evolved to allow us to follow conversations?

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9
Q

Agnosias

A

Higher level sensory deficits

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10
Q

Movement agnosia

A

Subject cannot ‘see’ movement

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11
Q

Prosopagnosia

A

Subject cannot recognise faces

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12
Q

Associative agnosia

A

Type of visual agnosia
Patient cannot recognise, name, or use objects appropriately. But can identify objects by selecting correct drawing, and can draw object accurately

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13
Q

Apperceptive agnosia

A

Type of visual agnosia
Patient can name an object is appropriate perceptual cues are present but cannot draw object. Also impaired at ‘naming’ object if presented if presented in unusual view.

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14
Q

Declarative vs procedural memory systems

Definitions?
Brain regions implicated?

A

Squire suggests that pattern of memory loss for anterograde amnesiacs gives evidence for distinction.

Declarative: facts, events. Suggested to have evolved more recently, depend on e.g temporal lone & diencephalon.

Procedural: knowledge gained through performance, Skill, habits, priming, conditioning etc. Brain systems less well defined, may include basal ganglia, cerebellum.

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