the aphasiology of a.r. luria
TRANSCRIPT
J. Neurolin@~rics, Volume 4, Number I, pp. 1-18. 1989. 091 l-6044189 $3.00 + .OO Printed in Great Britain 0 1989 Pergamon Press plc
The Aphasiology of A. R. Luria
Lluis Barraquer-Bordasi
Autonomous University of Barcelona
ABSTRACT
Luria’s aphasiology and its features are presented. The author introduces some
considerations concerning relations and contrasts of Luria’s view and those of other
outstanding aphasiologists.
INTRODUCTION
In the second half of the last century and long before being termed as such,
aphasiology began to be used in clinical and pathological methodology and
contributed to its development.
After the Second World War, while not abandoning interest in the distribution
and topography of lesions that result in different clinical pictures of aphasia,
descriptions were directed along other lines. For example, emphasis was placed on
the dichotomies: fluency/ non-fluency, conservation of repetition (although this
obviously cannot be considered a particular “function”)/affecting of repetition.
Above all, linguistics was applied in a greater degree to aphasiology, mainly with
respect to the contraposition between the ability of syntagmatic combination and
paradigmatic choice. Chomsky’s ideas with respect to performance/ competency
and the distinction between superficial and deep structures were also explored.
Luria’s aphasiology is a modern contribution; generally, it is distinguished from
the norms by its own semiological descriptions and an attempt at its own
classification of the different types of aphasia, types that Luria himself outlined
with more or less precision and that do not correspond to those generally accepted.
Luria tried to “overcome” the classical phenomenological descriptions of
2 Journal of Neurolinguistics, Volume 4, Number 1 (1989)
aphasias and searched for partialfbctors that resulted in different basic types. rhis
author conceived three stages of aphasiology.
(a) The first “localizationistic” stage, based on the fact that the description ofthe
supposed basic clinical types was often accompanied by the attempt to find a
limited localization of the language processes in the surrounding cerebral arcas.
Until a few years ago, most of the descriptions of aphasias (although one cannot
ignore the “dynamic” currents characterized by much more “overt” signs, first
described by Jackson) were kept, if not in this strict field. at least within the
branches that more or less arose from it.
(b) The second “neuropsychological” stage, in search of the,fhcror.v iniria/!t,a/trr&
as a result of the focal lesions. This is an attempt to understand the basic
mechanisms of language.
(c) A third ~‘~~urodynam~c” stage, in the Pavlovian sense, with the idea of
understanding the basic symptoms of aphasias in terms of prrrliuf cl7atzg~j.r of this
lineage. In this field, Luria refers to two problems: (i) clisordcrs ofthe “ruk O#
jiww “, in the regulation of cortical functions, in which case weak stimulations
would determine reactions as much as or stronger than intense or large stimu-
lations: in this manner the “highly- selective nlu~tidimensional matrix”. which
constitutes language. would be impaired. This would result in the appearance of
“matrices of contextual associations”. origin of verbal paraphasias. Such disorders
would appear to electively affect thel,ostPriorpurt.v of the“language areas”: and (ii)
lust 01’ irort>rul “neural plasticit_\,“, with the appearance of “pcrtholo~~ic~al inertia”,
expressed in the language sphere by the appearance of perseverations; this would
occur partjculariy in the cases where the lesions involve the unterior purrs of the
“language areas”.
Luria placed his own contributions within the scope of neuropsychology.
estimating that the analysis of hasic,fuctor.s that support the different types of’
language disorders signified an important step in the development of aphasiolopy.
He considered the development of the analysis of “neurodynamic” mechanisms as a
new step that had just been undertaken.
On the basis of his analysis of “partial factors” that would result in the different
“basic types” of aphasia, Luria distinguished and discussed these types in detail in
the following manner.
Aeousijc~-A~nosic or Sensorial Aphasia as a Result of Posterior Temporal Lesions
Luria derived this form of aphasia from theabsence of a well-defined function or
linguistic component. the phonological component. In order to construct the
sounds of speech -.- and to understand them -- Luria and Hutton (1977) empha-
sized that we must be able to qualify sounds: stated otherwise, we must include
sounds in systems of phonemes, basic units of speech. “This qualification is done by
The Aphasiology of A.R. Luria 3
the secondary zones of the auditory cortex, particularly the region termed Wer-
nicke’s area.” Consequently, the basic defect that appears in this region is the luck of
differentiation of the phonemes. This is not an auditory defect, as Wernicke
supposed, nor an intellectual defect, as Marie (1926) implied, but rather “the ability
to convert elementary sounds into complex sounds, phonemically organized, is
affected.” This phonemic organization varies from one language to another and,
for example, characteristics such as “hard” and “soft” or “low” and “loud”, which
are pertinent to one of them, lack a differential value for many others. As a
consequence of this fundamental lack, patients with acoustic-agnosic aphasia
would be incapable qf distinguishing between ver]’ similar “oppositional” and
“correlational”phonemes that differ in onlv one characteristic (for example, they
repeat “bapa” as “ba-ba” or “pa-pa”). These disorders are characteristic of a lesion
of the secondary (auditory) zone of the temporal lobe and adjacent zones. This
modal (acoustic) disorder of systematic hearing (limited to the language sphere)
“must cause a dissociation of sounds and meariings of words, which is basic in the
sensorial aphasic syndrome”. Luria himself underlined the words and this permits us to see how the author recognized the break between the semiological level and
the semantic level of the linguistic sign that occurs in this type of aphasia, thus
approaching - perhaps more than apparent ~ the position of the school of
Alajouanine (1968) among disorders of verbal comprehension. It alone would be
genetically, Luria makes the whole defect depend on the disorder of phonemic
anaf.vsis, that is, on the first of the three physiopathological levels described by
Alajouanine (1968); among disorders of verbal comprehension. It alone would be
responsible for the final “attack” on the significance of the words.
Word repetition is seriously affected. Spontaneous language is deprived qf
substantives and can adopt the form of a “salad of words”, in which phonemic
paraphasias appear, even though the patient is able to make himself understood
because of intonation, rhythm, etc. But there exists, for the reason we just
described, an “alienation of the significance of words”. The fact of an amnesic
aspect that the patient shows in searching for a word does not improve by giving
the observer the oral outline of it.
In the “rare” cases of true verbal deafness, the disorder of phonemic hearing
would occur separately.
In more posterior temporal lesions, there is a disturbance of nominativefunction
of language, connected with an inability to evoke visual images as f~ response to a
given word. The patient presents acknowledged difficulties in drawing the figure of
the named object.
Although recognizing the presence and importance of the disorder in discrimi-
nating phonemes, which Luria emphasized so much, Blumstein et al. (1976)
concluded their analysis of phonological factors in disorders of comprehension in
4 Journal of Neurolinguistics, Volume 4, Number I (1989)
different types of aphasia, by judging that a dejtict in phonemic hearing curlnot
ucccwnt .for the comprehension disorder ,found in Wernicke’s aphasia.
Acoustic-Amnesic Aphasia
Acoustic -amnesic aphasia resulting from medioten~pora//esion.s. is located in the
centre of the temporal gyrus or in the back of the temporal lobe. The defect would
take on the form of an alteration qf audio~~erhal memor.,’ or distinct awustic
umnesic, alterations. The patient cannot retain a short series of sounds. syllables or
words in his memory; he confuses elements in the series or some elements disappear
from his memory, which implies a d<fec,t in retention qfpermanent audiolir7,~ui.~tic,
recordings. This defect has a modally specific (auditory) character. It is based,
according to Luria, on an increasing mutual inhibition of auditory signals that
leads to a peculiar reduction in the order qf successive uwustic, perception. If the
intervals between elements in the series are longer, this inhibitory effect decreases:
each stimulus is better consolidated and retention is better. There is no “alienation
of the significance of the word”. There is a “disappearance” of the acoustic structure
01’ the words.
Semantic Aphasia
According to Luria, semantic uphasia originates from a disturhunc,e, at the level
of s~~mholic simultaneous s.vnthesis (“quasi-spatial”), dependent on a lesion c$thr
supramodal third parietal injtirior zone (angular gyrus and supramarginal gyrus,
areas 39 and 40 of Brodmann) or, more broadly. the parieto-temporo-occipital
zone. This region is very characteristic of the human brain and it does not become
morphologically mature until about age 7. The patient presents amnesic l,erhu/
d+cts in the strictest sense, that improve when the oral outline of the word i\
offered. For Luria, the “dynamic disturbances of the law of force” of the local
cortical function (in the Pavlovian sense) that occur in such lesions can lead to an
equally probable multitude of possibilities of association, either of the phonetic
nature (we would have to say phonological to keep to thedifferentiation of Lecours
and Lhermitte (1976)), morphological nature or semantic nature, from which
emerge all types of’paraphasias (phonemic and nominal, of the morphological or
semantic type). The difficulty in finding words is mainly- concentrated in the
designation of objects (substantives) and less in that of qualities (adjectivea) and
actions (verbs). What would be altered would be the designation of conc~rete
objects. not the abstract category. This would be related to the d$ficulties that such
patients show in carrying out the visual representations of the corresponding
objects (Tsvetkova 1977). Such patients, although thqv under.ftand the.rignifi’c,clnc,r
of the individual r<-ords, cannot understand the significance ofthe constrwtion a.? (I
The Aphasiology of A.R. Luria 5
whole. They cannot appreciate the significance.of the logicogrammatical relation-
ships. They can understand the “communication of events”, but not that of
“relationships” (in the terminology of Svedelius). A typical example is given by the
structure of the attributive genitive case (they cannot distinguish between “the
brother of the father” and “the father of the brother” or “the cross is under the
triangle” and “the triangle is under the cross”) which, in contrast to simpler
constructions, such as the partitive (“piece of bread”), “cannot be visualized in
concrete terms, but they express certain abstract relationships”(an idea that Luria
proposed and even underlined). Nor do they understand sentences such as:
“Tatiana is darker than Sonia, but blonder than Katherine.” The patient presents a
kind of “receptive agrammatism,” at least in a certain dimension. In this manner,
the comprehension of syntagmas offering a definite structuration is electively lost,
which expresses the disintegration of certain semantic schemes. The picture is
associated with a disturbance in arithmetic ability, constructive apraxia, etc.
Two very characteristic features of Luria’s ideas are the following.
(a) On the one hand, he places the break in simultaneous synthesis, implicated as
a primary factor in this type of aphasia, in the line of disorders with a “yuasi-
spatial” basis. “It is well known,” stated the author, “that lesions of the inferior part
of the left parietal zone inevitably results in disorders of orientation and space,
which are associated with serious defects in calculation and an inability to
understand complex logico-grammatical constructions.” Here, Luria wants to refer
to the existence of disorders within the “interior psychological space”, which would
prevent the capture of “quasi-spatial” relationships implicated in sentences such as
those previously referred to. Lesions of the inferior parts of the left parietal zones.
in eliminating the factor of simultaneous spatial synthesis, result in - states Luria
- a disorder of these complicated forms of verbal behaviour.
(b) The other great feature of Luria’s ideas that we want to mention here refers to
the declared opposition between the serial and sequential disorder, which depends
on lesions of the premotor cortex and simultaneously, concurrently, the “quasi-
spatial” disorder, resulting from inferior parietal or parieto-occipito-temporal
lesions. Jakobson (I 964) picked up this opposition formulated by Luria and placed
it as one of his three basic dichotomies in the estimation of different types of
aphasia.
The symptoms accompanying semantic aphasia would reflect the same disorder of “simultaneous synthesis”. Hence, disorders in spatial orientation, constructive
apraxia and acalculia.
Hier et al. (1980) studied three cases of semantic aphasia, basically adhering to
Luria’s ideas. For two patients, the CAT revealed infarcts at the left parieto-
6 Journal of Neurolinguistics, Volume 4, Number 1 (1989)
occipital junction and the third patient presented bilateral haemorrhagic lesions at
the temporo-parieto-occipital junction. The three patients also presented construc-
tive apraxia and elements of Gerstmann’s syndrome. The authors suggested that
“the aphasic as well as spatial disorder of patients with semantic aphasia can be
manifestations of a common defect in the perception of spatial relationships,
produced by a lesion in the left temporo-parieto-occipital region.” Apart from the
fact that the inclusion of the temporal topographic component can be unnecessary,
we want to personally emphasize that as much as the disorder defined as semantic in
such cases has a “parallelism” to the spatial and, even though its “analogous
structure” is found, so to speak, in other situations, the semantic level of language
(that of meanings), is affected in itself. To explore this would imply. among other
things, raising the idea of aphasia defined as “semantic” (\ji& irr!ru).
Lhermitte et al. (1976), Melice-Ledent et ul. (1976) and Gainotti e/ (I/. (I 983) have
been concerned, in one way or another. with this.
Afferent or Apraxic Motor Aphasia
A.fjivent or apraxic motor aphasia depends on an q~fi~t-tmt altrration of the
movements qf the speech apparatus, caused by a lesion oj’the rolandiic~ operculrrm
and the ir$v?or parts qf the post-rolandk area. Such a loss of precise oral
movements eliminates one of the physiological requirements for correct verbal
expression. The basic disorder would originate in a~~ositionalapruxia c;f’thespeech
organs in the search for suitable articular movements for the different sounds
(articular schemes qf “articulernes”: ” basic units of motor language”).
In the most severe cases, the patient cannot find a single combination of the
necessary movements for the pronunciation of the proper sound. In the mild cases,
the substitutions begin to take on a more concrete form. confusing, for example,
labial sounds (“b” for “p” or for “m”). The writing is also affected, as the graphemes
for which articulation is similar, are substituted one for the other.
Lecours (1980) stated that he had never observed a iesion limited t(J the left
ascending parietal gyrus, which undoubtedly leads to a v’ery cautious attitude
towards the anatomo-physio-clinical idea that Luria postulated for the aphasia he
defined as afferent motor or kinesthetic. Nevertheless, Lhermitte pt u/. (1980)
described a kinesthetic motor aphasia syndrome associated with a “pseudo-
thalamic” sensitive defect syndrome resulting from a partial left superficial .silvian
infarct, revealed by a CAT. Neurolinguistic study of this case revealed that the
patient had a disorder of oral productions characterized by a high incidence of the
substitutions of articulation. differentiated from the arthric disorders, as well as the
phonemic jargon. They conclude that “kinesthetic aphasia would be differentiated
by this clinical specificity and by the site of the lesion: anterior parietai lesion of the
The Aphasiology of A.R. Lurk 7
dominant hemisphere”. But they cannot define or even approximate the frequency
with which it occurs.
Luria recalled the positions of Marie (1926) (anarthria), Alajouanine et al. ( 1939)
(syndrome of phonetic disintegration), and Bay (1964) (cortical dysarthria),
“approximating” them to his kinesthetic motor aphasia, although he defined the
basic defect as “apraxic”, a “reduction” that Alajouanine and Lhermitte (I 960) did
not accept. For the rest, the lesions causing a syndrome of phonetic disintegration
were identified in the inferior portion of the ascending frontal gyrus or in the second
frontal gyrus (Lecours and Lhermitte 1976; Puel cf al. 1984).
Efferent Motor Aphasia
Efferent motor aphasia is a consequence of the disorders of motility that,
according to Luria, are created by lesions of thepre-motor zone, relapsing in such a
case concretely in the sphere of motility that intervenes in oral expression. There is
an inertia of the “articulemes”. The patient loses the ability to pass without a
solution of continuity from one articular position to another.
Pronunciation of sounds in serial combination is severely affected. The dynamic
aspect of the verbal activity, the fluidity, is lost. There are perseverations. But the
ability to pronounce “pure” sounds in individual form is retained. The essential
elements of this form of aphasia are the loss of the serial or sequential organization
of language, a result of the pathologic inertia of the individual articular impulses,
and the disorder of the interior language that develops after the acute clinical
picture, in subsequent states, is connected with motor agrammatism. Trying to
repeat sentences, the patient is only able to reproduce some words, usua/l~
substantives. His spontaneous language is transformed into an enumeration of
objects, but in spite of this, he cannot express a thought in the.form of aproposition.
He has lost the predicative significance of’ wlords.
These last aspects of the description that Luria presents of his “efferent motor
aphasia” inevitably remind us of Pribram’s (1971) idea with respect to “predi-
cation”, as a basis of the “productivity” (Jakobson 1964) of language.
In his book, Fundamentos de Neurolingiiistica (Fundamentals of Neurolinguis-
tics), Luria (1980) places and studies separately the disorders of the syntagmatic
organization of verbal codification, in patients with “telegraphic style”, from those
with complex forms of “efferent motor aphasia”, which implies separating, at least
up to a certain point, the agrammatism of “Broca’s aphasia”.
Luria states that in cases of lesions of the inferior zones of the pre-motor area, the
disturbance in codification of expression acquires a different, more specific charac-
ter, compared to that observed in “dynamic aphasia”. The main component
involved in this case is the predicative structure of expression, while its denomina-
tive components remain intact. If such a disturbance is severe, a “telegraphic style”
8 Journal of Neur~li~guistjes, Votume 4, Number 1 (1989)
results, in which the predicative structure of coherent speech disintegrates and
speech, as a whole, consists of only “nominative” components.
According to Luria, in the less severe cases or in some states of regression, the
“telegraphic style” is replaced by a lesser form ofagrammatism, in which the simple
forms of predicative organization of expression (such as the simple subject-predi-
cate struture) are made possible, while the more complex structures (for example,
the complex subordinated intercalates) and the observation of rules of agreement,
etc., are affected.
Finally, Luria states that there is a “third group ofcases”(and the third is between
quotation marks, to separate it from dynamic aphasia and “telegraphic style”), with
a clinical picture of efferent motor aphasia, jt.irh disorder of’rlrc kinetic t~ekmf~~ c!f
\tvrds andpathoiogic inertia. This last factor, probably related .-- he states --- to
deep lesion foci in the anterior zones of language. is not in itself a speech defect, but
it makes this disorder more severe and results in the complete inability to produce
coherent speech, which requires the possibility of fluid steps from one element to
another of oral expression. “Such defects;” Luria emphasires. “constitute the main
characteristic of the form of aphasia usually known as Broca’s aphasia,” It 15
important to recognize Luria’s point of view regarding the importance that
“pathologic inertia” would have in this “very classic” form of aphasia (it would be
connected, in a certain manner, to the loss of fluidity of oral expression) as well as in
the anatomo-clinical field, the value given, in the appearance of this inertia, to the
“severe” or “penetrating” character of the lesion. Let us remember here that
Hecaen and Consoli (1973) were able to find very different characteristics in their
patients with lesions in Broca’s area; they were superficial. deep or penetrating.
Dynamic Aphasia
Dynamic aphasia occurs, generally, as a result of lesions y$‘the ir@+iorpar-rs q/
thefkontal lohe, anterior to Broca’s area. Its distinguishing characteristic is that
even though the ability to utter words and repeat sentences remains intact, the
patient finds himself completell.lackingspontaneorts language and very rarely does
he use it to communicate. The involvement of different parts of the premotor zone
of the more anterior frontal cortex gives different nuances to the clinical picture. In
dynamic aphasia, there are no disorders: (i) of the external organization, either
auditory (as in sensorial aphasia) or motor (as in the two variants of this, which
Luria distinguishes); or (ii) of the internal, logico-grammatical organization (as in
the case of semantic aphasia), all these sectors of language remaining intact. But
there is a loss of the spontaneity, ~~Ianguage, to use an expression of Kleist’s ( i 934)
to characterize the disorder of his frontal patients. Luria extracts the defect that
dynamic aphasia expresses from a stage of “interior language”. “preliminary
scheme” of a “theme”, which must be verbally expressed. Remember that for
The Aphasioiogy of A.R. Luria 9
Vygotski (1962) this necessary stage of interior language has a predicative function.
Therefore, one might state that, generally, the “predication” would be compro-
mised, although at different levels, in both dynamic aphasia and efferent motor
aphasia.
This type of disorder usually becomes evident when the patient is questioned; the
questions initiate an echolalic repetition. If, on the other hand, he is asked to givea
long narration, he only gives brief, simplified, elementary responses. This is more
evident in writing, although writing by dictation remains intact. The loss of the
ability to narrate is characteristic.
In one of his works. Luria expressed himself as follows: “. . . in cases of severe
lesions of the frontal lobes, the patient is unable to express his intentions and
thoughts. either in the verbal or written forms”. “I will never forget,” stated the
author, “a letter written by a woman who had a severe lesion in the frontal lobe. to
the famous neurosurgeon, Professor Burdenko. ‘Dear Professor,‘she wrote, ‘I want
to tell you that I want to tell you that I want to tell you that I want to tell you.. .‘.
and she filled four pages of the letter without taking another step!”
Commenting on dynamic aphasia, Jakobson (1963) emphasized that the ability
for monologue is selectively lost in this disorder.
As we just mentioned, according to Luria, the basic element of this aphasia, at
least for the most part, would be a disorder of the interior language. “In some of
those cases,” as written in F#~d~~e~r~s de ~eur~~jng~isfica (Luria 1980), “repeti-
tive coherent speech remains intact. but, as a consequence of the disorders of the
‘interior language’ and the formation of ‘deep syntactic structures’, the active
creation of what many authors define as ‘linear scheme of the sentence’ becomes
impossible and the patient is unable to formulate a spontaneous expression or
convert his thought in developed speech.”
It is very interesting to note the reference Luria makes, as we saw previously, of
the presence of echolalia in his “dynamic aphasia”, as it raises the problem of
“approximation” between it and the classical “transcortical motor aphasia”.
In Jakobson’s (1963) view, dynamic aphasia can be considered as a definite form
of destructuration of contextual language, respecting its basic code relatively well.
Luria described the localization of lesions producing dynamic aphasia, and
implicated a disorder of the posterior frontal and premotor zones of the kft
hemisphere.
For Luria, his dynamic aphasia “is identical”, in part, with the form of aphasia
described by Head (1926) as “verbal aphasia”. But other authors compared,
instead, the latter with Broca’s aphasia of the “classics”.
With respect to the idea of dynamic aphasia, if one wants to characterize it by a
loss of monologue with dialogue remaining intact, it can be placed in the study
carried out by Ramier and Hecaen (1970) regarding the defects of verbalfluenc?~.
10 Journal of Neurolinguistics, Volume 4, Number 1 (1989)
This defect is particularly evident in left frontal lesions (Miller. Benton), but it also
appears, although to a lesser degree, in the right frontal lesions and appears to
depend (according to Ramier and HCcaen (1970)) on the interaction of two factors:
the loss of the incitement to action, connected with ,frontal lesion. and lqft
laferalization, by hemispheric “dominance”. The defect is analyzed by asking the
patient to give, in a determined amount of time, the most possible number of words
starting with certain letters and placing certain restrictions(no proper names, etc.).
There is a relationship with disorders defined by frontal lesions located in front of
“Broca’s area”: loss of spontaneity of language, etc.
Tissot (1966) believed that the form Luria defined as “semantic”is very similar to
that which Head (1926) defined in the same manner, and heconsideredthat in both
cases this tkfinition \t’as inadequate; “unfortunate”, he stated. The nominal
aphasia of Head (1926), “in the linguistic sense,” stated Tissot, “should be
classified as semantic.” For the same reason, it should not be what Head so termed.
as in its content it is similar to what Luria resorted to giving the same definition.
Therefore, according to Tissot (1966), the expression “semantic” would not be
justified either in Iuria’s recent descriptions or the older ones of Head. “Indeed.”
stated this author. “for the patients with this disorder, the separate words have not
lost their significance: rather their arrangement in the speech chain, their reciprocal
relationships. as well as the indication of their relationships with functional
monemes. their subordination. and coordination, are no longer grasped.“Spcaking
properly, this disturbance could not be defined as semantic except in the measur-e in
which the meaning of most of the words is determined partly by the context in
which they appear. The current genesis of the concept through the context would be
compromised in this form of aphasia. But the basic disorder would be based on the
disturbance of the system of relationships between the different signs of what is
stated. “We find it difficult,” stated T&sot (1966), “to find an univocal linguistic
explanation.“This author hastens to indicate that this is not even Luria’s intention.
who, in what he terms semantic aphasia, sees a disorder of language secondary to a
much more general disturbance of a “complex function of simultaneous spatial
temporal synthesis”.
What Tissot does is to bring his comments to this“base”levelpostulated by Luria.
For him. when Luria talks of a “loss” of the “complex simultaneous synthesis”, he
means. among other things, a d(fficu1t.i. in anal.txzing a complex simrritaneous
datum in a series that de\velops in time and inverse!)?. Tissot approximates this
aphasiological appreciation to the linguistic criterion of Tesniere (1959). who,
according to what the former explained, in constructing his structural synthesis,
states that “to talk is to transform a structural order into a linear order”, while
“understanding is to transform a linear order into a structural order”, as he suggest:,
it, by means of a spatial scheme, through which the function of each word in the
The Aphasiology of A.R. Luria 11
sentence would be indicated. For this linguist, syntax would consist of the study of
such a structure, while morphology would be limited to the study of signs that
would facilitate the transformation of that structural order to a linear order.
Tesniere’s (1959) analysis develops a proposition by Martinet (1960), inasmuch as it
states that the true reason for syntax is to try to explain how one can reduce a fact of
experience, that in itself is not a succession, into a linear succession of discrete
elements,
Tissot continues to explain that in “semantic aphasia” conceived according to
Luria, one of the model difficulties would be the impossibility to grasp, to
und~rsfand. the value of word.? as a~~nctio~z of‘context. For Luria, as for Head,
continues Tissot, the defect of actualization of the contextual sense is connected
with the loss of the possibility, as much to express as to understand, all the
relationships that connect the words in the sentence. “Is it possible to raise the
question,” Tissot asks himself, “if the two phenomena are unconditionally connec-
ted or not?” Be that as it may, these disturbances are the central point of the context
and belong, therefore, to the syntagmatic or contrast function. Thus, for this
author, the “semantic aphasia” of Head and Luria would involve the syntagmatic
central point rather than the semantic level, while the aphasia truly relative to this
other great central point of language would be what Head defines as “nominal”,
erroneously superimposed or approximated to “amnesic aphasia” by many.
Tissot emphasizes that while both Head and Luria give importance to the
parieta( t0pograph.y of lesions that produce a so-called “semantic aphasia”, these
are, instead, ternporal(in accordance with Alajouanine and Lhermitte (I 960)) when
there is a break between significant and signification, this disturbance being
situated in the central point of the lexicon, of the system of paradigm, playing there
the function of opposition. Precisely such a break of the link between signification
is the main fact, for Tissot, of fme semantic aphasia; this is that termed nominal in
the descriptions by Head. In such a case the lack of the correct, appropriate word is
characteristic and is replaced by a periphrasis.
The erroneous form in which, both for Head and Luria, semantic aphasia would
have been delineated, leads Tissot to examine in detail the dissociation that the
aphasic disturbances can create between the two levels: (i) the level of sense, for
one; and (ii) the level that includes at the same time, in Tesniere’s (1959) concept
previously referred to, the structural and linear order of the sentence.
Tissot states that the two levels are not independent, as the second one supports
the first (on the level of sense), but they cannot be confused, he argues. Tissot
explains that subjects with “semantic aphasia”(in the sense of Head and Luria, that
is. in the sense of the lack of the contextual support) could have kept the structural
order as well as the linear order of the sentence, but, for them, such a level would
have lost the value of the support of sense.’ One could perhaps say that the
12 Journal of Neurolinguistics, Volume 4, Number I (1989)
morphosyntax would become powerless, insufficient, to open access to the level of
sense. this being lost in the contextual “dilution”(converted from support and light
to obstruction and darkness). But this would occur in the specific form at :hr
expense of the loss or erosion of sense( or of significance) of the specified monemes of
a certain type. placed in key positions of linear syntagma. These would be w70~7~~17t~s
with a ke>’ “relational” sense, as are “more than”, “less than” (pairs that we might.
perhaps. define as “syntemes”), “greater”, “ lesser” (or “larger” and “smaller”). “of
(genitive in its attributive function). A branching transformational concept would
permit us to situate the L‘Io~~u.~” of the change producing the loss of semantics ot
what is stated in such cases. We could state that, just as in aphasia c~~u.wt1 !)I’ {I
temporal lesion. a semantic d&w can occur,fi-om the loss qf’the \,alur cif’~hr .sigr~
that a moneme (the minimal sign) has, in Luria’s semantic aphasia, t/w afj&iiu,y t jf’
thr .semantic value ~.ould take plaw at another IeLaeI, that of’the mtrrllal oyuui-
zation of’certain s.l~ntaKmas.
In a comparison of Luria’s classification with others found in the present
literature. it can be stated that those that are closer to a “clinical empiricism’”
emphasize the value of the dichotomy between decreased fluidity and illtact or
exaggerated fluidity (with a tendency towards logorrhea), as well as t.hat u hich
establishes the presence or not of a manifested disturbance of repetition (which, as
Brown (1972) emphasizes, is not, obviously. a linguistic function that can he
individualized).
On the other hand, many anatomo-clinical classifications tend to be supported
by or even exaggerate the separation between aphasias caused by anterior lesions,
whose prototype is Broca’s aphasia, and the aphasias caused by posterior ie\ions.
centered on Wernicke’s aphasia. One is led to the first classification of “motor”
aphasia, and the second, of “sensorial” aphasia, thus reducing the quesuon to an
outline that is both caricatural and incorrect. Geschwind (1984) stated that hc had
repeatedly objected to such a sensori-motor classification as being inaccurate.
Thus, for example. in Broca’s aphasia, there are disorders of comprehension, II!
particular of grammatical comprehension. But, even the terms “motor” and
“sensorial” are not the most appropriate to define the disturbances air language.
especially at specified levels.
In fact, a thorough examination in terms of aphasiology would require. a> has
already been done by others, detailed examination both of the linguistic factors and
those related to neural organization, as well as a balanced approximation between
the two fields. Kean (1984) stated that whereas the structure of language (gram-
mar). the process of language for production and comprehension. and neuro-
anatomy and neurophysiology of language are all conceptually distincl. from each
other, “the study of the aphasias is not itself a conceptual distinct domam
in the sense that there could ever be a characterization of an independent
The Aphasialogy of A.R. Luria 13
level of conceptualization and a representation of human linguistic capacity”.
To speak of cerebral zones in relation to some defined as “articulemes” seems to
us to approach too closely to the old hypotheses of some “centres” (although we
know that Luria thought in terms of “complex functional systems”) in relation to
some “images”.
The neurofinguistic classrjkation tendency is, in fact, a corollary of the classic
aphasiological tradition associated with linguistic knowledge. These classifications
“attempt to integrate the models of contemporary linguistics with the recent
aquisitions in the knowledge of the anatomo-functional organization ofthe brain”.
For Gainotti et af. (1977), the attempts of Hecaen, the directions of Tissot and the
systematization of Luria enter into this sphere. Gainotti and colleagues ascribed to
the neurolinguistic tendency that attempts to differentiate the strictly linguistic
components of aphasic verbal conduct from those other extralinguistic compo- nents. We want to point out and retain the following two elements.
(a) Aphasia must be considered as a whole.
(b) The different clinical forms of aphasia are probably due to the super-
imposition of extralinguistic disorders over this central disintegration of language.
The model proposed by Gainotti et al. (1977) is derived from some hypotheses of
generative linguistics and, in particular, the distinction established by Chomsky
between the levels of competence and realization or actuation. The first of these is
considered as a group of rules and interiorized processes, which constitute the
linguistic knowledge of the subject, while the second is considered as the actuali-
zation of such competency in a concrete situation, in which the verbal realization is
defined, not only by the mentioned linguistic competency, but also by non-
linguistic factors (perceptive and motor, praxic, mnesic, etc.). According to
Chomsky, a put~olog~ spec$c to language is oniy caused b_v disorders ofcompe- Ience. Among the disorders placed “befow” the level of competency. we would
mention, as do Gainotti and colleagues, “dynamic” aphasia of Luria, the “syn-
drome of phonetic disintegration” (anarthria) of Alajouanine and colleagues,
“cortical dysart hria” of Bay ( 1964), “speech apraxia” of Darley et al. ( 1975) and
other North American authors. Gainotti and colleagues disagree with Hecaen and
his school insofar as this latter group denies the existence of a break in competency
(only accepting the disintegration of some factors of realization) in any of the forms
of aphasia.
Gainotti and colleagues only want to emphasize “the fact that in many clinical
forms of aphasia there is some involvement of semantic (lexical) structures of
language”. Study of some aspects of comprehension of oral language in aphasias
suggested to Gainotti and colleagues that “ in semantic jargons, the verbal defect is
not due to involvement of one or more components of the system of realization
abilities, but, rather, the break in the true level of integration of language”. For NEL 411-B
14 Journal of Neurolinguistics, Volume 4, Number 1 (1989)
them, “the break in the semantic level of integration of language is a basic disorder
in many forms of aphasia”. Patients with amnestic aphasia can present important
errors in semantic discrimination. Moreover, many aphasic patients (Gainotti and
Lemma (1976) and other authors) presented even an impairment of the semantic
sphere that went beyond the verbal field.
We conclude with a brief mention of present-day problems concerning the
written language. Those who maintain the traditional position on the role of
phonemic process in writing, Luria included, maintain that all writing depends on
phonemic mediation. In reality, as argue Shallice and Heilman’s school (Roeltgen
and colleagues), the systems that can intervene in writing are diverse. A phono-
logical system can intervene in the conversion of a phoneme into a grapheme when
one attempts to write unfamiliar words or pronounceable chains of letters that are
not true words. In contrast, there is a lexical system (of evocation of the whole
word) that can be important in writing familiar words, irregular words -~ that
cannot be spelt out by direct conversion of the phoneme to grapheme ~ and
ambiguous words. Roeltgen and Heilman (1984) proposed the existence of two
systems used in the ability to spell: one lexical-semantic and the other phono-
logical. Each one can be affected separately. Lesions also can occur in different
sites. In lexical agraphia, they are localized in the posterior part of the angular
gyrus, while in phonetics, the lesions involve the supramarginal or insular gyrus and
spares the angular gyrus.
Concrete reference to the field of written language includes one of the particular
modifications to be done in the concepts in Luria. Many others can be formulated,
either in a particular field such as this or of a more general nature. But this is beyond
the perspectives of this report.
ACKNOWLEDGEMENTS
The author wishes to thank Drs Jordan Grafman and Irene Litvan for the English
translation of the manuscript.
NOTES
1. Please send all correspondence and reprint requests to: Lluis Barraquer- Bordas, Neurology Department, Sta. Creu i St Pau Hospital, Avgda, St.
Antoni Ma. Claret, 167 HO8025 Barcelona, Cataslonia, Spain,
The Aphasiology of A.R. Luria 15
REFERENCES
Alajouanine, Th. 1968 L’Aphasie et le Iangage p~tho~ogiq~e, Paris: J. B. Bailliere.
Alajouanine, l-h. and F. Lhermitte.
1960 “Les troubles de activites expressives du langage dans l’aphasia.
leurs relations avec les Apraxies,” Revue Neurologique 102,604-633. Alajouanine, Th., A. Ombredane and M. Durand
1939 Le syndrome de desint~gr~t~on phon~tique dans ~‘aphasie. Paris:
Masson.
Bay, E.
1964 “Principles of Classification and their Influence on our Concepts of
Aphasia,” in Disorders of Languages, A. V.S. De Reuck and
M. O’Connor (eds), London: Churchill.
Benton, A. L.
1968 “Differential Behavioral Effects in Frontal Lobe Disease,” Neuro- psychologia 6, 53-60.
Blumstein, S. E., E. Baker and H. Goodglass
1976 “Phonological Factors in Auditory Comprehension in Aphasia,”
~~europs~ch~~ogiff 15, 19-30.
Brown, J. W.
1972 Aphasia, Apraxia and Agnosia. Clinical and Theoretical Aspects,
Illinois: Charles C. Thomas Springfield
Darley, F, L., A. E. Aronson and J.R. Brown
1975 Motor Speech Disorders, Philadelphia: Saunders,
Gainotti, G., C. Caltagirone, G. Miceli, C. Silveri and G. Viila
1983 “Recherches sur la d&integration semantico-lexicale dans l’aphasie,”
in Centenario de la neurologia en espafia, Barcelona: Hospital de Sant
Pau, Servei de Neurologia.
Gainotti, G. and M. A. Lemmo
1976 “Comprehension of Symbolic Gestures in Aphasia,” Brain and .I_an-
guage 3,45 l-460. Gainotti, G., G. Miceli and C. Caltagirone
1977 “A Neurolinguistic Model for the Study of Aphasia,” European Neuro-
logy 15, 20-24. Geschwind, N,
1984 “Neural Mechanisms, Aphasia and Theories of Language,“ in Biologi-
cal Perspectives on Language, D.Caplan, A. Roth Lecours and A. Smith (eds.), Cambridge, MA: MIT Press,
16 Journal of Neur~linguistics, Volume 4, Number 1 (1989)
Head, H.
1926 Aphasia and Kindred Disorders qf Speech, Cambridge: Cambridge
University Press.
H&zaen, H. and S. Consoli
1973 “Anatyse des troubles du langage au COW-S des l&ions de j’aire de
Broca,” Neurops):rho/ogia 11, 377-388.
Hier, D. B., S. I. Mogil, N. P. Ribin and G. R. Komros
1980 “Semantic Aphasia: A Neglected Entity,” Brain and Language 10,
120-131.
Jakobson, R.
1963 Essais de f~ngi~istique g&&a/e, Paris: Minuit.
1964 “Toward a Linguistic Typology of Aphasic Impairments,” in Disorders
c~f Language, A. V. S. De Reuck and M. O’Connor (eds.), London:
Churchill.
Kean, M. L.
1984 “Linguistic Analysis of Aphasic Syndromes: The Doing and Undoing
of Aphasia Research,” in Biological Perspectives on Language,
D. Caplan, A. Roth Lecoursand A. Smith(eds. ), Cambridge. MA: MIT
Press.
Kleist, K.
1934 ~ehir~patho~og~e, Leipzig: Barth.
Lecours, A. R. 1980 “Correlations anatomo-cliniques de I’aphasie. La zone du langage.”
Revue Neurologique 136, 59 I-608.
Lecours, A. R. and F. Lhermitte 1976 “The ‘Pure Form’ of the Phonetic Desintegration Syndrome (Pure
Anaesthesia): Anatomo-clinical Report of a Historical Case.” Brain
and Language 3, 88-l 13.
1979 L’Aphasie, Paris: Flammarion.
Lhermitte, F. and J. Derouesnt 1976 “L’Aphasia amn&sique: etude de 2.5 cas.” Revue ~~~l~ro~~~g~que 132,
669-680.
Lhermitte, F., M. Desi, J. L. Signoret, and G. Deloche
1980 “Aphasie kinCsthtsique associte a un syndrome pseudothalamique.”
Revue Neurologique 136, 657-688.
Luria, A. R.
1964 “Factors and Forms of Aphasia,” in Disorders of ~~~g~~age.~, A. V. S.
De Reuck and M. O’Connor (eds.), London: Churchill.
I974 Cerebro y Lenguaje, La Afasia Traumcitica Sindromes, Esploraciones?*
Tratamiento, Barcelona: Fontanella.
The Aphasiology of A.R. Luris 17
1974 El Cerebro en Accidn, Barcelona: Fontanella.
1977 “On Quasi-aphasic Speech Disturbances in Lesions of the Deep Struc-
tures of the Brain,” Brain and Language 4,432-459.
1980 Fundamentos de Neurolingiiistica, Barcelona: Toray-Masson.
Luria, A. R. and J.T. Hutton
1977 “A Modern Assessment of the Basic Forms of Aphasia,” Brain and
Language 4, 129- 15 1.
Marie, P.
1926 “Presentation de malades atteints d’anartrie par lesion de l’hemis-
phere gauche du cerveau,” in Travaux et Memoires, X, Paris: Masson,
Martinet, A.
1960 Elements de linguistique generale, Paris: Colin.
Melice-Ledent, S., G. Gainotti., P. Messerli and R. Tissot
1976 “Logique Clementaire et champs semantiques dans l’aphasie,” Revue
Neurologique 132, 343-359.
Pribram, K. H. 197 1 Languages of the Brain. Experimental Paradoxes and Principles in
Neuropsychology,, London: Prentice Hall.
Puel, M., J. F. Demonet, D. Cardebat, et al.
1984 “Aphasies sous-corticales: etude neurolinguistique avec scanner X de
cas,” Revue Neurologique 140, 695-7 10.
Ramier. A. M. and H. Hecaen
1970 “Role respectif des atteintes frontales et de la lateralisation lesion-
ncllc dans le deficits de la fluence verbale,” Revue Neurologique
123, 17-22.
Roeltgen, D. P. and K. M. Heilman
1984 “Lexical Agraphia: Further Support for the Two-System Hypothesis
of Linguistic Aphasia,” Bruin 107, 8 1 l-827.
Shallice, T.
1981 “Phonological Agraphia and the Lexical Route in Writing,” Brain 104,
4 12-429.
Tesniere, L. 1959 Elements de syntaxe structurale, Paris: Klincksieck, edit.
Tissot, R.
1966 Neuropsychopathologie de I’aphasie, Paris: Masson.
Tsvetkova, L. S.
1977 Reeducacidn de1 Lenguaje, la Lectura y la Escritura, Barcelona: Fon-
tanella.
18 Journal of Neurolinguistics, Volume 4, Number I (1989)
Vygotsky. L. s.
1962 Thought andlanguage, E. Hausmann and G. Vaker (eds.), Cambridge,
MA: MIT Press.