Neuropsychology of amnesia

Dr Rohini N Kathavate

Forms of memory: Larry Squire’s 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

Barrick’s ‘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

Memory loss gradients in RA are

called Ribot gradients

x

retrograde

amnesia

anterograde

amnesia

lesion present past

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20

40

60

80

100

Amnesie patient

Normal forgetting

An example of retrograde

amnesia patient data

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0.1

0.2

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75-'8465-'7455-'6445-'5435-'44

Controls (n=16)

Korsakoff's (n=6)

Alzheimer's (n=8)

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)

Trace system

(neocortex)

Modulatory system

(basal forbrain)

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

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

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

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 mirror-image

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

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

Clinical presentation of amnesia

• Age

• Degenerative disorders

• Vascular disease

• Anoxia

• Korsakoff (vitamin B deficiency)

Clinical presentation of amnesia (con’d)

• 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

• 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