Neuropsychology of amnesia

1. Neuropsychology of amnesia Lecture (Chapter 9) Jaap Murre murre@psy.uva.nl

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 memoriesMemory loss gradients in RA are called Ribot gradients

9. Normal forgetting anterograde amnesia retrograde 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. Connections to and from the hippocampus

16. Anatomy of the hippocampus

18. Hippocampus has an excellent overview of the entire cortex

19. Diencephalon: dorsomedial nucleus and the mammillary bodies

20. 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

21. Example of a simple heteroassociative memory of the Willshaw type 1 0 0 1 1 0 0 0 1 0 1 1 1 1 0 1 0 0 0 0 1 0 1 1 1 0 1 0 1 0 0 0 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1

22. Example of pattern retrieval (1 0 0 1 1 0) 0 0 1 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 2 2 3 3 2 Sum = 3 Div by 3 = 1 0 0 1 1 0

23. Example of successful pattern completion using a subpattern (1 0 0 1 1 0) 0 0 1 0 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 1 1 2 2 1 Sum = 2 Div by 2 = 1 0 0 1 1 0

24. Example graceful degradation: small lesions have small effects (1 0 0 1 1 0) 0 0 1 0 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 3 2 1 2 3 1 Sum = 3 Div by 3 = 1 0 0 0 1 0

25. Trace-Link model: structure

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

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

28. 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

29. Stages in episodic learning

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

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

32. 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

33. 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

34. 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

35. 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

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

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

38. 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

39. 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

40. Next lecture • Implicit memory • Dementia