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Grodzinsky's latest stand – or, just how specific are “lesion-specific” deficits?

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Abstract

Deficits observed in Broca's aphasia are much more general than Grodzinsky acknowledges. Broca's aphasics have a broad range of problems in lexical and morphological comprehension; furthermore, the classic “agrammatic” syntactic profile is observed over many populations. Finally, Broca's area is implicated in the performance of many linguistic and nonlinguistic tasks.
Grodzinsky’s Latest Stand - or, just how specific are
"lesion-specific" deficits?
Frederic Dick & Elizabeth Bates
Center for Research in Language, University of California, San Diego,
La Jolla, CA 92092-0526.
fdick@cogsci.ucsd.edu -- bates@crl.ucsd.edu
The Behavioral and Brain Sciences, 2000, 23(1), 29-29.
Abstract
Deficits observed in Broca's aphasia are much more general than Grodzinsky acknowledges. Broca's aphasics have a broad
range of problems in lexical and morphological comprehension; furthermore, the classic "agrammatic" syntactic profile is
observed over many populations. Finally, Broca's area is implicated in the performance of many linguistic and non-
linguistic tasks.
Yosef Grodzinsky (YG) has penned a highly
imaginative account of aphasic deficits and their neural
correlates, the latest in a series of proposals that he has
put forward in the last 15 years for a grammar-specific
faculty in the human brain (e.g. Grodzinsky, 1984).
His proposals are famous for their strength, clarity and
falsifiability. Below we provide evidence that falsifies
his latest stand.
First, YG claims that the receptive deficit in
Broca’s aphasia is restricted primarily (perhaps exclu-
sively) to grammar (e.g. “the patients seem to have no
impairment to their lexicon in comprehension, namely,
the part of the lexicon that interacts with sentence
grammar is intact.” Section 2.1). This is misleading.
It is well established that Broca’s aphasics have marked
deficits in both phonological and lexical processing,
receptively and expressively (Goodglass, 1993). In fact,
some of the first demonstrations of impaired lexical
priming in Broca’s aphasia were conducted at the same
institution where YG conducts his English-language
work (e.g. reduced, delayed or deviant word-word prim-
ing in Prather, Shapiro, Zurif, & Swinney, 1991; see
also Milberg, Blumstein & Dworetzky, 1988).
Second, YG asserts (Section 2.1) that the gram-
matical comprehension deficit in Broca’s aphasia is
quite restricted, affecting syntactic movement operations
while leaving other aspects of grammar intact (such as
computation of agreement and case). This is simply
untrue. There is now a large cross-linguistic literature
showing that Broca’s aphasics (and other groups as
well) are markedly impaired in the use of agreement and
case information to assign agent-patient roles (Bates,
Friederici, & Wulfeck, 1987; Heeschen, 1980; Mac-
Whinney, Osmán-Sági, & Slobin, 1991). Furthermore,
although these patients often perform above chance on
grammaticality judgment tasks, they are significantly
less accurate in detecting subject-verb agreement errors
than violations of movement (Devescovi et al., 1997;
Wulfeck, Bates, & Capasso, 1991).
Third, the core of YG’s argument revolves around a
specific type of syntactic deficit that is supposed to be
unique to Broca’s aphasia: a deficit in the movement
operations associated with (inter alia) the processing of
non-standard word order. This is supposed to result in
chance performance on passives and object clefts despite
above-chance performance on actives and subject clefts.
In fact, this very pattern has been observed in all forms
of aphasia. For example, Dick, Bates, Wulfeck and
Dronkers (1998) compared a large number of anomics,
Wernicke’s, conduction, and Broca’s aphasics and found
cases with YG’s signature “agrammatic profile” in all
aphasic groups, including anomics (i.e. patients with
word-finding deficits who do not display clinically
significant signs of expressive agrammatism). The
presence or absence of this agrammatic profile also
failed to correlate with any particular lesion site, and
appeared often in patients with lesions sparing Broca’s
area. We note that the same profile is observed in
children who are still acquiring their language, and it
can be reproduced in college students who have to
perform exactly the same task under “stressful” con-
ditions (e.g. a combination of low-pass filtering and
compression of speech). In short, this profile has
absolutely no localizing value.
Finally, YG insists that the neural tissue in and
around Broca's area is specialized for and dedicated to
these syntactic operations, declaring that “the neuro-
linguistic localizing schema of language perception may
not have permeated the clinical literature, yet it is
currently accepted in cognitive neuroscience.” In fact,
very much the opposite is true. Not only do functional
imaging studies show language-related activation in
widely distributed and overlapping networks (see
Müller, this volume, for further comments), but a
steadily increasing number of studies show that regions
in and around Broca’s area are activated during non-
2
linguistic tasks, such as object manipulation, mental
imagery of tools, and sequential finger tapping cued by
a drawn hand (Krams, Rushworth, Deiber, Frackowiak,
& Passingham, 1998; Rizzolatti & Arbib, 1998). Such
"promiscuity" of activation does not lend much support
to a language-specific role for Broca's area.
To summarize: The “core data” of agrammatism
that YG uses to define the putative role of Broca’s area
is observed in a wide range of populations, with dif-
ferent etiologies, including normal adults processing
under stress. Patients with damage in and around this
region display a range of deficits inside and outside of
the grammar. Finally, imaging studies of normals
show that Broca’s area itself is involved in many
different linguistic and nonlinguistic tasks. In short,
the pattern of selective deficits and activations that are
essential to YG's proposal are not so selective after all.
*Supported by NIDCD R01-DC00216 and by an
NIDCD fellowship to FD.
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