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Aphasiology
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The phonetic—phonemic dichotomy

in aphasiology
a b a c
André Roch Lecours & Jean–Luc Nespoulous
a
Laboratoire Théophile–Alajouanine , Centre de recherche
du Centre hospitalier Côte-des-Neiges , Montréal
b
Faculté de Médecine, Université de Montréal
c
Département de Linguistique et Philologie , Université de
Montréal
Published online: 29 May 2007.

To cite this article: André Roch Lecours & Jean–Luc Nespoulous (1988) The
phonetic—phonemic dichotomy in aphasiology, Aphasiology, 2:3-4, 329-336, DOI:
10.1080/02687038808248933

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 APHASIOLOGY, 1988, VOL.2, NO. 314, 329-336

The phonetic-phonemic dichotomy in

aphasiolog y

A N D R E R O C H L E C O U R S ’ and J E A N - L U C
N E S P 0 U L O U S’
Laboratoire Theophile-Alajouanine, Centre de recherche du Centre hospitalier
CBte-des-Neiges, Montreal
‘Faculte de MPdecine, Universite de Montrtal
’Dipartement dr Linguistique et Philologic, Universite de Montreal
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One of the few semiological dichotomies which have stood the test of time in clinical
as well as research aphasiology is the one qualifying speech production with regard to
fluency. To the best of o u r knowledge, it was first explicitly recognized by Baillarger
(1865) during the 1860s, as Broca (1865) was asserting the innateness of left cerebral
dominance for language and Trousseau (1864) was successfully attempting to relabel
‘alalia’ and ‘aphemia’ as ‘aphasia’. Although the pertinency of Baillarger’s dichotomy
was never to be challenged thereafter, it took a century before systematic
documentation of it was undertaken (Goodglass, Quadfasel & Timberlake 1964).
The subject matter of the present paper is a particular aspect of the fluent versus
non-fluent dichotomy, more precisely the one related to the absence versus the
presence, within a particular aphasia symptom-complex, of phonetic anomalies, i. e.,
of a motor dysfunction specifically impairing the production of the phonatory
movements subserving speech production. As a matter of fact, this particular aspect
of neurological semiology had been an object of research among aphasiologists long
before aphasiology acquired its name together with a relative autonomy as a field of
scientific investigation. It is our intention to summarize, using the aphasiological
lexicon of 1988 (usually without mention of original terminologies), how the
phonetic-phonemic opposition has been successively considered by researchers
identifying themselves-with various degrees of dogniatism-as neurologists,
neurolinguists or neuropsycholinguists.

Neurologists (18251988)
In Western Europe from the 1820s and until the first World War, being known as one
knowledgeable about the language disorders that result from brain diseases was an
asset for anyone aiming at a significant academic career in medicine. For those who
saw the convolutions of the brain behind Gall’s phrenology of the skull, the way was
to correlate the surface manifestations of various language disorders with the
localization of their causal cerebral lesions. Bouillaud (1825), for instance, believed
that the anatomo-clinical method would provide ultimate responses as to brain-
language relationships. O n the other hand, those who could not conceive of the brain
as a modular entity, and/or who were inclined to give credit to ears as much as to eyes,
listened to surface manifestations more than they looked a t damaged brains. They

Address for correspondence: Andre Roch Lecours, 4565 Chemin de la Reine-Marie, Montreal,
Quebec H3W 1W5, Canada.
 330 AndrP Roch Lecours and Jean-Luc Nespoulous

relied on some general implicit or explicit knowledge of the grammars of their

respective languages. Thus, and albeit with hesitations, they identified linguistic
subcomponents and processes which they suspected to be at fault in aphasia. O ne such
subcomponent was articulation. For instance, more than twenty years before the term
aphasia was coined, the Dean of the Faculty of Montpellier taught his students about
‘asynergetic alalia’, in which the patient could no longer exert cotemporal control on
the movements of his peripheral speech organs, and about ‘alalia with verbal
amnesia’, a primordial manifestation of which was ‘paralalia’, a deviant behaviour
resulting from ‘paramnesia’, a cognitive dysfunction. An individual with the latter
condition would control his speech muscles normally but might, for instance, fluently
utter ‘/symylman/’ instead of ‘/myzylman/’, ‘/sErE/’ instead of ‘IrEzEI’, and so forth.
Target words were retrieved but, in speech production, ‘the letters and syllables were
interverted’ (Lordat 1843).
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At the turn of the century or soon thereafter, and whether siding with Dejerine or
with Pierre Marie (Klippel 1908), a well-bred neurologist was bound to distinguish
between three types of acquired speech disorders impairing word production: (a) the
dysarthrias, caused by various subcortical lesions, (b) motor aphasia, caused by
certain prerolandic lesions, which could occur in a pure form although it usually was
but one semiological feature of the symptom-complex associated to Broca’s name,
and (c) phonemic paraphasia, caused by certain retrorolandic lesions, which occurred
in various types of fluent aphasia. Articulation was impaired in the first two
conditions because speech muscles were weak, dystonic or uncoordinated, whereas it
was normal in the third. The effects of automatic-voluntary dissociation could be
observed in motor aphasia and phonemic paraphrasia although not in the dysarthrias.

Neurolinguists (1939-1988)
In relation to our subject matter, two important books were published in 1939. The
first one was entitled Grundxuge der Phonologie by Nicolas Sergueevitch Troubetzkoy.
It explained that phonetics deals with the articulatory and acoustic description of
phonemes, whereas phonology focuses upon more abstract linguistic properties that
are shared or not shared by the phonemes of natural languages. The second book, Le
Syndrome de Disintigration Phone‘tique duns I’Aphasie, by Thtophile Alajouanine, Andrt
Ombredane and Marguerite Durand, successfully aimed at the description of the
phonetic disorders which impair speech production in Broca’s aphasia. The authors
hinted a t phenomena such as partial devoicing, imperfect co-articulation and so forth,
and showed the possibility of interaction between theoretical linguistics and clinical
aphasiology. It is probably fair to assert that neurolinguistics was born with the
publication ofthis second book. (At all events, and albeit as a third author, Marguerite
Durand, was no doubt the first linguist to feel comfortable testing brain-damaged
patients in a hospital).
The neurolinguistic undertaking is mostly concerned with providing abstract
characterizations of deviant speech structures by reference to linguistic theory rather
than in the ways such structures are processed by the human mind and its subserving
brain. For instance:
(1) Buckingham (1980) claimed that the segmental errors ofnormal speakers and
those of fluent aphasics are qualitatively similar, Dressler (1982) that they are not.
(2) Blumstein (1973) led a phonological study of speech errors in Broca’s,
conduction and Wernicke’s aphasia. She proceeded to featural, markedness and
 T h e phonetic-phonemic dichotomy in aphasiology 331

contextual analyses of errors as well as to a study of error types and directions. O n the
whole, her characterizations turned out to be the same whatever the taxonomical
label. Her conclusion was that, as claimed by Jakobson (1968), the error patterns of
aphasics-just as those of children learning a mother language or of adults learning a
second language-are not related to loci of brain lesions but are rather the outcome of
the way in which the phonological system is structured and organized within any
given language.
(3) Nespoulous and colleagues (1982, 1983, 1984), on the other hand, although
acknowledging that most aphasics tend to substitute unvoiced to voiced consonants,
presented data indicating that this phenomenon reaches significance level in Broca’s
although not (and by far) in conduction aphasics. Moreover, voice onset time was
found to be nearly normal in all types of aphasia with the exception of Broca’s
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(Blumstein, Cooper, Zurif and Caramazza 1977, Blumstein, Cooper, Goodglass,

Statlender and Gottleib 1980, Itoh, Sasanuma, Tatsumi, Murakami, Fukusako and
Suzuki 1982). These facts could be taken to indicate the existence ofsome relationship
between loci of lesions, processing dysfunctions, and linguistic characterization of
errors.
(4) Shankweiler and Studdert-Kennedy (1967) have suggested that the cerebral
representation of vocal segments is less lateralized than that of consonants, a
phenomenon also approached by Goodglass (1973) from the developmental
standpoint. This dissociation was found to exist to a greater degree for English than
for Japanese (Tsunoda 1971), which is probably linked to the greater distinctive role of
vowels in the latter.
(5) The latest phonological models (Halle and Vergnaud 1980, Hayes 1981) have
made it possible to study the role of syllabic constraints in the genesis of segmental
errors in aphasia (Btland 1985). Moreover, the analysis of a corpus of phonemic
paraphasias by reference to the theory of ‘charm and government’ (Kaye,
Lowenstamm and Vergnaud 1985) has suggested that several clinical forms of aphasia
(Broca’s and conduction included) can comprise a properly phonological dysfunc-
tion, the same whatever the clinical form (Valdois 1987).

Neuropsycholinguistics (1956-1988)
When Roman Jakobson (1956) characterized Broca’s versus Wernicke’s aphasia as
contiguity versus similarity disorders, and still more when, for instance, he
characterized Luria’s afferent motor aphasia as a disorder in the encoding of
simultaneously produced units (Jakobson 1964), he showed interest in psycholinguis-
tic processes as well as in linguistic and neurological structures. The complementarity
between structural linguistic characterizations and brain-compatible psycholinguistic
models has since imposed itself. It has become a rule, in aphasiology, to attempt to
include the psycholinguistic dimension to one’s research. With respect to the
phonetic-phonemic opposition, this preoccupation has been visible in a number of
works dealing with aphasiological phonetics. For instance, it has been claimed that,
due to categorical perception and/or to a phonological ‘sieve effect’ (Troubetzkoy
1939), phonetic distortions are often misinterpreted as phonemic substitutions
(MacNeilage 1982). As observed in Broca’s aphasia, devoicing could thus witness to a
phonetic dysfunction: a t fault would then be thc temporal control of speech
production, i.e., the synchronous implementation of articulatory gestures required
 332 Andre‘ Rach Lecours and Jean-Luc NeSp@i4/0i45

for the adequate production of target segments (Keller 1984). Underlying scgmcntal
targets would rcmain canonical and sublcxical processcs flawless.
All voicing parameters have not been found to bc equally disturbcd in Broca’s
aphasia. Thus, vowel duration is preserved in prcconsonantal position (shortcr bcforc
voiceless than before voiced stops). One can take this as indicating that the
programming of the [+ voice] feature is not impaired in phonetic disintcgration
(Duffy and G a w k 1984, Tuller 1984, Baum and Blumstein 1987, Nespoulous,
Trcmblay and Lecours, in preparation).
Pucl, Nespoulous, Bonaft? and Rascol (1980) havc suggcsted that the phonctic
disturbance is not entirely the samc in pure anarthria as opposed to Broca’s aphasia. In
the former, the primordial disturbances involves [place], a feature with very many
dcgrecs of freedom, whereas it involves binary featurcs such as [+/-voice] in thc
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latter. This might bc taken to plead in favour of a further processing dichotomy,

intrinsic this time to the phonetic level.
The samc preoccupation has also permeated aphasiological phonology. For
instance: (1) Whcn producing scquences of phonemic approximations to a givcn
word, conduction, although not Wcrnicke’s aphasics showcd a regular trend toward
thc conventional target form. This was suggested to indicate that the intcrnal model of
the target words remained unimpaircd in conduction but not in Wernickc’s aphasia
(Joanette, Keller and Lccours 1980). (2) This intcrnal model was considered as an
underlying as opposed to a superficial phonological representation, and the
pathological process responsible for the repetition disorder of conduction aphasics
was suggcsted to be immediately distal to the former (Caplan, Vanier and Baker 1986,
Btland, Caplan and Nespoulous, submittcd).
(3) Illiterates have been shown capable of stripping initial syllables but not initial
phonemes from spokcn neologisms; it was thereforc suggested that becoming aware
of thc phonemic units of speech is a by-product of alphabetization (Cary and Morais
1980, Morais, Cary, Alegria and Bertelson 1979). Onc therefore wonders whether
this observation entails the prediction that the charactcristic dysechophemia of
conduction aphasia should be linguistically differcnt among the school-educated as
opposcd to illiterates (Lecours, Mehler, Parentc et al., in press). If any, what should
the differencc(s) be betwecn a phonemic paraphasia and a syllabic paraphasia? (4) The
phonemic and formal verbal paraphasias of conduction aphasics were suggested to be
superficially different manifestations of a single dysfunction (Lccours, Delochc and
Lhermitte 1974). (5) Given favourablc evolution, the symptom-complex of
Wernicke’s neologistic jargon will merge into that of conduction aphasia (Bucking-
ham and Kertesz 1976). A most striking characteristic of such a diachrony is that a
paticnt whose discoursc originally comprised numerous neologisms becomes onc
whose discourse comprises numerous recognizablc-i. e. targeted-phonemic para-
phasias. Does the difference between neologisms and phonemic paraphasias depend
mostly on the decoder’s rather than the encoder’s abilities? (6) But there is evidencc
that the neologisms of Wernicke’s jargonaphasics arc not always targeted (Bucking-
ham 1985). O n e could arguc that, at least in entirely neologistic jargon, speech
production is utterly asemantic (Lecours 1982). Obviously, the dysfunction leading to
thc production of this type of ncologism must be different, at least in part, from that
leading to the production of phonemic paraphasias.
 The phonetic-phorlernic d i h t o t t l y in aplinsiology 333

Beyond the chapels (1988)

In csscncc, currcnt aphasiological teachings concerning the phonetic-phoncmic
opposition are twofold.
(1) As behaviourally manifest in the production of the phonemic paraphasias of
subjects with conduction aphasia due to left supramarginal and/or postcrior
temporal lesions, a phonological processing disorder points at impairment of
those processes specifically subserving the selection of particular lexical-
phonological representations and/or the sublcxical operations (Shattuck-
Hufnagel 1979) through which such a representation must be reprocessed-at
both the syllabic and segmental levcl-before being, as it were, sent to
phonetic-motor modules in view of its articulatory production (Buckingham
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1985, Ncspoulous, Joanctte, Ska, Caplan and Lecours 1987).

(2) As behaviourally manifest in the phonctic disintegration of subjects with pure
anarthria or Broca’s aphasia due to left preccntral or inferior frontal opercular
lesions, a phonetic processing disorder points a t impairment in thc cotemporal
articulation of the features corrcsponding to adequately programmed
phonological representations.
Evidcncc is the following:
(1) In the former: (a) a sizeable production of displacement errors (with or
without substitution) as well as of grossly off-target word-like entities
(interpreted as indicating a sublexical phonemic proccssing deficit) and (b) thc
absence of both articulatory distortions and of clear-cut preferential tcndencics
in single-feature segmental substitutions (Buckingham 1985, Lecours and
Lhermittc 1969, Ncspoulous et n l . 1984, 1987, Poncet Degos, Deloche and
Lccours 1972).
(2) In the latter: (a) thc presence ofarticulatory distortions and (b) the existence of
clear-cut prefcrential tendencies in single-fcaturc segmental substitutions
(Kohn 1985, Lecours and Lhermitte 1969, Nespoulous et nl. 1982, 1983, 1984,
Trost and Cantcr 1974).
But l’aplinsie est itne (as Marie held in 1926) and dichotomies are bound to be
somewhat misleading. O n the one hand, acoustical analyses of speech production in
Wcrnickc’s aphasia have evidenced the existence, in this prototypically fluent aphasia,
of subtle phonetic alterations (Blumstein e t a ] . 1977, 1980). In this respect, Sabouraud,
Gagncpain and Chatel (1969) claimed, on the basis of oscillographic data, that thcre
exist threc typcs of phonetic anomalies in aphasia: onc common to Broca’s and
Wernickc’s aphasics, onc specific to thc formcr and the third to the latter. I t remains an
open qucstion whether such alterations arc related to anomaly in auditory feedback
(Alajouaninc, Lhermitte, Ledoux, Renaud and Vignolo 1964) or to some more
general effect of brain damage on speech production.
O n the other hand, not all the segmental errors of Uroca’s aphasics can be
interpreted as the outcome of disrupted phonetic processing: the (relatively few)
metatheses and assimilations of Broca’s aphasics do not appear to be phonetically
constrained; consonantal substitutions involving place, manner and/or voicing
can-progressively more often, with favourable evolution-lead to the production of
rntircly normal segments. Therefore, it remains for one to determine whether these
arc (still) phonctically constrained by the intrinsic articulatory complexity of the
 334 Andre‘ Roch Lecoun aridJean-Lwc Nespoulous

segments or phonologically constrained by markedness. Moreover, since articulatory

compensation is usually not accessible to Broca’s aphasics (Sussman, Marquardt,
Hutchinson and MacNeilage 1986), one might suggest that, with time passing, they
resort automatically to phonologically predictable strategies in order to compcnsate a t
best for their (still) phonetically constrained deficit.
This being said, it is quite clear that contemporary neuropsycholinguists-is it not
the fate of prefixes to lose their meaning?-have either failed or neglected to rclate the
dysfunctions of their processing modules (Fodor 1983) to lesions of the biological
modules that harbour them. Imprecise ncuroanatomical notions such as ‘anterior’ and
‘posterior’ lesions are still considered as acceptable. With the advent of both
sophisticated neurosciences and sophisticated cognitive sciences, the hiatus between
brain and mind has dcepened rather than shallowed. Although it has become a classic
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of grantmanship to insist on the possibility, given modern imaging techniques, of

apprehending ‘on line’ where and when cognitive processes take place, we arc still
very far from an ‘integrated cognitive science . . . the mind’s new science’ (Gardner
1985).

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