Neuropsychology of amnesia

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

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?

Forms of memory: Larry Squires

memory taxonomy

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
Barricks permastore)

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

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

The French neurologist Ribot

discovered more than 100 years
ago that in retrograde amnesia
one tends to loose recent
memories

100
80
60

Normal forgetting

40
20
Amnesie patient

retrograde
amnesia
past

lesion

anterograde
amnesia
present

An example of retrograde
amnesia patient data
Controls (n=16)
Korsakoff's (n=6)

0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0

Alzheimer's (n=8)

35-'44

45-'54

55-'64

65-'74

75-'84

Kopelman (1989)
News events test

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

The TraceLink model is an abstraction of

these areas
Link system (hippocampus)

Modulatory system
(basal forbrain)
Trace system
(neocortex)

The position of the hippocampus

in the brain

There are two hippocampi in the

brain!

Connections to and from the

hippocampus

Anatomy of the hippocampus

Hippocampus has an
excellent overview
of the entire cortex

Hippocampus

Hippocampus

Entorhinal cortex

Entorhinal cortex

36

TF

TH

V1

Perirhinal Parahippocampal
cortex
cortex

7b

7a
Visual
areas

46

Somatosensory
and motor
areas

P-B

P-I

3a

Unimodal and polymodal

association areas
(frontal, temporal, and parietal lobes)

3b

To and from sensory organs,

via subcortical pathways

(a)

(b)

Diencephalon: dorsomedial nucleus

and the mammillary bodies

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

Example of a simple heteroassociative

memory of the Willshaw type

0
0
1
0
1
1

1
0
1
0
1
0

0
0
0
1
1
1

1 0 0 1
0 0 1 0
1 1 0 1
1

1
1
0
1

0
1
0
1

1 1 1 1
1
1 1
1
1 1 1 1 1 1
1 1
1 1

Example of pattern retrieval

(1 0 0 1 1 0)
0
0
1
0
1
1
Sum = 3
Div by 3 =

1
1
1
1
3
1

1
1
1
2
0

1 1

1 1
1
1 1
1
2 3
0 1

1 1
1 1
1
3 2
1 0

Example of successful pattern

completion using a subpattern
(1 0 0 1 1 0)
0
0
1
0
0
1
1
Sum = 2
Div by 2 =

1
1
1
1
2
1

1
1
1
1
0

1 1

1 1
1
1 1
1
1 2
0 1

1 1
1 1
1
2 1
1 0

Example graceful degradation:

small lesions have small effects
(1 0 0 1 1 0)
0
0
1
0
1
1
Sum = 3
Div by 3 =

1
1
1
1
1
3
1

1
1

1
1
1 1 1 1 1
1
1 1
2 1 2 3 1
0 0 0 1 0

Trace-Link model: structure

System 1: Trace system

Function: Substrate for bulk storage of
memories, association machine
Corresponds roughly to neocortex

System 2: Link system

Function: Initial scaffold for episodes
Corresponds roughly to hippocampus and
certain temporal and perhaps frontal areas

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

Stages in episodic learning

Retrograde amnesia
Primary cause: loss of links
Ribot gradients
Shrinkage

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

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 mirrorimage of amnesia

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

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

No consolidation in semantic dementia

Severe loss of trace

connections

Stage 3 learning strongly

impaired

Stage-2 learning proceeds

as normal

Non-rehearsed memories
will be lost

Clinical presentation of amnesia

Age
Degenerative disorders
Vascular disease
Anoxia
Korsakoff (vitamin B deficiency)

Clinical presentation of amnesia (cond)

Focal brain damage

Closed-head injury
Transient global amnesia (TGA)
Electroconvulsive therapy
Psychogenic (functional) amnesia

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

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