MTL amnesics

Question 1

Corkin (1996/1984)

Answer 1

• HM’s radiology findings showed he had more extensive damage to HC formation than WH (specifically in entorhinal area) as well as adamage to adjacent perirhinal cortex
• ties in with him having most severe AA compared to RB, WM etc

also (1984):

• formal testing of HM revealed RG of up to 11 years before surgery
• but became amnesic at young age (27) so if he had been older, testing might have revealed more extensive, temporally graded RG

Question 2

Scoville and Milner 1957

Answer 2

• studied HM + 9 others
• bilateral MTL damage is cause of AA, and AA will always be observed if this occurs
• only unilateral = selective deficits

MTL amnesics show that MTL not needed for either STM or LTM
= needed for conversion of STM to LTM (consolidation)

Question 3

Zola-Morgan (1986)

Answer 3

• patient RB (memory impairment caused by ischaemia)
• first reported case of human amnesia where rigorous neuropsychological testing and detailed postmortem neuropathological findings demonstrated that damaged limited to the HC formation was sufficient to produce AA
• marked anterograde amnesia, little if any retrograde amnesia (maybe the year or two before ischaemic event), no other cognitive impairments
• bilateral lesion involving whole of CA1 region of HC
• lack of RG = HC is not used for storage of remote memories
  intact priming, so consistent with distinction between declarative and non-declarative memory (HC is only needed for the former)

Question 4

Davis (1984)

Answer 4

• animal model of AA

- experimentally induced ischaemia in rats damages CA1 and causes long-term deficit in new learning ability

Question 5

Zola-Morgan (1994)

Answer 5

• in monkeys, damage to HC is sufficient to cause AA

- severity of memory impairment increases with increasing damage to MTL

Question 6

Rempel-Clower (1996)

Answer 6

• GD = bilateral lesion of HC region involving most of CA1 (some subiculum cell loss). moderately severe AA, little RG
• LM = complete loss of CA1 and extensive loss of CA3 pyramidal cells, CA2 partially intact. moderately severe AA, but more severe / extensive RG (up to 15 years)
• WH = bilateral loss of CA1 cells, some loss of CA2, nearly complete loss of CA3 bilaterally (so damage to all HC cell fields). prominent holes in DG (abnormal granule cell layer), cell loss in subiculum and in EC (layer III worst). most severe AA and had RG involving as much as 25 years

1. bilateral damage limited primarily to CA1 is sufficient to produce moderately severe AA
2. bilateral damage beyond CA1 but still limited to HC formation can produce more severe memory impairment
3. extensive, temporally graded amnesia covering 15 years or more can occur after damage limited to HC formation
   i.e. severity of memory impairment depends on locus and extent of damage
   + damage limited primarily to CA1 field (patients RB and GD) caused minimal RG

RG gradient = memory worse for more recent events / faces than those acquired a longer time ago (less reliance on MTL, stored in neocortex)

Question 7

Squire + Zola-Morgan 1991

Answer 7

• animal model of MTL amnesia in monkeys
• lesion HC = worse performance on DNMTS task (except for very short delays)
• H+ lesion (HC, some of EC and parahippocampal cortices) = even worse
• H++ extended to include perirhinal and all EC) = worst performance (similar to HM)
• lesioned monkeys can acquire procedural skills
• also show RG (object discrimination task, learned 100 associations before lesion)
  = MTL damage impairs conversion of memory from STM to LTM