neuropsycology of amnesia

1. Neuropsychology of amnesia
Dr Rohini N Kathavate

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

3. 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’)

4. 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

5. 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

6. 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

7. x
retrograde
amnesia
anterograde
amnesia
lesion presentpast
0
20
40
60
80
100
Amnesie patient
Normal forgetting

8. An example of retrograde
amnesia patient data
0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
75-'8465-'7455-'6445-'5435-'44
Controls (n=16)
Korsakoff's (n=6)
Alzheimer's (n=8)
Kopelman (1989)
News events test

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

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

11. The position of the hippocampus
in the brain

12. There are two hippocampi in the
brain!

13. Connections to and from the
hippocampus

14. Anatomy of the hippocampus

16. Hippocampus
Entorhinal cortex
7a
36 TF TH 46
7b
3aP-IP-BV1M 3b
Visual
areas
Somato-
sensory
and motor
areas
To and from sensory organs,
via subcortical pathways
Hippocampus
Entorhinal cortex
Unimodal and polymodal
association areas
(frontal, temporal, and parietal lobes)
Parahippocampal
cortex
Perirhinal
cortex
(b)(a)
Hippocampus has an
excellent overview
of the entire cortex

17. Diencephalon: dorsomedial nucleus
and the mammillary bodies

18. 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

19. Trace-Link model: structure

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

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

22. 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

23. Stages in episodic learning

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

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

26. 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

27. 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

28. 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

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

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

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

32. 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

33. Comments
• 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