aphasia and brain organization

8/10/2019 Aphasia and Brain Organization

1/204


2/204

PH SI and

BR IN

ORG NIZ TION


3/204


4/204

P

H

S

I

n

d

B

R

I

N

O

R

G

N

I

Z

T

IO

N

lvarReinvang

Sum

ums

Hos

pital

m

ul

lustil

ulc of

Psy

cholo

gy

of

O

slo

Os

lo

mwa

y

S

PR

ING

ER

S

CIE

NC

E

BU

SIN

ES

SM

E

DIA

, L

LC


5/204

Library o

f Congress Ca

taloging

in

Pub

lication Data

Re

invang, lvar.

Aphasia and b

rain organizati

on.

A ppl

ied psycholing

uistics and com

municat ion di

sorders)

Bibliograph

y: p

Includes inde

x.

I

Aphasia.

2 Cogni t ive dis

orders.

3.B

ra in-

Woun

ds

an

d injuri

es-Complicati

ons

an

d sequelae.

4 Neuropsychol

ogy.

I

Title.

II Series.

R

C424.7.R45

1985

6 6.

85'52

85-9545

IS

BN 978-1-4757

-9216-4 ISB

N 978-1-4757-9

214-0 eBook)

DOI 10.1

007/978-1-4757

-9214-0

1985 Sp

ringer Science+

Business Media

New York

Originall

y published by P

lenum Press, Ne

w York in 1985

Softcov

er reprint

of

the

hardcover Ist ed

ition 198 5

All rights rese

rved

N o p

art of this b

ook may bc rep

roduced, store

d in a retrieval

system,

or

tr a

nsmitted,

in any form

or by any m

eans, electronic

, mechanical, p

hotocopying,

microfilming,

recording, o

r otherwise,

without wri t ten

permission fro

m the Publishe

r


6/204

PR

EF CE

This book

presents

t

he

work on aphas ia c

oming

out of

the

Ins t

i tute

for A ph

as ia a

nd

S

troke

in orw

ay during its

10

y

ears of exis

tence.

R ath

er

than

rev

iewing pre

vious ly

presen

ted

w o

rk, it

was my des ire

to give a

unified an

alysis

and discussion

of our acc

umula ted

data.

T heem

pirical bas i

s for

the

ana

lysis is a fa

irly lar ge

group 2

49

pa

tients)

inve

stigated

with

a s tand a

rd , com pre

hens ive

set

of proced

ures .

Tests of language functions

must

be developed

anew

for each

langua

ge,

but

com

parison o

f my findin

gs

withother recen t c

ompre-

h

ens ive s tu

dies of aph

asi a is facil

iated

by

clo

se parallels

i

n

tes tm e

th -

ods

C ha

pt er 2). The

classificat

ion sys tem

used is cur

rent ly

the m

ost

a

cceptedneu

rological sy

stem, b

ut

I

have opera

tionalized

it for resear

ch

purpo

ses

C

hapte r3).

The analy

ses

presented

are

based

on the view t

hat aphas ia is

an aspe

ct o f a m ul

t id imen s ion

al dis tu rba

nce of bra i

n function.

Find-

ings o

f associated

dis turban

ces and

vari

at ions

in the aphasic c

ondi t ion

over t ime

h

ave

b

een dismissed

b

y

some a

s irrelevan

t to

thestud

y

of

ap

has ia as a

languag e d

eficit. M y v

iew is

that this rich

and com ple

x

set of fin

dings give

s im

portant clues to

the

organiz

a t ion of b

ra in

func

tions

inhumans I

presen

t

analys

es of

the

re

la t ionship

of aphasia

to neuro

psychologi

cal disorde

rs

in

conce

ptual organ

ization,m e

mory ,

v

isuospatial

abilities

an

d

apraxia

C ha p ters

4 5,

and

6)

, and Is

tudy

the variat ions

wi

th

tim e o

f t

he

aphas

ic cond itio

n C hapte r

8).

N

o studyof

aphas ia is

complete

withou

t an

a

nalysisof

its clin-

ic

oanatom ic

al basis. Te

sting

the a

ssumptions

of the cl

assical mode

l

of a

phas ia , I c

an only pa

rt ly confirm

them. M

y analyses

reveal

that


7/204

vi

PREFACE

in many cases

interach ans

be

tween sev

erallesion

sites are

im

portant

in

deter

min ingd ef

icits

that

ar

e of ten

thought tohav

e a mo re c

ircum-

scribed clinicoanatomicalbasis.

In ta k

ing such a

broad v iew

of aphasia,

my

theoret

ical fram ew

ork

h

as been influenc

ed

by

conc

epts from g

enera l sy s

tems theor

y. The

theoretical

chaptersof

the book C

hapters1

and 9 presen

t and deve

lop

this

type of ap

proach suf

ficiently to

account fo

r the main

aspects of

my findings

an

d

to sugg

es t some

new lines o

f investiga

tion for

the

future.

I sh

ould l ike to

acknow le

dge the he

lp

and

su

pport of sev

eral

friends

and

colleagues. First of all, K

Sundet

perform ed the statistical

ana

lyses

an

d di

scussed all

th

e

st

atistical pr

oblems

with

m

e

P. B

arens te in ex

amined

my CT scans

and scored

the

m in

a s

tandard-

ized sys

tem.

K

W i

llmes

made available to

me

the

sy

s tem for an

alysis

of

CT

scan

s used

in the Aa c h en

aphas ia lab

oratory.

He also adv i

sed

me on problem

s of choos

ing app rop

riate s tatist

ical m odels

. My w ife,

T. Bjorg, d id

the

ar tw or

k for

the

bo

ok. A spec

ial w

ard

o

f thanks to

M. Tay

lor Sarno ,

who read

an earlier ve

rs ion of th

is mon

ograph an

d

gave m e every he lp

and

encouragementto deve lop i t for publication.

F

inally, Im

ust th

ank

the

N o r w egian

Nat ional H

eal th Asso

ciation

f

or theirs

upport of

my work d

uring several y

ears, inc lu

d ing

the

t im

e

period

during

w hic

h the bo ok

w

as w ritte

n .

IVAR

REINV NG


8/204


9/204


10/204

CONTEN

TS

ix

Chapter

5 M

emoryand Lea

rning Defi

cits

5 1

Normal

M em or y

71

5 1 1

Verbal Me

m ory

7

2

5 1 2 Ve

rbal Learni

ng

73

5 1 3 Th

e Relation

of Verbal Memo

ry

and

Lear

ning to La

nguage Fun

ct ion

73

52 Verb

alM e m o ry

and

Learn

ing in A ph

asics

74

5

2 1 Verbal

M em or y

74

5

2 2 Verba

l Learning

76

5 3

N onverba l

M em or y

a

nd

Learnin

g

77

5 4

Conc lus

ion

78

5 5 P

resent S

tudy

79

5 5 1 Te

sts

80

5 5

2 The S t

ructure of Memo

ry

in

A phas ia

~

55 3 Rel

ations of M

em ory to A

phas ia

Group

89

5

5 4 Discu

ssion

93

55 5 Con

clus ion

95

Chapter 6

Defe

cts

o

f Vi

sualNonv

erbal bilities

61 Visua

l Nonverba

l Funct ion

s in A p h a s

ia

97

6 1 1

Apraxia

99

6 2 Th

e

Prese

nt

Study

101

6 2 1 Test

s of Nonve

rbal Abiliti

es

1

01

6 2 2

Tests of

M otor Func

tion

103

6 2

3 Apraxi

a

103

6

2 4 Resu

lts

104

6 2 5

Discussio

n

1

06

Chapt

er

7

Localiza

tion of

Le

sion in

p

hasia

7 1

S tatus of

theLocaliza

tion Model

7 2

ew

an

didates

for Statu

s as

1

09

Langua

ge Areas

110


11/204

x

CO N TEN

TS

70201

T h

e Limbic

Sys tem 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 110

7

2 2

T he Len

ticular Zon

e

0

0 0 0 0 0 0 0 0 0 0

0 0 0 0 111

7 2 3

Medial Struc tures

0 00 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 11 2

7 3

T he Pres

en t S tudy 0 0 0 0

0 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 0

0 113

70301

M e

thod 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0

115

7 3 2

Results 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0

00 0 0 7

7 3

3 A

nalysis of T

est Pa ram

eters 0 0 0 0 0 0 0 0

00 119

7

03 40

Lesions and

Their C

ontext 0 0 0 0 0 0

0 0 0 0 0 121

7 40

C onclu

s ion 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 0

00 0 28

Chapter

Rec

overy an

d Pr

ognosis

801 T h

e Recovery

Process 0 0 0 0

00 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 12

9

8 2

Reco

veryof No

nverbal Fu

nct ions 0 0 0 0 0 0

0 0 0 0 0 131

8 3 P

rognosis 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 1

31

8

40 M e

chan isms

of Recovery

0

00 0 0 0 0 0 0 0 0

00 0 0 0 0 0 13

3

8 401

R elearnin

g

or

Facili

tation 0 0 0 0 0 0 0

0 0 0 0 0 133

84020

R eorganization of Function

0 0 0 0 0 0 0 00 0 134

8 4030

Release

of Vicario

us N eura l

S tr

uctures

and

Functiona

l Relocaliz

ation 34

8 40

40

C om

plem enta ry

R edifferen

tiation of

Funct io

n 00 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 13

5

8 5

ThePrese

n t S tudy 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0

0 136

8050

1

Recov

ery P at tern

0 0

00 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 36

8 5 2

P

rognosis 0 0 0 0

00 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 0 141

8 53

Relations

between

Fundionsin

A cute

an

d

Chronic Pa

tients 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 4

4

805 40

C onclu

sions 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 14 5

C

hapter

The

rganized

R

esponse

of the

rain to

Injury

901

Evidence

for O rgan iz

ed C omple

xity 0 0 0 0 0 0 0 0

148

9

2

A Prop ose d System icMode l

0 0

0 0 0 0 0 0 0 0 0

00 0 0 149

9

0201

A

bstrac t Mo

del 0 0 0 0 0 0 0 0 0

00 0 0 0 0 0 0 0 0

00 49


12/204

CONTENTS

xi

9.2.2. Neural Model

151

9.2.3. Clinical Evidence on Hemispheric

Relationships . . . . . . . . . . . . . . . . . . . . . . . 152

9.2.4. Within Hemispheric Specialization

and

Differentiation in umans . . . . . . . . . . 154

9.2.5. The Effect of Lesions and the Systemic

Basis of Recovery . . . . . . . . . . . . . . . . . . . 155

9.3. Testing the Model

158

9.3.1. Application of the Model to the Present

Findings . . . . . . . . . . . . . . . . . . . . . . . . . . .

159

9.3.2. General Applications of the Model 16

9.4. Concluding Remarks

161

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165

ppendix

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

181

ndex 193


13/204

PPRO CHES TO THE

STUDY OF PH SI

1 1 Clinical and

Theoretical

pproaches

The study of aphasia

may

be motivated by clinical as weil as theoretical

considerations.

t

has been

estimated

that about

1 million people suffer

from aphasia

in the

United States (Sarno, 1980). In

Sweden the

inci-

dence of aphasia

has

been estimated

at

60

per

100,000 inhabitants

per

year (Broman, Lindholm, Melin, 1967), and in

Norway Petlund

(1970) estimated the prevalence at .09 . The most frequent cause of

aphasia is strake, which is itself a common disease in an elderly

population. Whereas the risk of strake in the fifth decade of life is

.2 , the corresponding risk in the seventh decade is 2.0 (Mar-

quardsen

1969).

Add

the

fact

that

20 to 25 of

strake

patients

are

initially aphasic (Brust, Schafer, Richter, Bruun, 1976), and the

magnitude of the clinical problems becomes striking. In this context,

the need for practical and reliable methods of testing is apparent. A

classification system with knowledge of associated neurological and

neuropsychological deficits, prognosis, and

underlying

pathology is

a prerequisite for

sound

treatment.

From a theoretical point of view,

aphasia

has, since the time of

the founding papers of Broca

(1861)

and Wernicke (1874), presented

a unique

opportunity

to study

the

relationship of

the

brain to

higher

mental functions.

The

theoretical

problern may

however be

1


14/204

2

CHAPTER 1

fonnulated in different ways,

and

different methodological approaches

may be chosen.

A clinically

based

research strategy includes the following steps:

1.

Observing naturally occurring associations and dissociations

of symptoms. These groupings are referred to as syndromes, with

the

understanding that

they are clinically useful fictions.

2.

Distinguishing between theoretically meaningful associations

phenomena associated because they reflect the same function)

and

theoretically meaningless associations (associations

produced

by the

oretically uninteresting combinations of functions). The

methods used

include psychometric analysis,

post

ho

control of

the

lesion variable

(as the size of the lesion is believed to be the

most

significant factor

in producing spurious associations of symptoms), and experimental

control of the task variable. The result is a structural analysis of the

function involved.

An

alternative research strategy is based on

assumptions

about

the

nature

of language in the normal case.

t is fair to say that, recently, theoretically oriented efforts have

had

the

goal of analyzing (decomposing)

the

cognitive-linguistic proc

ess into constituent subfunctions and assigning

neural

correlates to

these subfunctions. In order to attain the goal of accounting for proc

essing, the internal computational steps of subfunctions and their

ordering must be specified for a given type of task.

Progress in linguistics has led to models of the

subcomponents

of the language function, and to possible rules for relating linguistic

symbols to each other. The structural school of linguistics has influ

enced

aphasiology

through

the works of Jakobsan (1971), whereas in

more recent times the transformational generative model of linguistics

presented

by Chomsky

1965) has

been

influential.

The tenn

neurolinguisti s

(Hecaen Dubois, 1971; Whitaker, 1971)

stands for

an

interdisciplinary

study

of aphasia

based on

neurology

and linguistics.

In

an

influential paper, Arbib and Caplan 1979)

argued

that

neurolinguistics must make an effort to give a computational account

of processing and that this can be approached by converging efforts

of

neurolinguistics, psycholinguistics,

artificial intelligence,

and

neurophysiology.

In the summary of Caplan (1982), the first steps are


15/204

APPROACHES TO THE STUDY OF APHASIA

1 The Ievel at which the nature of computation is expressed. With

respect to human language, Marshall suggests that generative transfor-

mational theories of grammar provide a characterization of

the

structures

relevant to language,

that

is, a characterization of the features of the

mental object attained.

2.

The Ievel

at

which algorithms

that implement

a computation are

characterized. Marshall suggests

that

work

on

parsing strategies,

both

implemented

and

based

on

the results of psychological experimentation,

provides

an

example of the beginnings of a characterization of the psy-

chological steps which are operative in the

attainment

of

the

linguistic

structures of Level 1

3. The Ievel at which an algorithm is committed to particular mech-

anisms, which has been

the

traditional preserve within psycholinguistics

of the aphasiologist. (p.

423

3

Clinical and theoretical motivations have been closely wedded

in the history of the

study

of aphasia. t

has been assumed that

theoretical inferences could be drawn with confidence on the basis

of clinical observation of the association

and

dissociation of phenom-

ena,

and

that the

syndrome

is a significant

unit

for theoretical analysis.

Only recently has the closeness or fruitfulness of this alliance been

questioned. According

toMarshall

(1982),

there will be some models

ofbrain

organization within which the

demands

of clinical diagnosis

and

theoretical

understanding

pull in diametrically

opposed

directions. (p.

404

For the neurolinguist, the unit of analysis is language, and

assumptions about a language function are

independently

motivated

from studies in linguistics and psycholinguistics. t

does

not follow,

however, that aphasia

n

toto

or

subsets of aphasia phenomena are

wholly interpretable as a failure in

subfundians or

processing stages

of the language function. l t is interesting to follow the increasing

divisions of clinical and neurolinguistic studies. In

the

1970s

there

was

optimism that the major clinical

syndromes

of aphasia could be

given a neurolinguistic analysis referring to breakdown in major blocks

of linguistic subfunctions (Caramazza Bemdt, 1978 . The more recent

attitude is that only selected aphasic symptoms, including agram-

matism and some forms of dyslexia and agraphia, can be usefully

studied,

and

then

preferably in selected cases

with

'

1

pure defects.

Taking the

stand that

there are only

two

approaches

to

aphasi(l-

the clinical, which takes the patient as

an

unanalyzed whole as its

unit of study, and the theoretical, which takes the language function


16/204

4

CHAPTER 1

and nonclinical models of it as its units of study-grossly disregards

a third approach.

This

approach

may

be

termed

neuropsychological

and

takes

the

syndrome as its unit of analysis. t follows the step of the clinical

research procedure as outlined above. When the outlines and divi

sions of a functional domain have been established with gross neu

rological correlates, then one of two options may be chosen.

One

is

to say that this is as far as one can get in clinical group studies, and

selected patients with more specific deficits offer the only opportunity

to advance the study by clinical material or methods. Another option,

however, is to say

that syndromes

are meaningful indicators of

the

multidimensional response of the brain to localized injury. They are

indications of the organizing principles at work in the efforts of

the

whole brain to maintain optimal functioning, as

much

as they are

indications of

the

contributions of the missing parts.

Although neurolinguistic analysis is strong on detailed func

tional analysis and specification of processing, it has difficulty justi

fying its selection of study

material

and

its notion of relevant

case

We

have no

theoretical metric for

measuring

the pureness

of functional

deficits, and it

may

well be

that

sharply delineated behavioral

symp

toms are the consequence of highly complex functional interactions.

The findings from analyses of

pure

deficits can be applied to more

complex cases only if one

assumes

that pure deficits can be conca

tenated

without giving rise to

strong

interaction effects. See Shallice,

1979, for a discussion of the problems

and

advantages of single-case

studies.)

Neuropsychological analysis is weak on detailed

function-and

process analysis. The existence of

some

alleged syndromes may be

questioned on empirical

grounds

e.g., the criticism of Benton, 1961,

of the Gerstman syndrome). Neuropsychological analysis has the

advantage of not requiring an independently motivated theoretical

model

and

provides much of the necessary framework for more

sophisticated analysis by giving a normative background for gradation

of performances.

f

the phenomena under study are interactive, then

syndromes

may reflect the emergent properties of factors combined

in

a larger system,

and

a description of the relationship of

the

variables

for different parametric values is a necessary part of a complete the

oretical analysis.


17/204

APPROACHES TO THE STUDY OF APHASIA 5

1.2.

Historical Approaches

The

present

conceptions of aphasia date back to

the

continental

European neurological tradition before and

around

the

turn

of the

century. This tradition has a main stream,

represented by

Wernicke

1874) and Lichtheim 1885) and several tributaries with supplemen-

tary approaches (Marie, 1906; Jackson, as summarized

by

Head, 1915,

1926; Goldstein, 1948; Luria, 1970; Jakobson, 1971; Hecaen Dubois,

1971). To a surprising degree,

the

mainstream of thinking

around the

turn

of the century is still a dominant

mode

of

thought

(Benson

Geschwind, 1977). Because all classical thories are centered

on

con-

cepts of localization of function, it is useful to give a more general

characteristic of localization theory before discussing the controversies.

1.2 .1. Localization Theory

of

Language to Brain

elation

No

author can be taken as the foremost representative of local-

ization theory. The following is

the

present author's summary of the

essential features of

the

theory implied

by authors

who

use

terms

like

language area or speech center to describe

the

neurological basis

of the language functions:

1.

The brain contains areas with specialized functions, beyond

the sensory

and

motor areas. Normally, one cerebral

hemisphere

contains all

the

structures necessary

and

sufficient for language. This

hemisphere

is said

tobe

dominant (for language). Normally,

the

left

hemisphere

is dominant,

but

in some instances,

these

structures may

be distributed

between the hemispheres

or

may

be located entirely

in the right hemisphere.

2.

Within the dominant hemisphere, there is also specialization,

so

that

some areas are of critical importance to the language function

and some are not. The structures necessary for language (language

areas) are commonly believed tobe cortical, and

tobe

located in the

temporal

and

frontal Iobes. There are, however, different theories

and formulations of which specific areas are important and how far

their functions are differentiated.

3.

Different parts of

the

language areas are specialized for dif-

ferent functions. Differently localized lesions in the language areas

give rise to varied clinical syndromes.

By

focusing

on the

features


18/204

6

CHAPTER 1

that

show

the most consistent relationships to the locus of injury, a

definition of types of aphasia can be given. t is

not assumed

that all

pathological performances in aphasia

show

a lawful relationship to

the locus of injury. Alternative classifications built

on

principles other

than clinicopathological correlation may be chosen but would have

to prove their advantage for special purposes. Again, there are dif-

ferent alternative formulations of which are the major

and

minor

aphasic syndromes and what is their specific relationship to the locus

of injury.

4

Language areas have fiber connections with one another and

with

other

areas. In the classicallocalization theories, these Connec-

tions are believed to have very simple functions of transmitting stim-

uli, thereby triggering the activity characteristic of the area receiving

the stimulus. More complex information on the results of previous

stages of analysis may also be transmitted, thereby

adding

or inte-

grating the activity of several connected areas before a motor response

is emitted. This simple conception of the functioning of connecting

fibers has led to their being

named

association

fibers

and to their areas

of convergence being called

association

areas Although it

has

not been

done

in classical localization theory, it is entirely possible,

without

abandoning localization theory altogether, to explore the hypothesis

that association fibers have more complex functions than believed.

The localization theory

has

been criticized both on general

conceptual grounds and with respect to some of its more specific

statements about the nature of aphasia

and

the types of aphasic

disturbances.

t is worthwhile to pause and note that none of these criticisms

question the existence of a correlation between the type of aphasia

and the locus of the lesion. Even authors often identified as antilo-

calizationalists, like Jackson see Head, 1915), Marie 1906), Head

1926), and Goldstein 1948), never denied the existence of clinico-

pathological correlation.

1 2 2

Criticism

of Basic Premises

The criticisms most often advanced may be summarized

under

three points:


19/204


7

1. t is impossible or unacceptable to try to localize normallan-

guage, a criticism stated forcefully by Jackson (see Head, 1915 .

2.

The mixture of behavioral

and

neurological

terms

of classi

fications is ill-conceived

and

confusing. This criticism, too, is

closely connected

with the work of Jackson (see Head, 1915).

3. The general form of

the theory

(connectionism

or

associa

tionism) is

outdated and has been shown

tobe

inadequate.

Both Head (1926)

and

Pribram (1971) have stated this argu

ment forcefully.

Regarding the alleged nonlocalizability of

normallanguage,

it is

appropriate to stress

the

difficulty of using observational clinical data

as a basis for inference about normal processes. In particular it is

unwise

to

name

centers on

the

direct basis of lesion locus

and

symptom

description. This is

no more than

to

say that phrenology

is

outdatedas

a model of neuropsychological research.

On

the basis of

observation

that

patients

with

certain lesions have difficulty

in

naming

objects, we would be unwise in inferring that the locus of the lesion

is normally

the

locus of object

names.

But

assume

that

characteristics

of this naming

difficulty can be

teased out further by

experimental

variation of conditions

and

can

be shown

to deviate from

normal

performance by certain parameters. We

would have

then a basis for

hypothesizing an underlying process, which can then, again hypo-

thetically,

be

related to a given neurological structure.

The hypotheses

may

very well have implications that could also

be tested

on

normal

individuals by

means

of behavioral measures.

The criticism is correct if it is reformulated to

say that

no

hypoth-

esis assigning normal processes to given neurological structures should

be accepted on clinical evidence alone. The declaration that

language

cannot be

localized, however,

seems

to

be

an arbitrary conceptual

decision

that any

function

with

a definite relation to a

neural

locus

cannot be called language

Mixing behavioral

and

neurological classification was called

psychoneurology

by

Jackson (see

Head,

1915). There is danger of

tautological reasoning if concepts from one category are used to define

those from another. f

frontal

aphasia

is

defined

as

the type of aphasia

resulting from frontal injury, then the question of the frontal locali

zation of this

syndrome has

already

been

settled

by

definition.


20/204

8

CHAPTER I

However, if care is taken to define behavioral categories in behavior

terms and neurological categories in anatomical terms,

then

there

should

be

no

objection to

studying

the relationships

between

the two.

With the

advent

of more sophisticated statistical techniques, the

question of the behavioral validity of aphasia types can be raised: Are

there naturally occurring clusters of aphasia symptoms,

and if so, do

they correspond to the classically described types of aphasia?

t

must

be recognized that the answer to this question depends on the patient

group studied. The agent of injury

may

be

such

as to

produce

diffuse

lesions, as in metabolic or anoxic lesions.

t

may also produce discrete

lesions,

but

of several anatomically distinct structures

not

known

to

have a common function. This combination of lesions

may

weil occur

in

cerebrovascular disease, where structures may be damaged together

by

virtue of having a common blood supply. In

penetrating

head

injuries, again, the lesion may be discrete and weil defined but may

not follow the demarcation lines drawn by anatomy. Rather than

injuring one well-defined anatomical structure completely, it

may

incompletely injure three.

odern

statistical studies started

with

Weisenburg

and

McBride

1935) and continued with Jones and Wepman 1961) and Schuell,

Jenkins, and Carroll (1962). All these studies rejected classical clas

sification schemes but are open to the criticism of Iack of control of

localization of the

lesion. Recent studies

by

Goodglass

and

Kaplan

1972) and Kertesz and

Phipps

1977) indicate that

an

extension and

refinement of classificatory schemes within the framework of a clas

sical clinicopathological model are a likely development.

I agree wholeheartedly with the critics of classical localization

theory that associationism is an inadequate theory for explaining the

complex activity of the nervous system. Hughlings Jackson was aware

of this point. From his studies of epilepsy, he described a certain dass

of symptoms as release symptoms, that is, symptoms caused

by

a

loss of inhibition. In his hierarchial model, the alleged loss of the

propositionallevel of function and the emergence of autornahe speech

are the primary example ofthistype of deficit in aphasia. In modern

times, several authors, among them Pribram (1971), have rejected

associationism

and

have

proposed

more complex theoretical models.

As noted above (p. 6), localization theory does not presuppose

associationism, although the two theories have been closely linked


21/204


historically. The inadequacy of

an

associationist model of

the

brain,

tagether

with

the

criticisms discussed above,

should not

lead to aban

doning the

concept of localization of function. Localization

theory

should,

however, be modified and modernized. The specific content

of an adequate theory is largely unknown.

t

is, however, of some

interest to discuss

what

general features

an adequate

theory

must

have.

1 2 3 Criticisms of Assumptions Regarding

the

Nature of phasia

or

the

Types

of phasie

Disturbances

The following criticisms will be discussed:

1

Language

cannot

be distinguished from intelligence. Aphasia

is symptomatic of a more general intellectual disturbance

(Marie, 1906; Bay, 1962).

2. Different forms of aphasia do not exist; only

aphasia

with

different additional disturbances exists (Bay, 1962; Schuell,

Jenkins Jimenez-Pabon, 1965).

Jackson (see Head, 1915) proposed that language is

integrated

in

several levels of mental functioning. Aphasia is

not

a disturbance

of an anatomically localized language mechanism or process; rather,

it reflects mental regression from a propositional

11

Ievel of functioning

to lower levels. Speech

in

emotional context is preserved,

but prop-

ositional speech is lost. Other influential thinkers

supported

this posi

tion.

l t

was adopted

by

Head (1926),

who echoed

Jackson's statement

that an aphasic is in a certain sense lame in his thinking, and by

P. Marie 1906}, who said that aphasia is a special sort of intelligence

defect. In modern times Bay

1962) has

been a strong advocate of

the view that a conceptual disturbance is inherent in aphasia.

The position of Wernicke (1874) on this issue was clear:

The spoken and written narne of an object is not a

new

attribute of

the object. t is

thus

clearly different frorn the actual sensory rnemory

irnages of the object. Only the latter make up

the

concept of the object.

Disturbance of the concepts of things with which

we

deal in the process

of thinking are always disturbances of intelligence. Disturbances of speech,

on the contrary, cause difficulties only in the use of the conventional

means of representation of the concepts. (p.63)


22/204

10

CHAPT

ER 1

Th

e con

sequ

enceo

f th is

issue

for r

esear

ch see

m s to

be to

que

s

tion

whet

her a

cons

isten

t defe

ct in

inte

lligen

ce c

an be

foun

d in

aphasics.

f

so, it is necessaryto postulate

n

inherent l ink be tw een

tho

ught

nd

langu

age b

eyond

thep

lausi

ble as

sum p

tiont

h t th

e lan

g

uage

distur

bance

m ak

es n

ins tru

m en

t for th

ough

t le ss

avail

able.

A

w

ay o

f dem

onstr

ating

a def

ect of

intel

ligenc

e is t

o sho

w tha

t, giv

en

a def

ect in

perf

o rmin

g a ta

sk w i

th lan

guag

e mat

erial,

it is p

ossib

le to

dem

onstra

te th

e def

ect ev

en if

the v

erbal

elem

ents

of the

task

are

rem

oved.

The

availa

ble re

searc

h on

hem i

spher

ic asy

m m e

try o

nly pa

rtly

supportsthe notion of material-specific functions of the tw o hemi

sph

eres(

Milne

r,

197

4;

Ga

zzani

ga

Ledo

ux 19

78), nd

dif

feren

ces in

th

e cog

nitive

m od

e of

opera

tion

of the

two

hem

isphe

res mus

t b

e

con

sidere

d. (Fo

r revi

ew, s

ee Bra

dsha

w

n

d

N ettl

eton,

1981.

) Rese

arch

on

in t

ellige

nce in

apha

sia, s

um m

arized

in L

ebrun

nd

H oop

s (197

4),

indic

ates s

om e

reduc

tioni

n spe

cific n

onve

rbal t

asks, but

t

he ro

le of

the

size o

f the

injur

y in

expla

ining

such

defec

ts is

uncer

tain .

The

evid

ence

on th

e issu

e is n

ot str

onge

noug

h to l

ead us

to ab

ando

n the

theoryof localized language function. The facts nd their in terp re

ta

tiona

re d i

scusse

d fur

ther i

n C h

apter

6.

The s

econd

c hall

enge

to loc

alizat

ion th

eory nd

th

e clin

icopa

th

ologic

al m o

del i

s the

quest

ion o

f w he

therd

iffere

nt ty

pes o

f apha

sia

exist

. The

posit

ion ta

ken

by an

tiloca

lizatio

nists

is tha

t diff

erent

syn

drom e

s exi

st afte

r diff

erent

ly loc

alized

lesio

ns, but

the

y sho

u ldn

ot

be

calle

d diff

erent

form

s of a

phasi

a. Th

ey sh

ould

r the

rbe s

een a

s

aph

asia w

ith d

iffere

nt, dd

ed d

isturb

ance

s. Ma

rie

1

906)

s

tated

tha t

Bro

ca aph

asia

is the

comb

inatio

n ofa

phas

ia nd

anar

thria.

This

is the

holis

tic in

terpre

tation

of a

phasi

a , w h

ich h

as al

so be

en po

pula

r in

m

odern

time

s th r

ough

the w

ork o

f Sch

uell t al

1965

).

Ther

e is no

dou

bt tha

t, ina

phasi

a, var

iations

in pe

rform

ance

can of

ten be

obse

rved,

so

thats

om ep

atien

ts hav

e dis

propo

rtiona

te dif

ficulti

es w i

th spe

aking

,

w

riting

, read

ing,

o r au

ditory

ana

lysis.

Som

etim e

s suc

h var

iation

s

dete

rm in

e the

classi

ficati

on of

the t

ype o

f aph

asia.

W het

her o

r not

such

distur

banc

es of

perfo

rm an

ce sh

ould

be ca

lled d

istur

bance

of

la

ngua

ge is

partl

y a c

oncep

tual

questi

on. B

enso

n nd

G es

chw in

d

1977)

defin

ed lan

guag

e as

perce

ption

of ver

bal se

nsory

stim

uli, in

te

gratio

n oft

hese

stim u

li w ith

prio

r know

ledg

e, nd

activ

ation

of ve

rbal


23/204


24/204


25/204

APP

ROAC

HESTO

THE

STUDY

OF A

PHAS

IA

13

d

ifficu

lty of

deriv

ing te

stabl

e pred

ictio

ns. G

enera

l syst

em s t

h eory

is

no t

a testa

ble th

eory

but on

ly a f

ramew

ork f

or de

velopi

ng m

ore de

tailed

theorieswi th in a specific field.

13

1 App

licati

ons of

Syste

ms The

oryCo

ncepts

in

N

europ

sychol

ogy

A

com p

rehen

sive r

eview

of th

is top

ic is

be

yond

t

he scope

of th i

s

ch

apter

.Few

a

utho

rs re

fer ex

plicitl

yto sy

s tem

s theo

ry its

elf,

and ver

y

many

u s

e con

cepts

t

hat

a

re re

lated

to sy

s t ems

theo

ry in

one

way

or

anoth

er . H

ere I

focu

s esp

eciall

y

on

s ta te

m e n t

s em

phas i

z ing

th

e

dynamic, interactive

nature

of b rain funct ion

and

the nature

of sy m p

to

m s a

s an

organ

ized r

espon

se o f

the w

ho le

brain

after

injur

y .

O

ne

cont

ext i

n w

hich

the

dynam

ic

n

ature

of fun

ction

-to

loca

lizatio

n rel

a t ions

hips h

as

bee

n muc

h

d

ebate

d is

the

s

tudy

o

f t

he

on to

g en y

of th

e cere

bral l

a teral

izat io

n of

the

lan

guag

e fun

ction.

Len

neb

erg

1967)

s u m m

arize

d

theevide

nce

and co

nclud

ed t

hat lan

guag

e

is

gradu

al ly

latera

lized

after

bein

g init

ially b

ilater

ally

rep res

en ted

.

Sinc

e the

n it h

as

been

re

cogni

zed

tha

t

th i

s v iew

is o

versta

ted. T

here

is ev idence ofearlyspecialization ofthe left hemisphere for lan g u age

(D

enni

s W

hitak

er, 19

77),

and fo

r seve

ral as

pects

of lan

guag

e,

ther

e

are

no

in

dicat

ions

of co

n t inui

ng la

terali

zation

. As

p

ointe

d ou

t

b

y

M osc

owitc

h (197

7), c

u r ren

t test

smay

t

ap only

very

low

levels

o f

lin

guist

ic pro

cessin

g ,

and

w

heth

er h igh

e r

ord

er

li

nguis

tic pro

cesse

s

do

inde

ed

b

ecom

e pro

gress

ively

m ore

latera

lized

wit

h age is

open

to

de

bate

(p. 2

04).

Se

ines 1

974)

gave

an ex

tensiv

e rev

iew o

f t

he role o

f the

corpu

s

ca l losum

inestablishing hemispheric

spec ial iza t ion.

With poorly

devel

oped

c

o rt ico

-cor t

ical C

o n n e

ct ion

s ,

recip

rocal

sp

ecial

izatio

n

deve

lops o

nly s

o far

as st

ructu

ral as

ym m e

tries

allow

. Wit

h cal

losal

a

genes

is, th

ere is

an in

dicat

ion o

fgrea

ter l ik

eliho

od of

b

ilater

allan

guage

repr

esen t

a t ion

a

nd a h ig

h er in

ciden

ce of

retar

dat io

n in

l

an

guag

e dev

elopm

ent .

The d

evelo

pme

nt of h

emi s

pher i

cspec

ializa

tion

fo

r lan

guage

in no

rmal s

may

b

e

re

la ted

to rela

tively

late

m yeli

n izat i

on

of

callosa

l fibe

rs (Ya

kovlev

Le

cours

,

1

967).

Sein

es 1

974) co

m m e

nted:

The evidence in support of the view that CC (corp us cal losum ) m ay

b

e respo

nsible

for th e

e stabl

ishm en

t o fla n

guage

laterali

zation

is th

us

no

t

str o

ng,

but

at

leas

t it has

thead

van tag

e o fbei

ng rel a

tively e

asyto

confirm

o

r disco

nfi rm .

This v

ie w di

ffers fr

om the

trad i

t ional

in hibi

tory th

eory


26/204


27/204


28/204

1

6

C

HAPTER 1

T he insiste

nce on

the

interactive

, dyn

amic proper t ies

of

neural

fu

nctions is

in agreeme

nt with

a

sys tems

theo ry app

roach. Th

is

approach

is

furtherdevelopedin

an

eloquent statement

of h is p osi t ion

by

Kinsbo

urne 1982

):

There ar

e no discontin

uitie s in the

brain. No independent

ch

anne ls

traverse it, nor

is its territ

ory divisible i

n to areas that house auton

omaus

processes No

Simula

tion of

h

uman

behaviour , howe

ver impre

ssively

successful

in im personat

ing its model

, is capable o

f revealing how

the

human

mind arrive

s

at

the s ame

outcome , un l

ess i t

i

s based

on

a ne twork

mech

anism. p. 412

1.3.2 Localizat

ion

of Function in Ligh

t of

Systems T

heory

t is possi

ble to class

ify neurop

sychologic

al theories

according

to

thei r posi t

ion on

the

two

dicho

tom ies of l

ocalization

ve

rsus non-

loc

alization

and systemi

c vers

us

no

nsystemic .

I will first

describe

the

d icho

tom y

betwe

en

nonloc

alizat ion and

localiza

tion views

and

then

show how

these v iews a re

m odified

by

in

troducing

the

co

ncept of

systemi

c functioni

ng.

1. Nonloc

alization

nonsy

stemic

T

he t

heory

s

ays tha

t

fun

ctions a re

diffuse

ly represen

tedin a str

ucturally re

latively un

differentiate

d brain.

eural net

works have

been

d

escr ibed a

s analtern

at ive to lo

calized

functional

cente rs . Th

e alternativ

e , h o w e v e

r , se

ems hard

to recon

cile

w

iththe

h ig

h ly specifi

c str

uctures

and patt

erns

of conn

ec t ions

foun

d

in modern neurosc

ience .

T he origina

l ideaof the neuron

network

as acontinuum

of nerve c

ells

of

Standard sha

pe

a

nd isotr

opic random

or

geometric

ally determin

ed)

connectivity propert ies has all

but

disappeared from

our

im age of the

centers of

the higher an

imals . Szent

agothai Ar

bib, 1975, p. 43

T h

erefore , be

cause

of th

e

kn

own

sp

ecif ity

and diversi ty o

f ana tomica

l

s t ruc tu re s

i

n the

brain

, th is

theor

y cannot be m

aintained for

the

fu

nc-

t ioning of t

he bra in a

s a w hole .

t m ay, how

ever ,

be

c

o n s ide red

for

ce

rta in func t

ions

in

re la

t ion to lim

ited bra in r

egions . Th

e thesis

that

lesion

s

within t

he

la

nguage areas g i

ve rise to

apha

sias

o

f v ary ing

severi t

y , bu

t not

o

f varying

type , exem

plifies this

p roposi t ion

.

2.

Localization

nonsyste

mic

Thi

s th

eory

s t

a tes th

at th

e

br

ain h

as

highl

y specific

and diversif

ied ana tomi

cal s t ruc tu

re s

with

eq

uallyspe -

cific

and diversifi

ed function

s. T he ext r

em e exam

ple is

phrenology


29/204


which says that the brain is a collection of

independently

working

organs.

The advantage of classical clinicopathological theory over

phren-

ology is that it

adds

the possibility of integrative action

by

postulating

connections between neural centers, as weil as the building

up

of

more complex functions

by

association. The theory is still nonsys

temic, so long as the presence of connection does not modify the

operations of localized functional centers. The Wernicke-Lichtheim

model uses the concept of localized functions to describe

and

explain

loss of function but

adds

aphasia syndromes (conduction aphasia,

transcortical aphasias) caused

by

isolation

or

disconnection of lan

guage areas.

An even more sophisticated step in analysis is taken when local

ized centers are connected in temporal sequence

and

shifting com

binations. These functional systems (see Luria, 1973) are

seen as

underlying normal performances. They arestill

not

systemically orga

nized in the sense of the

present

discussion, because the functioning

of a component is not modified by other components, barring the

special case of disconnection.

3. Nonlocalization systemic

Although acknowledging the highly

interconnected

nature of neural tissue, I have already rejected the

neural net as a sufficient model of the human nervaus system. As an

alternative to neural nets, Szentagothai

and

Arbib

1975)

described

more

modern

concepts,

based on

the idea of modules of

neuronal

organization. Although recognizing anatomical specificity, still

the

similarity of neuronal building blocks, called

modules throughout

the

cortex is stressed.

To make such a model systemic, it

would be

necessary to

assume

that

the pattern of interaction between neural elements (modules)

determines function, whereas this

pattern

can be set up

anywhere in

the brain, or at least

in

the cortex. Although such formulations are

more theoretically acceptable than simpler concepts in

the

nonsys

temic version of nonlocalization theory,

the

problern is to

show how

localized injury to a brain thus organized could result in a differential

deficit in the language function, with relative sparing of

other

func

tions. Hence, the introduction of a systemic dimension does

not

make

nonlocalization theories better able to explain the empirical findings.

Although rejecting this alternative as a model for the brain as a whole,


30/204


31/204


is the

main

clue to the systemic organization of cerebral representa

tion. In nonsystemic organization

the

additivity of effects is pre

served

but not

in

systemic organizations. Finally

the

degree of

changeability in the performance-to-structure relationship in recovery

can be used as additional relevant information.

1 4

The

resent Study

What

one undertakes as a research project is determined by

one

s

interests practicallimitations

and,

most

important

what

one

regards

as reasonably well established.

During the period of time in which the material for this study

was

collected

the

general services offered aphasic individuals in Nor

way

were unsatisfactory. Speech

therapy

services

were not

organized

and were available only in large cities or communities. No counseling

social

support,

or information pertaining specifically to the problems

connected with aphasia were given to families

and no

training in the

care

and

treatment

of aphasia patients

was

offered to hospital per

sonnel. As a first step to improve this situation the Institute for

Aphasia and Stroke

was

established in 1973 by a donation from the

National Health Association a private organization with the fight

against coronary

and

other vascular diseases as one of its goals.

The Institute for Aphasia and Stroke is a test laboratory located

in the

Sunnaas

Rehabilitation Hospital which is one of the municipal

hospitals of Oslo Norway. The staff of the institute consists of one

neuropsychologist

one

technician

and one

research associate. The

hospital has 226

beds and

admits patients with several kinds of func

tional disturbance with organic etiology offering physiotherapy

occupational therapy speech therapy and, in addition social and

medical services. Patients

may

be

admitted

for evaluation only or for

full treatment. The hospital offers only

inpatient

services; thus, the

patients

admitted

for treatment have severe physical handicaps

whereas patients with lighter physical defects are referred to other

institutions with outpatient services.

Because of its

unique

position

the

institution received appli

cations for admission from the entire country during the period of

this study. An attempt

was

made to see as

many

as possible of the


32/204

20

CH

APTER 1

pa t

ients for ev

aluat ion a

nd testing,

so as to ge

t a survey

of

t

he pop-

ulatio

n referred f

or treatmen

t . A l thoug

h no exact

figure can b

e given,

it

can

safely be sta ted that m ore

than

90

of thepat ients referred

wer

e teste

d .

The decisi

on to create

an aphas ia

registry w

as mot iva t

ed by the

des

ire for a sy

stematic r

egistration

of all avail

able inform

ation perti

nent

to the des

cription an

d evaluat io

n of the pa

t ien t g roup

. Th e regis

try shoul

d serve

primarily

as an ins

trument fo

r clinical r

esearch,

c

oncentra t in

g

o

n the co

nnect ion of

aphas ia with

other symp

toms and

on the d

evelopmen

t of ap

has ia with

t ime. The

results of

tests per

formed at the Institu te for A phas ia

and

Stroke form the

main

content

of the

registry, w

i th medica

l

an

d gen

eral

b

ackground

info

rmat ion

added.

As re

viewed abo

ve, a summ

ary of

theconsensus

in

1978, when

this

study s tar ted,

runs as fo

llows:

The clini

cally defin

ed

sy

ndromes

of apha

sia are s ta

ble enti t ies

wit

h a wel

l-def ined p

athological

substrate.

Because a

phasia is a

lin

gui

stic deficit,

a more refi

ned l inguis

tic analy sis

of langu ag

e per form

ances in the major syndromes will allow us to replace the static

tradi

tional

descriptio

ns of functio

ns as un

analyzed

wholes

wit

h

dy

nam ic pro

cess ing con

cepts

approachin

g

the

ideal of co

mplete com

puta t ion

al specifica

tion with n

eural corre

lates.

My d ifficul

ties with ac

cepting the

pos i t ion just

sum

marized were

b

ased

on

both m e

thodologic

al and con

ceptual wo

rries. First

of all, I

wor r ied abou

t the lo

osely d ef in

ed procedu

res for test

ing

a

nd def

ining

apha

s ic syndrom

es . A nec

essary first

step for cl

inical research

and

a step t

hat

m

ust be

taken anew

n each di

fferent lan g

uage

com

munity-

is to def

ine strict and

quantif i

able proced

ures for te

s t ing and

classi

ficatio

n. The sy

stem of m

yself and

my colleag

ues is desc

r ibed in

Cha p te

rs 2 and 3.

Sec

ond, I wor

r ied about the

seemin

gly i

nnocuous assump

tion

that

a

ph asia is a

lingu istic d

eficit. Rem

ernhering t

he papers by

Teuber

a

nd Weins te

in 1956),

by Weins t

ein 1964),

and by o th

ers showing

an assoc

iation of a

phas ia w i t

h some v is

ual reason

ing

a

nd le

a rn ing

tests,

as well as t

he many ex

iting papers by

Kimur

a see Kimu

ra, 1979)

on

the close a

ssociation o

f langua ge

and

h ighe

r

or

der

motor function

s,

I thoug

ht i t more a

ppropr ia te

to def ine

aphas ia at

the outset

as a

linguistic-c

ognitive de

fect.

lthough I in

no way wish t

o ques t ion the


33/204


21

reality of a language function separate from other cognitive functions,

it

may

still be the case that aphasia does

not

reflect

an

isolated dis

turbance of this function.

f

it

turnsout

that

only a few selected cases

demonstrate

pure

disturbances of language,

then

a scientific approach

to the great majority is needed. Maybe these cases can be viewed as

just mixed and can be explained as additions of defects observed

in isolation in the

pure

cases. But it may also be

that

important inter

actions are at work, so that mixe

syn romes

becomes a misnomer for

unanalyzed complexity.

Third, I worried about the generally simplistic approach to

the

effect of brain injuries evident in a deficit-oriented analysis.

t

seemed

to me that the multidimensional response of the brain to injury, as

weil as the variations over time of this response, was what

had

to be

described

and

accounted for. I was (and am) disturbed by

the

tend-

ency to stress regularity and to dismiss variability in the response of

the brain to injury as noise. Commenting on the relative success

of syndrome classification, Wernicke 1874) stated:

Only a particular period in the course of the disease should be con

sidered if

one

is to diagnose aphasia correctly.

On

the one hand the

general

phenomena

which accompany the onset of aphasia, as

they

do

that of most localized lesions of the brain, must have disappeared. On

the

other hand

however, the conditions ought not to have Iasted so long

that

the

possibility of compensation by the

other hemisphere

is already

present. (p.

69)

Here, the motivation of the neurological diagnostician to ignore infor

mation not pointing to the locus of the injury is clearly seen.

Poeck (1983b) echoed the same opinion:

l t

cannot be denied that a certain

number

of vascular aphasias (approx

imately 15%) cannot be classified in terms of

standard

or nonstandard

syndromes. The main reason, in

our

experience, is that the examination

is

done

too early, prior to the establishment of a weil defined syndrome

or at

the

late stage of recovery, with or

without the

effects of speech

therapy. (p. 80)

On the basis of these reflections, and having standardized the

necessary tools for measuring and classifying aphasic phenomena

(Chapters 2 and 3), I have therefore

undertaken

a broadly conceived

program of testing aphasics with neuropsychological tests. Informa

tion on lesions with CT -scans has been recorded when possible, and

repeated testing has been performed in order to chart as far as possible


34/204

CH

APTER

the e

xtrem

es of

para

metri

c valu

es in

apha

sia

conce

ived

of as

n

ex

perim

ent o

fnatu

re. I

will a

ttem p

t to gi

ve a s

ystem

s-the

ory-o

riente

d

account of the complexity of the aphasic condition.

t

m u st be rec

ogniz

ed th

a t th

e acco

unt f

alls s

hort o

f the

goal

of

n expe

rim e

ntal

analy

sis of

causa

lly si

gnific

ant fa

ctors

if suc

h n a

nalys

is can

be giv

en.

t

also

falls s

hort o

fthe

ideal

of a sp

ecific

ation

of the

actu

al pro

cessin

g

stag

es be

h ind

the p

erform

ance

sobs

erved

. I w o

uld s

till cla

im th

at at

th

e ver

y leas

t thi

s type

of a

nalys

is of

the or

ganiz

ed co

mple

xity o

f

lingui

stic-co

gniti

ve ph

enom

ena

und

er a set

of ex

treme

cond

itions

is

a valu

able

com p

lem e

nt to

other

sour

ces o

f info

rm at

ion a

bout

the

underly ing system.


35/204

OPER TION LIZ TION

OF MODEL

2 1 The odel

2

The goal is to select a model that, tothebest of

our

current knowledge,

captures

the

significant dimensions of clinical

syndromes

t

should

also account for the associations of

parameters

that are useful for

defining syndromes while leaving reasonable space for

within-

syndrome

variations.

The Wernicke-Lichtheim model underlies

the

terminology

and

the clinical classification systems most frequently used today.

t

is a

model within the localizationist tradition (Wernicke, 1874; Lichtheim,

1885), and it identifies

two

cortical areas

important

to

the

language

function,

the

Broca

and

Wernicke areas. The fibers associating

these

areas are assumed to run in the arcuate fasciculus. In addition, Lich

theim

assumed that transcortical fibers, via a hypothetical concept

center, can mediate information between the language areas. Dif

ferent forms of aphasia follow from lesions of different neurological

structures.

The localization of language areas is

shown in

Figure 2.1, and

the

types of aphasia resulting from differently located lesions are

shown

in Table 2.1.

A more detailed review of brain regions and the associated aphasia

types is given below. The review does not limit itself to statements

3


36/204

4

C

HAPT

ER 2

Fig

ure 2.

1. Loca

lization

of lan

guage

areas.

Legend

: 1)

an

ter ior

languag

e area

Broca

);

2) W ernic

ke area

; 3)

su

prama

rginal

gyrus;

4) ang

ular gy

rus.

by cla ss

ical

u

thors

but in

tends

to

sketc

h the

p res

en t -d

ay st

tuso

f

th is

m ode

l.

2

1 1

Broca

re

a

T

he Br

oca ar

ea is

locate

d in

th

e

th

i rd tr

an sv e

rse fr

ontal

conv

o

l

ution

, w hi

ch ca

n b e d

iv id e

d in t

o th re

e par

ts: th

e orb

ital, t

he tri

an

gular

,

nd th e o

percu

lar.

t

is th

e o pe

rcu la

r p r

t of

the

con

volu

tion

Table

2 1

Assumptions of

the

Wernicke Lichthe

im

Model

Typ

eof ap

has ia

B

roca

W e

rn icke

Globa

l

C

onduc t

ion

Ano

m ic

Is o

la tion syn

drome

Tr

anscort

ical mo

tor

Tr

anscor

ti cal se

n sory

Broca

area

W

ernick

earea

Locus

of lesi

on

Bro

ca nd

W ernic

ke area

s

A rcuat

e fasci

culus

A n g u

lar gyr

us

Exte

nsive n

eocorti

cal, sp

a ring B

roca

nd

W ernickeareas

Frontal

, spari

ng the

Broca a

rea

Pariet

o-occip

ital, sp

ar ing t

he Wer

nicke

area


37/204


38/204

6

CH

APTER 2

1977; M

ohr , 1976;

K erschens

te iner , Poe

ck, Huber,

Stachowia

ck,

W eniger , 1

975).

2.1.2. Poste

rior Languag

e rea

The p

os te r ior

language area

is compose

d ofparts

o

f

th

ete

mporal

neocorte

x,

th

e gyru

s su p r a m a r

g inal is , and th

e g

yrus an gular is

. The

Wernic

ke

area

is

defined in th

is

mo

nograph

as the t

e m p ora l part

o fthe

pos

terior languag

e

a

rea.

T here

seems to be a

gene

ral

ag

reement abou

t the pr

actical

rule

of

thumb fo

llow ed by ne

urosurgeon

s that the

an

terior

part

o f

the

tem

porallobe

up to

Labbe ' s ve

in can be e

xcised without

dire c

on-

sequenc

es

f

or

t

he

language func

t ion. In

neuroa

natomical t e rms

,

Heschl

s

g

yri a re

often g iven as

the

anterior Iimit of

the

W e r n i

cke

are

a . In reg

ard to the p o

ster ior, i t i

s general ly

agreed that

th is

area

is

continuou

s

wi

th the

supramarg

inal and

ang

ular gyri

. The main

disp ar i ty betw

een d iv

erse statem

entsand

diagrams

seems to be that

some

reg

ard

o

nly the

superior tem

pora l c o n v

olut ion as

re levant to

lang

uage, whereas

others

include

t

he

middle, and

some

a

uthors even

the inf

er ior, t emp

ora l gyr

us

(

Bogen B

ogen, 1976)

. Theresul t

s based

on

electric

al cortical s

t imula t ion in

local

anaesthesia

vary

am

ong e

ar ly

report

s (Penfield

R oberts,

1959), w

hich seem to

in dicate a

more

extens

ive area,

and la ter re

ports (

Rasmussen

M

ilner, 1975

; Fed io

van

B uren, 19

75), whi

ch f ind a more

restr icted

area. I have

adopte

d

the

def ini t ion

tha

tthe W

ernicke are

a consists o

f the

posterior

par

t of

the sup

erior and

middle

temporal gyri.

In the opinion of Galaburda (1982), the W ernicke area shows a

degree of ana

t o m ic diffe

rent iat ion, judge

d

by architecton

ic criteria,

closely sim

ilar to

th

at

of the Broc

a area. He

noted :

In fact, arch

itectonic simil

arities between anterior

and

posterior la

n-

guage

areas

and

the

over lap

in

their

conn

ect ional o rgan

izat ion make

it a

somewhat surprisi

ng

finding

tha

t le

sions in

e

ither

region produ

ce su ch

different

aphasic

sy

ndromes.

(p. 443

)

t should

be n

oted

however, that the

studi

es re fer red

to have

been performed

on

rhesus m onkeys Th

e

p o

ster io r l

anguage

area

has

evolved

out of pro

isocortex

located in the

tem

poral and p o

s-

terio

r insula

r

re

gion. t co n

tain s regio

n s o f

varying cytoarch

i tectonic


39/204

OPERATIONALIZATION OF A MODEL

27

differentiation, from primary auditory sensory cortex to more gen

eralized neocortex, found in

the

inferior parietal lobule

and the

temporo-occipital junction.

Wernicke

1874)

believed

that the

Wernicke area is a store of

auditory

ward

images

Klangbilder).

The condition after injury is there

fore characterized

by

difficulties

with

auditory language perception

(total or partial

ward

deafness) and disturbances of speech (because

the appropriate auditory images for stimulating motor representations

are disturbed).

Geschwind

1979)

stated:

Much

new

information has been

added

in

the past

100 years,

but

the

general principles Wernicke elaborated still seem valid. In this model the

underlying structure of an utterance arises in Wernicke s area. t is

then

transferred through the arcuate fasciculus to Broca s area where it evokes

a detailed and coordinated program for vocalization. (p.

187)

Wernicke aphasia is characterized by fluent, paraphasic speech

and

reduced auditory comprehension. Speech is

produced

without

effort and has complex grammatical structure. Informational content

is deficient (Goodglass Kaplan, 1972;

Huber

Stachowiack, Poeck,

Kerschensteiner, 1975). The term jargon aphasia is sometimes used

for cases in which speech is totally incomprehensible,

but

jargon is

not confined toWernicke aphasia (Benson Geschwind, 1977). Rep

etition is usually disturbed to the same degree as auditory compre

hension, whereas naming performances may vary. Reading and writing

are usually severely disturbed,

but in

some cases,

they

are preserved

(Lecours Rouillon, 1976).

The

supramarginal yrus

is continuous

with the

superiortemporal

gyrus. Wernicke

1874)

regarded the supramarginal gyrus as part of

a continuous perisylvian gyrus, anatomically and functionally contin

uaus

with

the superior temporal convolution. The stimulation

data

seem to

support

this view (Penfield Roberts, 1959; Rasmussen

Milner, 1975). The reason for giving special consideration to this gyrus

isthat the

probability of

an

auditory-language-comprehension defect

is markedly lower with a lesion of the supramarginal gyrus alone than

with a lesion of the superior temporal gyrus (Luria, 1970), whereas

the

probability of

reduced

fluency of speech

with

misarticulation

and

phoneme substitutions increases, possibly because of

the

proximity

to the primary somatosensory cortex. The possibility of finding a


40/204

28

CHAPTE

R 2

sy

ndrome corre

sponding to

co

nduction

aph

asia may

therefore

exist with

lesions o

f the supra

m arginal g

yrus . Cytoa

rchitectoni

c s tudies

by Gal-

aburda, LeM ay, Kem per,

and

G eschw ind

1978)

indicatethat thepart

of the su

p ramargina

l gyrus imm

ediate ly a

d jacent to

the

sup

erior

tem -

poral g

y rus may

be long to t

he audi tory

associatio

n cortex,

whereas

m or e p

er ipheral p

o r t ions

do not.

The an

gular yrus is c

onvent iona

lly def ined

and is ana

tomically

co

n tinuous w

ith the mid

d le tempor

al gyrus. A

ccording t

o Hensche

n

1922),

only five c

ases wit

h

s

elective inv

o lvem en t o

f the

a

ngular

gyrus

had bee

n publ i shed

up tothat

time. The

pat ients

wereall alexic

and

agraphic

but

had

no

aud i tory

comprehension

defect. Lesions of the

a

ngula r gyr

us occur o

ften wi

th more exten

sive involv

em ent of

the

poster ior

language a

rea.

A

uthors

who use

an extende

dconcept

ofthe

Wernick

e area usu

ally includ

e the angul

a r gyrus e

.g . , Marie,

1906;

D

ejerine, 1

914; Penfie

ld Rober

ts, 1959). W

ernicke

1874) accord

ed

no s

ta tus to

the

angu

lar gy

rus in conn

ect ion w

ith read ing an

dwrit ing

butassumed

that asso

ciation fib

ers from

the occipita

l lobe to

the

Werni

cke area we

renecessar

y for rea din

g . The ass

umption of

a special

im por tance of the

angular

gyrus for reading

and

w riting is widely

adopted

today. So

m e autho

rs also acco

rded it a sp

ecial funct

ion in

w or d

retrieval n

aming) Ge

schwind,

1967

b;

Luria,

1970).

Anomic

apha

sia

is ch

aracter ized

by f luent

speech

with m ar ked

shor tage o

f conte

nt

w

ords . Ther

e is little p

a raphas ia

as such,

but there are

attemp

ts to

subst i t

u te circuml

ocutions an

dvague d

escr iptions

for con

tent w ords .

C

omprehen

sion and repet

ition are g

ood , but

th

ere are sev

ere prob-

le

m s in read

ing an

d

w

riting Goo

dglass K

aplan, 197

2; Kertesz

,

1

979).

les

ion encom

pass ing

bothBroca an

dWernicke

areas produces

a global

aphasia Thi

s

may

be r e

garded as

a composi te

form of ap

has ia

th

at shou

ld not be clas

sified as a

n indep

endent type,

butclinically

it

has d

istinct feat

ures.

t

is c

haracter ize

d by severe

loss in

allla

nguage

modalit i

es , but t

he pa tien t is u

sual ly not mute

Ofte

n ,he or

she has

v

erbal s tereo

types , con

sist ing of c

onvent iona

l phrases

sw earing) or

m eaningle

sssyllabic c

ombinat ion

s. In audi t

o ry com pr e

hension , th

e re

is

also some a

bility to re

act to con cr

ete words ,

particularl

y if they ar

e

em otionall

y significan

t for the pa t

ient Stach

owiak, Hub

er , Kersch

en-

stein

er, Poeck,

Wenige

r, 1977).


41/204

OPERATIONALIZATION OF A MODEL

29

2

1 3 Arcuate

Fasciculus

Very precise descriptions of this cortico-cortical fiber

bundle

are

hard

to find. t has a compact middle

portion

sweeping around the insula

parallel to the circular sulcus. The

ends

fanout

and connect the infe

rior

and

middle frontal convolutions

with

large parts of the convexity

of the temporal lobe. The existence of a direct projection from

auditory

areas to a homologue of the Broca area has been confirmed in rhesus

monkeys

by

Pandya

and Galaburda (1980).

This fiber

bundle

is

one among

several structures

assumed

to

be of functional importance

in

connecting

the

posterior language area

with the Broca area. Wernicke believed

the

insula to have this func

tion, but this possibility is now considered unlikely, and in the neo

classical literature, the

arcuate fasciculus is accepted as the major

functional connection. Lesions of the fascicle result in a conduction

aphasia

with relatively fluent speech and

good comprehension,

but

repetition difficulty. Fluency may be less than

in

Wernicke aphasia,

because the patient makes frequent attempts to correct literal para

phasias

phoneme

substitution errors).

He

or

she may

go

through

a

series of approximations in attempting to correct his or her production

( zeroing in ). In addition to

good

auditory

comprehension,

there is

also often

good

reading comprehension (Benson, Sheremata, Bou

chard, Segarra, Price, Geschwind, 1973;

Green

Howes, 1977;

Benson Geschwind, 1977).

Lesions outside the language areas

mentioned

above may pro

duce

aphasia. This means not that the areas injured have language

functions,

but

that

the language areas normally interact

with

sur

rounding areas when language is integrated in complex behaviors.

The essential feature of

such

lesions producing aphasia is

that they

disconnect or isolate parts of the entire language areas from the sur

rounding

cortex.

Total isolation produces an isolated speech area syndrome. The

patient

has no

spontaneaus

speech but responds to questions. The

response is afmost f i l ~ w a y s a direct repetition of the question. Speech

is weil aiticulated ~ d tb:e patient repeats even long sentences 'He or

aphasia and brain organization

Documents