1. Neuropsychology of amnesia
Lecture (Chapter 9)
Jaap Murre

2. In this lecture We will review basic aspects of amnesia
We will try to locate memory in the brain and relate brain lesions to amnesia
We will make a start with dementia, looking at progressive semantic dementia

3. Before we embark on our study of amnesia
What types of memory are there?
If amnesia is a form of memory loss, what is forgetting?

4. Forms of memory: Larry Squire’s memory taxonomy

5. Forgetting There is currently no theory that explains why we forget
Forgetting seems to follow rather strict rules, but even these have not been fully explored
It is postulated that very well rehearsed knowledge will never be forgotten (Harry Barrick’s ‘permastore’)

6. Before looking at the anatomy and clinical aspects of amnesia
We will review a connectionist model of amnesia
It will not be necessary to review the technical aspects of this model
The model may help you to get an overall idea of what amnesia is

7. We will focus on some important characteristics
Anterograde amnesia (AA)
Implicit memory preserved
Retrograde amnesia (RA)
Ribot gradients
Pattern of correlations between AA and RA
No perfect correlation between AA and RA

8. The French neurologist Ribot discovered more than 100 years ago that in retrograde amnesia one tends to loose recent memories Memory loss gradients in RA are called Ribot gradients

9. x retrograde anterograde amnesia amnesia past lesion present
Normal forgetting
retrograde
amnesia
anterograde
amnesia x
past
lesion
present

10. An example of retrograde amnesia patient data
Kopelman (1989) News events test

11. Neuroanatomy of amnesia
Hippocampus
Adjacent areas such as entorhinal cortex and parahippocampal cortex
Basal forebrain nuclei
Diencephalon

12. The TraceLink model is an abstraction of these areas
Link system (hippocampus)
Modulatory system
(basal forbrain)
Trace system
(neocortex)

13. The position of the hippocampus in the brain

14. There are two hippocampi in the brain!

15. Parahippocampal gyrus and other structures

16. Connections to and from the hippocampus

17. Anatomy of the hippocampus

19. Connectivity within the hippocampus

20. Hippocampus has an
excellent overview
of the entire cortex

21. Diencephalon: dorsomedial nucleus and the mammillary bodies

22. Connectionist modelling
Based on an abstraction of the brain
Many simple processors (‘neurons’)
Exchange of simple signals over connections (‘axons and dendrites’)
Strength (‘synapse’) of the connections determines functioning of the network
Such neural networks can be taught a certain range of behaviors

23. Example of a simple heteroassociative memory of the Willshaw type 1 1 1

24. Example of pattern retrieval
( ) 1
Sum = 3
Div by 3 =

25. Example of successful pattern completion using a subpattern
( ) 1 1
Sum = 2
Div by 2 =

26. Example graceful degradation: small lesions have small effects
( ) 1 1
Sum = 3
Div by 3 =

27. Trace-Link model: structure

28. System 1: Trace system
Function: Substrate for bulk storage of memories, ‘association machine’
Corresponds roughly to neocortex

29. System 2: Link system Function: Initial ‘scaffold’ for episodes
Corresponds roughly to hippocampus and certain temporal and perhaps frontal areas

30. System 3: Modulatory system
Function: Control of plasticity
Involves at least parts of the hippocampus, amygdala, fornix, and certain nuclei in the basal forebrain and in the brain stem

31. Stages in episodic learning

32. Retrograde amnesia Primary cause: loss of links Ribot gradients
Shrinkage

33. Anterograde amnesia Primary cause: loss of modulatory system
Secondary cause: loss of links
Preserved implicit memory

34. Semantic dementia
The term was adopted recently to describe a new form of dementia, notably by Julie Snowden et al. (1989, 1994) and by John Hodges et al. (1992, 1994)
Semantic dementia is almost a mirror-image of amnesia

35. Neuropsychology of semantic dementia
Progressive loss of semantic knowledge
Word-finding problems
Comprehension difficulties
No problems with new learning
Lesions mainly located in the infero-lateral temporal cortex but (early in the disease) with sparing of the hippocampus

36. Semantic dementia in TraceLink
Primary cause: loss of trace-trace connections
Stage-3 (and 4) memories cannot be formed: no consolidation
The preservation of new memories will be dependent on constant rehearsal

37. No consolidation in semantic dementia
Severe loss of trace
connections
Stage-2 learning proceeds
as normal
Stage 3 learning strongly
impaired
Non-rehearsed memories
will be lost

38. Clinical presentation of amnesia
Age
Degenerative disorders
Vascular disease
Anoxia
Korsakoff (vitamin B deficiency)

39. Clinical presentation of amnesia (con’d)
Focal brain damage
Closed-head injury
Transient global amnesia (TGA)
Electroconvulsive therapy
Psychogenic (functional) amnesia

40. Rehabilitation of amnesia
There is no known treatment
Compensation will, thus, help the patient best:
‘memory book’
electronic agenda
Errorless learning is pioneered by Alan Baddeley and Barbara Wilson

41. Comments on the chapter
Very few people now believe that the amygdala plays a role in episodic memory
Most neurologists now accept the existence of focal retrograde amnesia (Kapur, 1993)
Animal studies (rats, primates) show clear evidence of Ribot gradients in the range 30 to 100 days

42. Next lecture
Implicit memory
Dementia