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Functional Deficits Underlying Amnesia. Lec 2docx Notes

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Functional Deficits Underlying Amnesia Historical attempts to understand amnesia

Lashley (1929)
- Wanted to search for the "engram" of memory  physical representation of memory in the brain / single biological locus of memory
- He researched this by looking at the measurement of behaviour before
+ after specific, carefully quantified , induced brain damage in rats
- He trained rats to perform specific tasks - for food rewards -then lesioned specific areas of the rats cortex - either before or after training
- Cortical lesions had specific effects on the acquisition + retention of knowledge - but the location of the rats cortical damage had no effect on the rats performance on the maze
- This led Lashley to conclude that memories are not localised - rather they are widely distributed across cortex
- Developed a theory of 'Mass Action'  rate, efficacy + accuracy of learning depends upon the amount of cortex available - deterioration of performance on the task is determined by the amount of tissue removed rather than its location
- Also developed idea of 'Equipotentiality'  one part of the cortex can take over the function of another part within a functional area of the brain - any tissue within that area can perform the function - therefore to destroy a function - all tissue in that area must be destroyed.

Penfield (1954)
- While conducting surgery to remove specific types of temporal loci which were causing epilepsy - noticed that stimulation of the temporal lobe induced vivid memory representations in patients

Can Penfield's results be otherwise explained?

Only small minority of patients (7%) stimulated in the temporal lobe gave memory like responses These memories had a dream like quality to them - inaccessible, fantasy like - are they really memories?
Some memories appeared to be false Memory experience was not tied to the location of stimuli - sometimes got memories when stimulated different locations
 The effects may have been a result of electrical discharges spreading to other brain sites

Case R.B. (Zola-Morgan, Squire & Amaral, 1986)

Early evidence suggested memory impairment could be localised to the medial temporal lobe (Glees & Griffith, 1952) Formal testing of H.M + 9 other patients - Scoville & Milner (1957) - led to the view that damage to the hippocampus was responsible for the amnesia

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