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Aspects of Aphasia
Department of Psychology, Moscow University, Moscow ( USSR)
One of the most i mpor t ant tasks in t he present -day st udy of language disorders, is
t o bri ng t hem within t he ambi t of moder n neur ol ogy and neur ophysi ol ogy; to find
fact ors underl yi ng language di sorders correspondi ng with different focal lesions of
the br ai n; and t o deduce t her ef r om some pri nci pal forms or syndromes of language
deficit. I t is well known t hat aphasi a represents a highly compl i cat ed f or m of disturb-
ance of symbolic f or mul at i on and expression, but this di st urbance needs a detailed
physi ol ogi cal analysis in or der t o include aphasi a within t he field of neurol ogy. The
wel l -known syndromes of sensory or mot or aphasia, of semantic or dynami c
aphasia, will be bet t er under st ood aft er careful psycho-physi ol ogi cal st udy of this
I n fol l owi ng this line of appr oach whi ch was st art ed some t hi rt y years ago, I pr opose
t o describe some dat a whi ch mi ght perhaps serve as compl ement ar y t o t he studies
upon aphasi a which have been done in Gr eat Britain. I shall begin with t he so-called
sensory aphasi a and aft erwards deal with cert ai n ot her types.
I t is well known t hat the left t empor al l obe (WERNICKE'S zone and the areas connect ed
t heret o) is regarded as represent i ng an i mpor t ant par t of the cortical t ermi nat i on of
t he audi t or y system, whi ch PAVLOV preferred to speak of as the acoust i c anal yser.
Thi s zone is very i nt i mat el y connect ed with t he left t empor al part s of t he speech area
of t he cor t ex and lesions t here result in a mar ked di st urbance in t he most compl i cat ed
f or ms of acoust i c analysis, and part i cul arl y in t he di scri mi nat i on of phonemes.
Experi ence wi t h many pat i ent s wi t h gunshot wounds and also with t umour s of
t he left t empor al lobe has demonst r at ed t hat the acui t y of heari ng can remai n un-
disturbed, but t hat the di scri mi nat i on of compl ex non-verbal sound-systems may
suffer. Thus t he di scri mi nat i on of ver y br i ef sounds or of cert ai n sound-series - - a b
c d as opposed t o a c d b - - c a n b e mar kedl y i mpai red. The di scri mi nat i on of speech
sounds (phonemes) is as a rule severely upset.
Wi t h slight injuries t here results a difficulty in the di scri mi nat i on of t he so-called
J. neurol. Sci. (1965) 2:278-287
correl at i ve or opposi t e phonemes only, whi ch possess mer el y one distinctive feat ure
as bet ween p/ b, d/t, v/ w, etc. Wi t h mor e severe injuries, however, even disjunctive
phonemes lose t hei r distinctiveness and the vi ct i m is unabl e t o single out verbal
sounds f r om a spoken word, and he t ends t o percei ve ver bal sounds as noises.
Fig. 1 illustrates the results of the t est i ng f or di scri mi nat i on of correl at i ve phonemes
in a series of 800 pat i ent s wi t h focal br ai n disease.
9 4 . 7 %
60 . Oo
4 0 0 %
3 0 25.
o /,
Fig. 1. Distribution of frequency of cases with impaired phonematic perception, according to the
localization of the cerebral lesion.
The loss of acoust i c and verbal acoust i c di scri mi nat i on is a pr i mar y f act or in the
case of lesions of the left t empor al lobe, and par t i cul ar l y of T1. But i f this f act or is
di st urbed, a series of secondar y s ympt oms will follow. Thus the pat i ent will become
unabl e to percei ve spoken speech and will t her eby fail to achi eve the compr ehens i on
of wor ds ( t r a v e l - - t r o u b l e - - d r a b b l e ) . He becomes unabl e t o name objects and
cannot utilize acoust i c clues. Me mor y t races of the spoken words cannot be ret ai ned
and the pat i ent ' s i mmedi at e acoust i c recall is t her eby weakened. Anal ysi s of the acous-
tic st ruct ure of the wor d is i mpai r ed and consequent l y the act of writing, so t hat he
makes ma ny charact eri st i c errors (see Fig. 2) al t hough still able t o copy wri t t en wor ds
and signs.
I f the upper par t s of the left t empor al zone are intact, and the lesion is si t uat ed
within the mi ddl e regi on of this zone, or in the white mat t er - - as in ma ny cases of
ot ogeni c abscess - - no consi derabl e di st urbance can be obser ved regardi ng phone-
mat i c hearing, but the whol e syndr ome descri bed above is present in slight f or m. The
pat i ent is able to repeat i sol at ed phonemes al t hough he may miss t hem in a
series of si mi l ar wor ds like z a b o r and z a p o r and s o b o r ( i . e . , fence, lock, cat hedral ).
He will be unabl e to repeat a series of words al t hough he can quite well r epeat a series
of movement s or of drawi ngs. He will be unabl e to r emember names or any r at her
unc ommon wor ds and cannot be assisted by pr ompt i ng. The serial or gani zat i on of
ver bal processes becomes much upset . Thi s is a syndr ome of a ki nd of acoust i c mnest i c
J. neurol. Sci. (1965)2:278-287
280 A.R. LURIA
aphasia and an instability of the verbal acoustic traces possibly represents the physio-
logical factor underlying this particular syndrome.
One of the most interesting features is that the prosodic and melodic components
of speech may be preserved intact and I recall the case of one well-known composer
Fig. 2. Writing to dictation carried out by patients with left-sided temporal lobe lesions. Patient 1
(attained the 7th grade): gasha (kasha, cereal); kora, (gora, mountain); criby (griby, mushroom);
storove (zdorovic, health); Patient 2 (attained the 7th grade): okurets (ogurets, cucumber); tiatel
(diatel, woodpecker); gonbaim (kombain, tractor);krovad (krovat, bed). Patient 3 (attained the 10th
grade): fopeega (sobaka, dog): lizda sholshod (listia shurshat, the leaves are rustling). Patient 4
(attained the 7th grade): gonmada (komnata, room); grukom blamiy (krogum plamia, the fire is all
around). Patient 5 (attained the 10th grade); ridid ptsita (letit ptiztra, the bird is flying).
who suffered from sensory aphasia but was still able to compose music, and indeed
wrote some of his best symphonies after his illness.
A lesion of the left temporal lobe consequently brings about a loss of phonematic
hearing as its primary factor, while secondarily, a syndrome of sensory aphasia arises
from this particular disturbance.
J. neurol. Sci. (1965) 2:278-287
It is possible to follow the same technique in making an analysis of the mot or aphasias.
For a long time it was believed that mot or aphasia represents a single or unitary
syndrome, that it is associated with a lesion of BROCA'S area, and that it results
from a loss of the mot or schemata of words, or - - if one wishes to use modern
t ermi n01~y - - the encoding process. However, this conception is doubtful and a
careful study of the physiology of movement leads us to a different conclusion.
As shown by a number of Russian physiologists efferent impulses themselves do
not suffice to provide precise sophisticated movements. There are at least two different
mechanisms which can be held responsible for an efficient mot or pattern or mot or
(1) An afferent and kinaesthetic background of a movement, which can be regarded
as the sole mechanism giving to the mot or impulses a proper address, and providing
correction of impulses in the flow of a mot or action (vide BERNSTEIN'S important
studies upon the physiological structure of movement).
(2) An efferent or kinetic mechanism which is responsible for the arrest or denerva-
tion of the first link of the movement; a plastic transition to the next link of the mot or
chain; and, as a result, a serial organised skilled movement.
It was found - - and this is very important for our approach to the problem of
mot or aphasia - - that both factors are connected with different regions of the cerebral
cortex. Thus the kinaesthetic factor is linked with the post-central parts of the brain,
while the kinetic factor is connected with the pre-motor zone. Consequently mot or
aphasia can be brought about by at least two different factors, and the whole field
of mot or aphasia needs to be divided into at least two quite distinct syndromes.
These are: (1) the syndrome of afferent or kinaesthetic mot or aphasia, resulting from
post-central lesions; and (2) the syndrome of efferent or kinetic mot or aphasia with
lesions of the premot or system. These two types of mot or aphasia may be studied
separately and in greater detail.
Afferent (or kinaesthetic) motor aphasia
NISSL VON MEYERNDORFF was probably one of the first to regard mot or aphasia as
resulting not from lesions of BROCA'S area but of the Rolandic operculum, realising
that it was the result of disturbance of the afferent part of the sensori-motor area.
The first case of BROCA himself proves this hypothesis. We know now that consider-
able deficit of the kinaesthetic basis of a movement can result from post-central
lesions, and that such lesions if involving the lower part of this area can bring about
a specific form of mot or aphasia. Lesions of the post-central area can result in a de-
fault in the addressing of the impulse to the proper group of muscles, resulting there-
fore in a kind of afferent paresis - - or an afferent apraxia - - as demonstrated else-
where by BAY. Electro-myographic study confirms this view (see Fig. 3). The result
of such a deficit is a difficulty in making the appropriate movement in a series of
tests of postural praxis.
If the lesion is situated within the lower parts of this region the same disturbances
are met with in the articulatory movements. The subject now becomes unable to
J. neurol . Sci . (1965) 2: 278 287
282 A. R. LURIA
Fig. 3. Electromyogram of the flexors and extensors of the hand i n a normal subj ect (a), and i n apat i ent
with a left post-central meni ngi oma (b)
Fig. 4. Wri t i ng to dictation performed by patients with afferent (kinaesthetic) mot or aphasia.
Khanat , khardat (khalat, coat); boni nki , boni nki (botinki, boot s); wagod (wagon, carriage), stol
(table) and slon (elephant): told to draw a table, he drew a table but writing remai ned incorrect;
par na (parta, desk), stot (stol, table), ShOt (slon, elephant), pat at a (palata, ward).
J. neurol. Sci. (1965) 2: 278- 287
pr oduce t he correct art i cul emes, or t o di fferent i at e such correl at i ve or si mi l ar art i cu-
lemes as b / p / m/ o r d/t/1. I n massi ve lesions and severe cases this i nabi l i t y i nvol ves
mor e discrete art i cul emes; wi t h smal l er lesions, a si mi l ar di st ur bance can be f ound as
t he result of mor e subt l e analysis. Thi s di st ur bance of fine sophi st i cat ed ar t i cul at or y
movement s is believed t o represent a pr i mar y f act or of afferent or ki naest het i c mot or
aphasi a.
As a secondar y (systemic) di st urbance fol l owi ng this fact or, one may include an
i nabi l i t y t o bri ng about a correct art i cul at i on of wor ds; a defect in the repet i t i on of
words and in the nami ng of obj ect s; at t i mes a di st ur bance in the act of readi ng
al oud, and even slight i mpai r ment in the compr ehensi on of words r ead al oud. There
is al so a t ypi cal di st ur bance of wri t i ng wi t h charact eri st i c er r or s wher eby for exampl e
1 is wri t t en i nst ead of r, (see Fig. 4) but cor r ect i on may come about by way of visual
anal ysers. A t ransi t i on f r om single wor ds t o whol e sent ence- pr oposi t i ons does not
entail any par t i cul ar t roubl e.
Ef f e r e nt or k i ne t i c mo t o r aphas i a
Thi s is quite a different t ype of mot or l anguage di st urbance, and is the resul t of a
lesion in t he l ower par t of the left pr e mot or zone, i . e. , BROCA'S area. Lesi ons of the
pr emot or zone do not resul t in any di st urbance of the ki naest het i c basis of movement s ;
these lesions are not accompani ed by any loss of the correct addressi ng of mot or
impulses, nor any s ympt oms of at axi a or post ur al apraxi a. The mos t i mpor t ant
pr i mar y defect in these cases is a loss of the ki net i c schema, or a di st urbance in skilled
movement s which is the resul t of an upset of the pr oper or gani sat i on of serial move-
ment s, a defect of dener vat i on of the first l i nk of a mot or chai n and a pl ast i c t ransi -
t i on to the next link. I f the lesion is l ocat ed wi t hi n t he upper por t i on of the pre-
mot or zone (field 6aft) we can witness a di st urbance of skilled movement s of the hands
(a dys- aut omat i sat i on of t appi ng, r hyt hmi cal movement s, kinetic melodies). Somet i mes,
if the lesion is deep and upset s the nor mal connect i ons of the pr emot or cort ex wi t h
the subcort i cal mot or ganglia, a series of per sever at or y s ympt oms may appear
i nvol vi ng movement s i ncl udi ng drawi ng and writing.
When the lesion dest roys the l ower par t of the left pr emot or zone ( Br oca' s area)
the same di st urbances can be met wi t h in speech. The kinetic mel odi es of speech
become dest royed, and the t r ansi t i on f r om one art i cul eme to anot her becomes i m-
possi bl e; and, al t hough the subject can make the correct art i cul at i on f or the first
par t of a word, he is unabl e to change when it comes t o the art i cul at i on of the next
par t (thus mo o - k h a may become mo o . . , m. . . ma) . I t is readi l y seen t hat the en-
codi ng process is now severely hi ndered by these defective ki net i c schemat a and
these difficulties pr oduce the pr i mar y f act or s of the efferent or kinetic mot or aphasi a.
I nabi l i t y t o name an obj ect or to pass f r om the expressi on of one wor d to the
next, and al so a loss of pr oposi t i onal speech as a kinetic unit, are the mos t significant
secondar y or syst emat i c results of this ki nd of pr i mar y di sorder, differing in different
stages of recovery, but all rel at i ng t o the same fact or. I t is significant t hat in these
pat i ent s di st urbances in wri t i ng have a highly distinctive char act er : writing of separ at e
letters ma y be intact, but the appr opr i at e or der of letters in a wor d is oft en lost.
Wri t i ng t hen becomes a process whi ch is t ot al l y dys- aut omat i zed, the posi t i on of
J. neurol. Sci. (1965) 2:278 287
284 A. R. LURIA
l e t t e r s c h a n g e s ( see Fi g. 5) a n d s o me t i me s t h e r e ma y b e a p e r s e v e r a t i o n ma k i n g t r a ns i -
t i o n f r o m o n e l e t t e r o r wo r d t o a n o t h e r q u i t e i mp o s s i b l e .
An i mp o r t a n t p o i n t is t h a t a s e v e r e i mp a i r me n t o f c o n t e x t u a l o r g a n i s a t i o n o f
s p e e c h ( R. JAKOBSON) c a n b e c o me a s i g n i f i c a n t s y mp t o m i n t hi s f o r m o f a p h a s i a , [ b e i n g
Fig. 5. Writing to di ct at i on carried out by a pat i ent with efferent (or kinetic) mot or aphasia. Patient
V (lesion of right front o-t emporal region). Two mont hs after original injury.
Pi ~ Ak ; Mu - + Mk ; Re ~ R i ; Mu ~ R ; B o - + Ku
Lom -+ Sak; Ri s ~ Kak; Shar -+ Shko; Don -+ Dkk
Patient D, wound of ant eri or speech zooe. Two mont hs after onset ; Nos (nos, nose); zus (zub, t oot h);
vos (sok, j ui ce); sos (son, dream).
Patient P, wound in left front o-t emporal region. Two mont hs after onset; mi -+ mi ; cho ~ chi;
su ~ si; ku -+ ku; pu -+ ku; ra --, chu.
Patient I, injury to Br oca' s area; mot or aphasia. Wri t i ng silently stal (steel), sit. The same, but with
teeth clenched upon prot ruded tongue, st ol ; krol, pit (plot, logs). Aft er visual exposure of t he wo r d . . .
polt. Af t er pronounci ng t he wor d a l o u d . . . p l o t .
Patient M, engineer. Lesi on of ri ght ant eri or speech zone (in a left-handed subject).window (okno)
Wi t h teeth clenched upon prot ruded t ongue oko, okno, no, onk, ononok. Aft er di ct at i on okno.
J. neurol. Sci. (1965) 2: 278-287.
the result of the same loss of kinetic organi sat i on of the phrase, and the i mpai rment of
prosodi c and mel odi c organi sat i on of speech can somet i mes go hand in hand with
severe det er i or at i on of the schema of the whole proposi t i on, developing the f or m of
the wel l -known sympt om of t el egrammat i sm, and a special syndrome of a loss of
Fig. 6. Writing to dictation by a patient with a deep posterior frontal tumour (perseveration of letters
is seen).
active proposi t i onal speech, which we call dynami c aphasia. All these sympt oms
require careful study, and it is possible t hat we shall find i mpor t ant mechanisms
of these disorders in the i mpai rment of inner speech which, accordi ng to VIGOTSK,
is decisive in the devel opment of a verbal kinetic mel ody. It is obvi ous t hat the phys-
iological mechani sm of t hat most i mpor t ant f or m of aphasic disorder, requires
special at t ent i on.
Hi t her t o we have dealt with the acoustic and art i cul at ory aspects of speech, but
it is obvi ous t hat disorders of l anguage may be far mor e compl ex in charact er and
entail a det eri orat i on in t he semantic organi sat i on of language. Broadl y speaking this
can be the result of any severe i mpai rment of t he cerebral cort ex bringing about organi c
dement i a, but we shall pr oceed t o seek semantic defects, in the nar r ow sense of the
word, which result f r om fact ors associated with a definite local lesion of the cortex.
The syndr ome of semantic aphasi a was well descri bed by HENRY HEAD and it is
difficult t o add t o his description. The i mpor t ant poi nt is t hat sympt oms of seman-
tic aphasi a can be observed in cases of lesions of t he left pari et al or t empor o- occi pi t o-
pari et al regions of t he cortex. Fur t her mor e t hey are cl earl y associated with disorders
of si mul t aneous and spatial schemata. In these patients t here is a difficulty in bringing
separat e component s t oget her t o f or m a coher ent whole, and also t o anal yse compl ex
spatial relationships. The di st urbance of spatial rel at i onshi ps has a very specific
J. neurol. Sci, (1965) 2:278-287
286 A.R. LURIA
feat ure. Not every spatial percept i on is upset in these cases, but pri mari l y t here occurs
an al t erat i on in t he percept i on of asymmet ri cal spatial schemata. Thus it is impossible
f or t he pat i ent t o distinguish right f r om left, and he fails in or i ent at i on within space, in
analyses of t he hands of a clock, t he post ure of fingers, and spatial rel at i ons as evi-
denced by geographi cal maps. This t ype of spatial synthesis requires t he associ at i on of
occipital (visual), t empor al (vestibular) and ret ro-cent ral (kinaesthetic) zones with a
synthesis of t he opt i cal percept i on of space, t oget her with differential local signs on t he
ri ght hand.
Di st urbance of the synthesis of asymmet ri cal spatial schemat a is pr obabl y one of the
al l -i mport ant fact ors underl yi ng some of the mor e compl ex sympt oms of semant i c
aphasia. Careful st udy has shown t hat not every type of meani ng is di st urbed in these
cases, but mai nl y the compr ehensi on of such relational schemat a as requi re the distinc-
t i on of asymmet ri cal spatial relationships.
Years of linguistic st udy were necessary before discovering such types of grammat i cal
st ruct ure which requi re an analysis of asymmet ri cal spatial relationships and which
are bel at ed pr oduct s of linguistic devel opment . Such types of const ruct i on i ndeed
exist, as f or example, possessive attributives (father' s brother as opposed t o brother's
father, or dog's master as opposed t o master's dog) which fol l owed the ol der forms
the father' s, his brother, etc. There is also the preposi t i onal const ruct i on (the circle
under the triangle, as opposed t o the triangle under the circle; or the spring is before
the summer as opposed t o the summer is before the spring), or even mor e compl ex
rel at i onal const ruct i ons (such as Jenny is older than Mary but younger than Betty).
Such kinds of grammat i cal st ruct ure are as a rule ext remel y difficult for patients with
pari et al lesions, and bri ng about confusion. Even l ong t rai ni ng does not result in
si mul t aneous compr ehensi on of these structures. Aft er a system of rehabi l i t at i on,
patients may event ual l y be able t o arrive at t he meani ng of such a const ruct i on by
means of using a l ong chai n of successive links of reasoning.
It is i mpor t ant t o realise t hat the same deficit of simultaneous spatial schemat a and
of an analysis of asymmet ri cal structures causes these patients t o show a mar ked
di st urbance of counting. Every ari t hmet i cal process, especially t hose utilizing the decimal
system and the mani pul at i on of numbers within the decimal system, requires an
oper at i on in such an asymmet ri cal quasi-spatial field. This being so, such operat i ons
are quite impossible f or this type of patient, not on account of any lack of abst rac-
tion, but because of a deficit within these spatial schemata.
I t is difficult t o discern the physiological fact ors which under l y this most com-
plicated f or m of disturbance. Fur t her experi ment al wor k is needed, and studies
al ong these lines are now in progress in our l aborat ory.
We have at t empt ed t o describe the mor e i mpor t ant f or ms of aphasi a and t o find
cert ai n fact ors which are f undament al f or these forms. Fr om this present dicussion
we shall omi t such very i mpor t ant probl ems as t hat ot her class of di st urbance which
involves t he regulating or cont rol l i ng f unct i on and the selective st ruct ure of the speech.
These disturbances are typical of quite a different type of di sorder of language and
t hought , one whi ch lies outside the pr obl em of aphasi a in a strict sense. They are the
i mpor t ant results of f r ont al l obe lesions and were the subject of a special paper
present ed in my book (LURIA 1962). It const i t ut es a specific and most i mpor t ant aspect
J. neurol. Sci. (1965) 2:278-287
of t he pr obl em of l anguage di sorders t hat meri t s a discussion all on its own.
I ma y concl ude wi t h a few final r emar ks. The appr oach pr esent ed does not in any
way cont r adi ct the anal ysi s of levels of l anguage di sorder advanced by HUGHLINGS
JACKSON a cent ur y ago. I t has as its obj ect t he anal ysi s of some i mpor t ant f act or s
underl yi ng aphasi a, and in t hat way it can serve as an at t empt t o make a psycho-
physi ol ogi cal anal ysi s of l anguage- pat hol ogy and bri ng t he pr obl em of aphasi a within
t he general cont ext of moder n neurol ogy.
A scientific appr oach to aphasi a requi res an anal ysi s of separat e fact ors underl yi ng
speech di sorders in different local lesions of the brai n.
The fol l owi ng basic f or ms of aphasi a are descri bed in this paper :
(1) Acoust i c aphasi a, wi t h l ocal i sat i on of the lesion in the left t empor al zone and
wi t h a di st urbance of acoust i c anal ysi s of speech sounds as a basic sympt om.
(2) Afferent (kinesthetic) mot or aphasi a, wi t h l oeal i sat i on of the lesion in post -
cent ral part s of the left hemi spher e and wi t h a di st urbance of art i cul at i on as a basi c
s ympt om.
(3) Efferent (kinetic) mot or aphasi a, wi t h l ocal i sat i on of the lesion in pr e mot or
par t s of the lett hemi spher e and the di st urbance of sequent i al or gani sat i on of speech
as a basi c s ympt om.
(4) Semant i c aphasi a, wi t h l ocal i sat i on of the l esi on in par i et o- occi pi t o- t empor al
par t s of the left hemi sphere and wi t h di st urbances of spat i al ( si mul t aneous) anal ysi s
and synthesis as a basic s ympt om.
LURIA, A. R. (1947) Traumatic Aphasia, Med. Acad. Press, Moscow (English translation at Mouton,
The Hague, 1964).
LURIA, A. R. (1962) Hi gher Cortical Functions in Man, University Press, Moscow (English translation
at Basic Books, New York, 1964).
neurol. Sci. (1965) 2:278-287