MODULARITY, DOMAIN SPECIFICITY AND
Center for Research in Language
THE DEVELOPMENT OF LANGUAGE
University of California, San Diego
Debates about the nature and evolution
of language often shed more heat than light, because they confuse three
logically separable issues: innateness, localization
and domain specificity. Proponents of innateness argue
that our ability to acquire a language is determined by genetic factors,
and mediated by a form of neural organization that is unique to our species.
Proponents of localization argue that our ability to process language is
localized to specific regions of the brain. Proponents of domain specificity
build on both these points, but add the further specification that our localized
language abilities are discontinuous from the rest of mind, separate and
"special", constituting what Chomsky (1988) has termed a "mental
The first claim has to be true at some level of analysis,
because we are indeed the only species that can acquire a language in its
full-fledged form (cf. Greenfield and Savage-Rumbaugh, 1991; Savage-Rumbaugh,
Murphy, Sevcik, Brakke, Williams and Rumbaugh (1993). The second claim is
also well attested. Indeed, one of the oldest findings in cognitive neuroscience
is the finding that lesions to specific regions of the left cerebral hemisphere
in adults usually lead to irreversible forms of language breakdown, or aphasia
-- although, as we shall see, there is still considerable controversy about
the nature of those symptoms (Bates and Wulfeck, 1989a&b). The real
debate revolves around the mental-organ claim. Are the mental structures
that support language "modular", discontinuous and dissociable
from all other perceptual and cognitive systems? Does the brain of the newborn
child contain neural structures that are destined to mediate language, and
language alone? The domain specificity view can be contrasted with an approach
in which language is viewed as an innate system, but one that involves a
reconfiguration of mental and neural systems that exist in other species
(Deacon, 1990a&b; Sereno, 1990), and which continue to serve at least
some non-linguistic functions in our own (Bates, Thal and Marchman, 1991;
Bates, Thal and Janowsky, 1992).
In this paper, I will provide arguments for innateness
and localization but against domain specificity, in research on adult
aphasia (the adult endpoint that is the source of most hypotheses about
early specialization for language), and in research on normal and abnormal
language development. I will begin with a brief explication of the modular
approach to language, and then describe some general arguments and specific
findings that support a different view, i.e. that "Language is a new
machine built out of old parts" (Bates, Bretherton and Snyder, 1988).
Modularity and domain specificity: What are they?
The word "module" is used in markedly different
ways by neuroscientists and behavioral scientists, a fact that has led to
considerable confusion and misunderstanding in interdisciplinary discussions
of brain and language. When a neuroscientist uses the word "module",
s/he is usually trying to underscore the conclusion that brains are structured,
with cells, columns, layers and/or regions that divide up the labor of information
processing in a variety of ways. In all fairness, there are few neuroscientists
or behavioral scientists who would quibble with this claim. Indeed, Karl
Lashley himself probably had something similar in mind, despite his notorious
claims about equipotentiality and mass action (Lashley, 1950). In cognitive
science and linguistics, the term "module" refers to a stronger
and more controversial claim, one that deserves some clarification before
The strongest and clearest definition of modularity in
cognitive science comes from Jerry Fodor's influential book Modularity
of mind (Fodor 1983; see also Fodor, 1985). Fodor begins his book
with an acknowledgment to psycholinguist Merrill Garrett, thanking him for
the inspiring line "Parsing is a reflex." This is, in fact, the
central theme in Fodor's book, and the version of modularity that most behavioral
scientists have in mind when they use this contentious word. A module is
a specialized, encapsulated mental organ that has evolved to handle specific
information types of enormous relevance to the species. Following the MIT
linguist Noam Chomsky (Chomsky, 1957; 1965; 1988), Fodor argues that human
language fits this definition of a module. Elaborating on this argument,
Fodor defines modules as cognitive systems (especially perceptual systems)
that meet nine specific criteria. Five of these criteria describe the way
that modules process information. These include encapsulation
(it is impossible to interfere with the inner workings of a module), unconsciousness
(it is difficult or impossible to think about or reflect upon the operations
of a module), speed (modules are very fast), shallow
outputs (modules provide limited output, without information about
the intervening steps that led to that output), and obligatory firing
(modules operate reflexively, providing pre-determined outputs for pre-determined
inputs regardless of the context). As Fodor himself acknowledges (Fodor,
1985), these five characteristics can also be found in acquired skills that
have been learned and practiced to the point of automaticity (Schneider
and Shiffrin, 1977; Norman and Shallice, 1980). Another three criteria pertain
to the biological status of modules, to distinguish these behavioral systems
from learned habits. These include ontogenetic universals
(i.e. modules develop in a characteristic sequence), localization
(i.e. modules are mediated by dedicated neural systems), and pathological
universals (i.e. modules break down in a characteristic fashion
following some insult to the system). It is assumed (although this assumption
may not be correct -- see below) that learned systems do not display these
particular regularities. The ninth and most important criterion is domain
specificity, i.e. the requirement that modules deal exclusively
with a single information type, albeit one of enormous relevance to the
species. Aside from language, other examples might include face recognition
in humans and other primates, echo location in bats, or fly detection in
the frog. Of course learned systems can also be domain-specific (e.g. typing,
driving or baseball), but they lack the instinctual base that characterizes
a "true" module. In the same vein, innate systems may exist that
operate across domains (see below for examples). However, in Fodor's judgment
such domain-general or "horizontal" modules are of much less interest
and may prove intractable to study, compared with domain-specific or "vertical"
modules like language and face recognition.
Fodor's version of modularity unifies the three claims
that language is innate, localized, and domain-specific. This is a thoroughly
reasonable proposal, but other forms of mental and neural organization are
possible. In fact, all logical combinations of innateness, domain specificity
and localization may be found in the minds and brains of higher organisms.
Here are a few possible examples.
(1) Well-defined regions of the brain may become specialized
for a particular function as a result of experience. In other words, learning
itself may serve to set up neural systems that are localized and
domain-specific, but not innate. A good example comes from positron
emission tomography studies of brain activity showing a region of visual
cortex that is specialized for words that follow the spelling rules of English
(Petersen, Fiez and Corbetta, 1992). Surely we would all agree that English
spelling is not part of our biological heritage (and if it is, it should
be clear to every teacher that such a module is not well fixed in the genome
of American students). The ultimate location of a "spelling module"
must be based on general facts about the organization of visual cortex,
and its connections to the auditory system (in particular, the areas with
primary responsibility for language -- see below).
(2) There may be a strong innate predisposition to set
up domain-specific functions in a form that is broadly distributed across
many different cortical regions, in patterns that vary widely from one individual
brain to another. In other words, these systems may be innate and
domain-specific, but not strongly localized. An example comes from
cortical stimulation showing that many different regions of the left hemisphere
can interrupt naming, although some sites are more vulnerable than others
(Ojemann, 1991; Burnstine, Lesser, Hart, Uematsu, Zinreich, Krauss, Fisher,
Vining, and Gordon, 1990; Lüders, Lesser, Dinner, Morris, Wyllie, and
Godoy, 1991; Lüders, Lesser, Hahn, Dinner, Morris, Resor and Harrison,
1986; Lüders, Lesser, Hahn, Dinner, Morris, Wyllie and Godoy, 1991).
(3) There may be systems that are innate and highly
localized, but not domain-specific. Instead, they are used to process
many different kinds of information. Posner's three different attentional
systems might be good candidates for this category (Posner and Driver, 1992).
In short, although evidence for localization is extremely
interesting, it is simply not germane to the problems of domain specificity
or innateness. Many studies of localization in adult animals (e.g. Goldman-Rakic,
1987) provide compelling evidence for regional specialization of a very
intricate sort under "default" developmental conditions. On the
other hand, there has been a veritable explosion of evidence for cortical
plasticity in vertebrates, showing how many alternative forms of organization
are possible when the default conditions do not hold (e.g. the "rewiring"
results of Frost, Sur, Killackey, O'Leary, Merzenich and others -- see Johnson,
1993, for a review). Indeed, some neuroscientsts have argued that experience
literally sculpts the brain into its final form (Merzenich, Nelson,
Stryker, Cynader, Schoppmann and Zook 1984; Rakic, 1975; Huttenlocher, 1990).
Hence localization and domain specificity may be the endpoints of learning
and development, but they are not necessarily the starting points (Karmiloff-Smith,
My arguments here will focus on domain specificity, but
first I should clarify that domain specificity itself can apply at several
different levels. A system may have unique properties at one level, while
it follows general laws at another. Table 1 lists five levels at which a
claim of domain specificity can be made: (1) the task or problem to be solved,
(2) the behaviors or skills that evolve (or emerge) to solve the problem,
(3) the knowledge or representations that must be present somewhere in the
mind/brain of an individual who can solve the problem and produce the requisite
behaviors, (4) the neural mechanisms or processors that are required to
sustain those representations, and (5) the genetic substrate that makes
1 - 4 possible (in interaction with some environment). What level do we
have in mind when we argue that language is "special"? Surely
we can agree that language represents a special response to a special problem,
i.e. the problem of mapping thoughts and concepts that are inherently non-linear
(or atemporal) onto a channel with heavy linear (temporal) constraints.
That is, symbols must be produced one at a time (one word or one sign),
fast enough to fall within memory constraints but clearly and efficiently
enough for successful production and comprehension. Human languages represent
a very broad set of possible solutions to this special problem, but taken
together (for all their similarities and differences), languages do not
really look very much like anything else that we do (i.e. Turkish and tennis
both take place in real time, but they do not look alike). Finally, we can
all agree that the detailed and unique set of behaviors that comprise language
must be supported by a detailed and unique set of mental/neural representations,
i.e., knowledge of Turkish cannot look very much like knowledge of tennis.
PROPOSED LEVELS OF ANALYSIS FOR THE DOMAIN SPECIFICITY, LOCALIZATION
AND INNATENESS OF LANGUAGE
DOMAIN SPECIFICITY LOCALIZATION INNATENESS
(UNIQUE TO LANGUAGE?) (RESTRICTED TO (GENETICALLY
SPECIFIC SITES?) DETERMINED?)
TASKS/PROBLEMS YES NO NO
TO BE SOLVED
BEHAVIORS/SOLUTIONS YES NO NO
REPRESENTATIONS/ YES NO NO
MECHANISMS NO YES YES
GENETIC SUBSTRATE NO YES (OF COURSE)
In other words, there is no controversy surrounding the
claim that language is "special" at the first three levels in
Table 1. The problem of language is unique, it is solved in a special way,
and the knowledge required to solve that problem does not look like anything
else we know. The real controversy revolves around the next two levels in
the chart. To solve a special problem, do we really have to have a special
information processor? Have we evolved new neural tissue, a new region or
a special form of computation that deals with language, and language alone?
And is that new mechanism guaranteed by its own special stretch of DNA?
These are the levels at which I part company with the Fodor/Chomsky view.
In the words of Eric Kandel (Kandel, Schwartz and Jessell, 1991, p.15):
"The functions localized to discrete
regions in the brain are not complex faculties of mind, but elementary operations.
More elaborate faculties are constructed from the serial and parallel (distributed)
interconnections of several brain regions."
Our challenge is to figure out how these older, simpler
neural systems have been reconfigured to solve the language problem. I will
argue that language is domain-specific at Levels 1 - 3 (the problem, its
behavioral solution, the representations that support behavior), but these
levels are not innate or localized. On the other hand, linguistic knowledge
is acquired and supported by processors that are innate and are localized,
but not domain-specific (that is, they can also process information from
General Arguments Against the Domain Specificity of Language
My own long-standing skepticism about the mental-organ
claim is based on four kinds of evidence: (1) phylogenetic recency, (2)
behavioral plasticity, (3) neural plasticity, (4) the arbitrariness of mappings
from form to meaning. None of these arguments constitute a disproof of domain
specificity, but together they weaken its plausibility.
(1) Phylogenetic recency. Bates et al. (1991) note
that the species on this earth have had a great deal of time to evolve ways
of dealing with light, gravity, motion, spatial organization, cause and
effect, and the boundaries of common objects and events. By contrast, language
is a newcomer -- about 30,000 years old by current best estimates. It is
hard to imagine how we could have developed elaborate, innate and domain-specific
mechanisms for language in a relatively short period of time (although "poverty
of the imagination" is an admittedly weak argument for any case, including
(2) Behavioral plasticity. Although one sometimes
reads in textbooks that languages are based on a host of universal principles,
the same everywhere, cross-linguistic research testifies to a surprising
variability in structure and function across natural languages (MacWhinney
and Bates, 1989, a volume based on studies of sentence processing in 15
different languages, as drastically different as Hungarian, Warlpiri and
Chinese; see also Wurm, 1993). To be sure, there are some similarities (e.g.
all languages have a semantics and a grammar). But the variability that
has been recorded so far greatly exceeds reports for other putatively innate
and domain-specific systems (including the oft-invoked example of birdsong).
Oral languages present a daunting range of possibilities, from Chinese (a
language with absolutely no inflections of any kind on nouns or verbs) to
Greenlandic Eskimo (a language in which a sentence can consist of a single
word with 8 - 12 prefixes, suffixes, and infixes). But an even more important
lesson comes from the fact that deaf communities have developed full-blown
linguistic systems in the visual-manual modality (e.g. Klima and Bellugi,
1988). If bats were suddenly deprived of echo location, would they develop
an equally complex and efficient system in some other modality, within two
generations? Probably not. To me, the very existence of languages like ASL
argues strongly against domain specificity -- although it does argue that
our species has a robust and passionate urge of some kind to communicate
our most complex thoughts, and a powerful set of information processing
mechanisms that permit us to solve this problem.
(3) Neural plasticity. In contrast with the best-known
examples of innate and domain-specific brain systems, the systems that support
languages also show an extraordinary and perhaps unprecedented degree of
neural plasticity. Research on the long-term effects of early focal brain
injury suggests that children with large lesions to the classic language
zones go on, more often than not, to attain levels of language ability that
are indistinguishable from normal (Bates et al., 1992; Thal, Marchman, Stiles,
Aram, Trauner, Nass and Bates, 1991; Marchman, Miller and Bates, 1991; Stiles
and Thal, 1993; Vargha-Khadem, Isaacs, Papaleloudi et al. 1991; Aram, 1988).
As Milner and her colleagues have shown (Rasmussen and Milner, 1977; Milner,
1993), this steady state can be achieved in a variety of ways. In roughly
40% of the adult survivors of early focal brain injury who received a sodium
amytal test to determine the hemispheric specialization for speech, language
production was interrupted by paralysis of the right hemisphere. Another
40% of this sample displayed left-hemisphere dominance for speech, suggesting
that some kind of reorganization has taken place within the left hemisphere.
The remaining 20% displayed some form of bilateral organization for speech,
with some language functions controlled by the left and others by the right.
This does not mean that the two hemispheres are initially
equipotential for language. For the last ten years, we have carried out
prospective studies of language development in children with focal injuries
to the left or right hemisphere. That is, we locate children with early
focal brain injury in the prelinguistic period (before six months of age),
and follow them through their first encounters with cognitive domains that
are lateralized in normal adults (e.g. language, spatial cognition, facial
affect). Our findings for language are largely compatible with retrospective
studies of the same populations, i.e. most children go on to achieve linguistic
abilities within the normal or low-normal range. However, it is also clear
that this reorganization takes place after an initial phase where regional
biases for language are evident (whether or not those biases map onto the
adult picture). Regardless of side, size or site of lesion, most children
with focal brain injury are delayed in the first stages of language production.
Receptive delays are not uniquely associated with left-hemisphere injury
at any point in the stages that we have studied so far, suggesting that
the acquisition of receptive control over language may be a bilateral phenemenon
(indeed, receptive deficits tend to be slightly greater with right-hemisphere
injury) On the other hand, recovery from initial delays in expressive language
does take longer (on average) in children with left-hemisphere injury. We
may conclude with some confidence that the recovery of language observed
in children with focal brain injury represents a true reorganization, an
alternative to the default model that is discovered after an initial delay.
The same degree of plasticity is not observed in other,
phylogenetically older cognitive domains (Stiles and Thal, 1993). Working
with the same population of children, Stiles and colleagues (Stiles-Davis,
1988; Stiles-Davis, Janowsky, Engel and Nass, 1988; Stiles and Nass, 1991)
have observed patterns of behavioral deficit along the lines that we would
expect from work on spatial cognitive deficits in adults (although the childhood
variants are more subtle). Reilly and colleagues have reported similar parallels
to the adult model in their research on facial affect in these children
(Reilly et al., 1994). Although it is difficult to compare apples and oranges,
it looks as though there may be more plasticity for language than we observe
in other perceptual and cognitive systems.
(4) Arbitrariness of form-meaning mapping. This
final point is a bit more difficult to summarize, but I think it is at least
as important as the first three. A defining characteristic of language (indeed,
one of its few universals) is the arbitrariness of the relationship between
sound and meaning (and, to a surprising degree, between signs and their
meanings in ASL). The words "dog", "chien", "perro",
"cane", "Hund", etc. do not in any way resemble the
fuzzy four-legged creatures that they signify. The same is true for the
relationship between grammatical forms and the communicative work that those
forms carry out. For example, depending on the language that one speaks,
basic information about "who did what to whom" can be signalled
through word order (as it is in English), case inflections on nouns (e.g.
Latin, Russian, Hungarian), agreement marking between subject and verb (a
major source of information in Italian, but only a minor source in English),
and a range of other cues. What does this have to do with modularity? If
one examines all the known examples of innate and domain-specific knowledge,
there is always some kind of a physical constant, a partial
isomorphism between the source of information in the world to which
the animal must respond, and the internal state that the animal must take
(at some level in the nervous system) in order to respond correctly. Consider,
for example, the "bug detector" in the retina of the frog (Lettvin,
Maturana, McCulloch and Pitts, 1959), or the line angle detectors located
in the visual cortex of kittens (Hubel and Wiesel, 1963). To evolve an innate
perceptual and/or motor system, it seems that nature needs something to
work with, something that holds still, something physically solid, constant,
reliable. Language lacks this property, and for that reason, I find it hard
to understand in concrete, material terms what an "innate language-specific
acquisition device" might look like.
As I have said, none of these are knock-down arguments
by themselves. They simply serve to put us on our guard, to raise an appropriate
level of skepticism in the face of claims about a grammar gene or a language
neuron. Let us turn now to some more specific claims about innateness, localization
and domain specificity, starting with the adult aphasia (the first test
case for localization and domain specificity in the history of cognitive
Arguments Based on Adult Aphasia
Let us assume, for the moment, that there is good evidence for localization
of language in our species, in high-probability default patterns that must
(I agree) mean that some kind of genetic bias is at work. Exactly what is
In the early stages of research on aphasia, it was generally
argued that Broca's aphasia (non-fluent with spared comprehension) results
from a breakdown in the motor aspects of language, while Wernicke's aphasia
(comprehension deficits in the presence of fluent speech) results from injury
to sensory areas. This characterization made reasonably good neuroanatomical
sense, in view of the fact that Broca's aphasia correlates with frontal
injury while Wernicke's aphasia is associated with posterior lesions, but
its fit to the behavioral data was always fairly loose. As Freud (1891/1953)
pointed out a hundred years ago, a sensory deficit cannot explain the severe
word-finding deficits and substitution errors that characterize the fluent
output observed in Wernicke's aphasia. In the 1970's, analogous problems
arose for the motor account of Broca's aphasia (Zurif and Caramazza, 1976;
Heilman and Scholes, 1976). In particular, careful experimental studies
showed that these patients also suffer from comprehension problems when
they are forced to rely on grammatical markers to interpret complex sentences
(e.g. patients could interpret "The apple was eaten by the boy",
but not "The boy was chased by the girl"). At this point, several
investigators offered an alternative view based on modular theories of linguistic
organization (e.g. Caramazza and Berndt, 1985). In particular, it was argued
that Broca's aphasics have lost the ability to comprehend or produce grammar
(resulting in telegraphic output, and subtle comprehension deficits that
are most evident when semantic information is too ambiguous to support sentence
interpretation). Conversely, the comprehension deficits and word-finding
problems observed in Wernicke's aphasia could be jointly and parsimoniously
explained if these patients have lost the ability to process content words.
This apparent double dissociation provided support for the idea that the
brain is organized into innate, domain-specific and localized modules for
grammar and semantics, respectively (see Gazzaniga, 1993, for arguments
along the same lines).
But this unifying view has also fallen on hard times.
More recent studies of language breakdown in aphasia have forced investigators
to abandon the idea of a "grammar box", i.e. neural tissue that
is devoted exclusively to grammar, and contains the representations that
are necessary for grammatical processing. To offer just a few examples,
there are (1) numerous studies showing that so-called agrammatic aphasics
can make remarkably fine-grained judgments of grammaticality (Linebarger,
Schwartz and Saffran, 1983; Wulfeck, 1987; Shankweiler, Crain, Gorrell and
Tuller, 1989; Wulfeck and Bates, 1991), and (2) a host of cross-linguistic
studies showing differences in the symptoms displayed by agrammatic patients
in different language communities -- differences that can only be explained
if we acknowledge that the patient still retains detailed knowledge of his/her
grammar (Bates, Wulfeck and MacWhinney, 1991; Menn and Obler, 1990). It
begins to look as though linguistic knowledge is broadly represented
in the adult brain -- a conclusion that is also supported by studies of
brain activity during normal language use (Petersen et al., 1992; Kutas
and Kluender, 1991). Some areas do play a more important role than others
in getting a particular process underway in real time, but the knowledge
itself is not strictly localized.
So what is localized? The classic sensorimotor view of
Broca's and Wernicke's aphasia has fallen by the wayside, and now the grammar/semantics
view has fallen as well. But their successor is still unnamed. Some investigators
have argued that left frontal regions are specialized for the rapid processes
required for fluent use of grammar, while posterior regions play a more
important role in controlled, strategic choice of words and sentence frames
(e.g. Frazier and Friederici, 1991; Zurif, Swinney and Garrett, 1990; Milberg
and Albert, 1991). These ideas are still distressingly vague, but they point
us in a new direction.
From a developmental perspective, the default pattern
of brain organization for language observed in adults can be viewed as the
end product of regional differences in neural computation and processing
that "attract" or "recruit" language processes under
default conditions. The perisylvian areas of the left hemisphere are not
"innate language tissue", any more than a tall child constitutes
an "innate basketball player". However, all other things being
equal, the left perisylvian areas will take over the language problem, and
the tall child has a very good chance of ending up on the basketball team.
This brings me to the problem of how (and where) language is acquired.
Arguments based on Normal and Abnormal Language Development
In line with Fodor's criterion for ontogenetic universals,
it is well known that children go through a series of universal stages in
language learning: from babbling in vowel sounds (around 3 months) to babbling
in consonants (between 6 - 9 months); from first signs of word comprehension
(from 8 - 10 months) to the onset of word production (averaging 12 months,
with a substantial range of individual variability); from the single-word
stage (from 12 - 20 months, on average) to the onset of word combinations;
from simple two-word strings (so-called telegraphic speech) to complex grammar
( evident in most normal children by three years of age). But can we conclude
that these milestones reflect the unfolding of a domain-specific module?
Probably not, at least not on the basis of the evidence that is currently
available (see Bates et al., 1992, for details). First of all, there is
enormous variability from one child to another in the onset and duration
of these stages. Second, there are important variations in this basic pattern
from one language to another (e.g. children who are exposed to a richly
inflected language like Turkish often display signs of productive grammar
in the one-word stage). Third, each of these milestones in early language
is correlated with specific changes outside the boundaries of language (e.g.
the use of familiar gestures like drinking, combing or putting a telephone
receiver to the ear as a way of "labelling" common objects --
gestures that appear in the hearing child right around the time that naming
takes off in the vocal modality). In other words, one cannot conclude that
the universal maturational timetable for language is really universal, or
that it is specific to language.
These problems of interpretation are compounded in research
on abnormal language development. Two recent examples illustrate the confusion
between innateness and domain specificity that has plagued this field, much
like the confusion between domain specificity and localization that has
characterized research on adult aphasia.
Petitto and Marentette (1991) published an influential
paper demonstrating that deaf infants exposed to sign language "babble"
with their hands, producing meaningless but systematic actions that are
not observed in hearing children. Furthermore, this form of manual babbling
occurs around 8 - 10 months of age, the point at which vocal babbling appears
in the hearing child. The authors conclude that language learning involves
innate abilities that are independent of modality (i.e. vocal or manual);
they also claim that these abilities are specific to language, providing
support for Chomsky's mental-organ claim. Their first conclusion is clearly
supported by the evidence, but the second is not. We have known for more
than 100 years that children begin to imitate novel actions (i.e. actions
that are not already in their repertoire) around 8 - 10 months. The more
systematic the adult input, the more systematic the child's imitation is
likely to be. Petitto and Marentette's demonstration of babbling in the
visual modality constitutes a particularly beautiful example of this interesting
but well-established fact. The kind of imitation that underlies babbling
is undoubtedly based upon abilities that are innate, and particularly well
developed in our species (human children imitate far better and more often
than any other primate (Greenfield and Savage-Rumbaugh, 1991; Chevalier-Skolnikoff,
1991), but proof of its existence does not, in itself, constitute evidence
in favor of the notion that language is "special".
A somewhat different example appeared in a letter to Nature
by Gopnik (1990; for further details see Gopnik and Crago, 1991), describing
preliminary results from a study of grammatical abilities in a family of
individuals suffering from some kind of genetically based disorder (see
also Tallal, Townsend, Curtiss and Wulfeck, 1991). Members of this family
have difficulty with particular aspects of grammar, including regular verb
inflections (e.g. the "-ed" in verbs like "walked" and
"kissed"). By contrast, they are reported to have less trouble
with irregular forms like "came" or "gave". This pattern
is offered as an example of an innate and domain-specific disorder, termed
"feature-blind dysphasia", and has been cited as evidence in favor
of Pinker's claim that regular and irregular forms are handled by separate
mental and perhaps neural mechanisms (Pinker, 1991). Shortly after Gopnik's
letter appeared, Nature published a rebuttal by Vargha-Khadem and Passingham
(1990; see also Fletcher, 1990), who have studied the same family for a
number of years. These authors point out that the members of this family
suffer from a much broader range of linguistic and non-linguistic deficits
than one might conclude from Gopnik's description. Their peculiar grammatical
symptoms are only the tip of an iceberg, one by-product of a disorder with
repercussions in many different areas of language and cognition, providing
further evidence for innateness but none for domain specificity (Marchman,
The above examples are part of a long tradition in neurolinguistics,
where unusual profiles of language ability and disability are cited as events
for the eccentricity and modularity of language. Some other "parade
cases" include Specific Language Impairment or SLI, and children with
By definition, specific language impairment (SLI) refers
to delays in receptive and/or expressive language development in children
with no other known form of neurological or cognitive impairment. However,
recent studies of SLI suggest that this definition may not be accurate (Cohen,
Gelinas, Lassonde and Geoffrey, 1991; Tallal, Stark and Mellits, 1985).
Although these children do not suffer from global forms of mental retardation,
they do show subtle impairments in aspects of cognition and/or perception
that are not specific to language. For example, many children with SLI experience
difficulty in processing rapid transitions in acoustic information (including
nonlinguistic stimuli). This may help to explain new studies comparing SLI
in English, Italian and Hebrew (Rom and Leonard, 1990; Leonard, Bortolini,
Caselli, McGregor and Sabbadini, in press) showing that the specific areas
of grammar that are most delayed vary from one language to another, and
the most vulnerable elements within each language appear to be those that
are low in ``phonological substance'' (i.e. salience). The subtle deficits
associated with SLI may also transcend the acoustic modality, affecting
certain kinds of manual gesture (Thal, Tobias and Morrison, 1991). Taken
together, these studies suggest that SLI may not be a purely linguistic
(or acoustic) phenomenon.
The strongest evidence to date in favor of domain specificity
comes from rare cases in which language appears to be remarkably spared
despite severe limitations in other cognitive domains. Etiologies associated
with this unusual profile include spina bifida and hydrocephalus, and a
rare form of mental retardation called Williams Syndrome, or WMS (Bellugi,
Bihrle, Neville, Jernigan and Doherty, 1991; Jernigan and Bellugi, 1990).
The dissociations observed in WMS prove that language can ``decouple'' from
mental age at some point in development. Nevertheless, recent studies of
WMS place constraints on the conclusion that language is a separate mental
system from the beginning. First, it is clear that language development
is seriously delayed in infants and preschool children with WMS, suggesting
that certain "cognitive infrastructures" must be in place before
language can be acquired (Thal, Bates and Bellugi, 1989). Second, studies
of older children with WMS demonstrate peculiar islands of sparing in some
non-linguistic domains (e.g. face recognition, and recognition of common
objects from an unfamiliar perspective), and unusual patterns of deficit
in other non-linguistic domains that are not at all comparable to the patterns
displayed by Down Syndrome children matched for mental age. Third, the language
of older children and adults with WMS includes some deviant characteristics
that are not observed in normal children. For example, in a word fluency
test in which WMS children and Down Syndrome controls were asked to generate
names for animals, Down Syndrome and normal controls tend to generate high-frequency
words like "dog" and "cat"; WMS individuals tend instead
to generate unusual, low-frequency items like "ibex" and "brontosaurus".
In view of such findings, it seems that WMS may not represent sparing of
normal language, but a completely different solution to the language problem,
achieved with a deviant form of information processing.
In short, the dissociations between language and cognition
observed in SLI (where language < cognition) and in Williams Syndrome
(where language > cognition) cannot be used to support a mental-organ
view. Things are just not that simple. Instead, these unusual profiles offer
further evidence for the behavioral and neural plasticity of language. There
are many ways to solve the problem of language learning. Some are more efficient
than others, to be sure, but the problem can be solved with several different
configurations of learning, memory, perception and cognition. This brings
us to my final point: How is it that language is learnable at all?
There is a branch of language acquisition research called
"learnability theory" (e.g. Lightfoot, 1991), which uses formal
analysis to determine the range of conditions under which different kinds
of grammars can (in principle) be learned. Until recently, most of this
research has been based upon the assumption that language learning in humans
is similar to language learning in serial digital computers, where a
priori hypotheses about grammatical rules are tested against strings
of input symbols, based on some combination of positive evidence ("here
is a sentence in the target language") and negative evidence ("here
is a sentence that is not permitted by the target language"). A famous
proof by Gold (1967) showed that a broad class of grammars (including generative
grammars of the sort described by Chomsky) could not be learned by a system
of this kind unless negative evidence was available in abundance, or strong
innate constraints were placed upon the kinds of hypotheses that the system
would consider. Since we know that human children are rarely given explicit
negative evidence, the learnability theory seems to require the conclusion
that children have an extensive store of innate and domain-specific grammatical
In the last two years, this conclusion has been challenged
by major breakthroughs in the application of a different kind of computer
architecture (called neural networks, connectionism, and/or parallel distributed
processing) to classic problems in language learnability. Because connectionism
makes a very different set of assumptions about the way that knowledge is
represented and acquired, Gold's pessimistic conclusions about language
learnability do not necessarily apply. This new era began in 1986 with a
simulation by Rumelhart and McClelland (1986) on the acquisition of the
English past tense, showing that connectionist networks go through stages
that are very similar to the ones displayed by children who are acquiring
English (producing and then recovering from rule-like overgeneralizations
like "comed" and "wented", in the absence of negative
evidence). This simulation has been severely criticized (see especially
Pinker and Prince, 1988; Kim, Pinker, Prince and Sandup, 1991). However,
a number of new works have appeared that get around these criticisms, replicating
and extending the Rumelhart-McClelland findings in several new directions
(Elman, 1990 and 1991; MacWhinney, 1991; Plunkett and Marchman, 1991 and
1993; Marchman, 1993). The most recent example comes from Marchman (1993),
who has "lesioned" neural networks at various points during learning
of the past tense (randomly eliminating between 2% - 44% of the connections
in the network). These simulations capture some classic "critical period"
effects in language learning (e.g. smaller, earlier lesions lead to better
outcomes; later, larger lesions lead to persistent problems in grammar),
showing that such effects can occur in the absence of "special"
maturational constraints (compare with Newport, 1990, and Elman, 1991).
In addition, Marchman's damaged systems found it more difficult to acquire
regular verbs (e.g. "walked") than irregulars (e.g. "came"),
proving that the specific pattern of deficits described by Gopnik
and by Pinker can result from non-specific forms of brain damage
in a general-purpose learning device. Such research on language learning
in neural networks is still in its infancy, and we do not know how far it
can go. But it promises to be an important tool, helping us to determine
just how much innate knowledge has to be in place for certain kinds of learning
In short, a great deal has been learned in the last few
years about the biological foundations for language development. Evidence
for innateness is good, but evidence for a domain-specific "mental
organ" is difficult to find. Instead, language learning appears to
be based on a relatively plastic mix of neural systems that also serve other
functions. I believe that this conclusion renders the mysteries of language
evolution at issue in this volume somewhat more tractable. That is, the
continuities that we have observed between language and other cognitive
systems make it easier to see how this capacity came about in the first
Aram, D.M. (1988). Language sequelae of unilateral brain lesions in children.
In F. Plum, (Ed.), Language, communication and the brain. New York: Raven
Bates, E., Bretherton, I., & Snyder, L. (1988). From
first words to grammar: Individual differences and dissociable mechanisms.
New York: Cambridge University Press.
Bates, E., Thal, D., & Janowsky, J. (1992). Early
language development and its neural correlates. In I. Rapin & S. Segalowitz
(Eds.), Handbook of neuropsychology, Vol. 7: Child neuropsychology. Amsterdam:
Bates, E., Thal, D. and Marchman, V. (1991). Symbols and
syntax: A Darwinian approach to language development. In N. Krasnegor, D.
Rumbaugh, E. Schiefelbusch and M. Studdert-Kennedy (Eds.), Biological and
behavioral determinants of language development. Hillsdale, NJ: Erlbaum,
29 - 65.
Bates, E. & Wulfeck, B. (1989a). Crosslinguistic studies
of aphasia. In B. MacWhinney & E. Bates (Eds.), The crosslinguistic
study of sentence processing. New York: Cambridge University Press.
Bates, E. & Wulfeck, B. (1989b). Comparative aphasiology:
A cross-linguistic approach to language breakdown. Aphasiology, 3, 111-142
Bates, E., Wulfeck, B. & MacWhinney, B. (1991). Crosslinguistic
research in aphasia: An overview. Brain and Language, 41, 123-148.
Burnstine, T.H., Lesser, R.P., Hart, J. Jr., Uematsu,
S., Zinreich,S.J., Krauss, G.L., Fisher, R.S., Vining, E.P., and Gordon,
B. (1990). Characterization of the basal temporal language area in patients
with left temporal lobe epilepsy. Neurology, 40(6), 966-970.
Bellugi, U., Bihrle, A., Neville, H., Jernigan, T. and
Doherty, S. (1991). Language, cognition and brain organization in a neurodevelopmental
disorder. In W. Gunnar and C. Nelson (Eds.), Developmental Behavioral Neuroscience.
Hillsdale, NJ: Erlbaum.
Caramazza, A. & Berndt, R. (1985). A multicomponent
view of agrammatic Broca's aphasia. In M.-L. Kean (Ed.), Agrammatism (pp.
27-63). New York: Academic Press.
Chevalier-Skolnikoff, S. (1991) Spontaneous tool use and
sensorimotor intelligence in Cebus compared with other monkeys and apes.
Behavioral and Brain Sciences, 14:2.
Chomsky, N. (1957). Syntactic structures. The Hague: Mouton.
Chomsky, N. (1965). Aspects of the theory of syntax. MIT
Chomsky, N. (1988) Language and problems of knowledge.
Cohen, H., Gelinas, C., Lassonde, M. and Geoffrey, G.
(1991). Auditory lateralization for speech in LI children. Brain and Language,
41, 395 - 401.
Deacon, T. (1990a). Brain-language coevolution. In J.A.
Hawkins and M. Gell-Mann (Eds.), The evolution of human languages: Proceedings
of the Santa Fe Institute Studies in the Sciences of Complexity. Addison-Wesley.
Deacon, T. (1990b). Rethinking mammalian brain evolution.
American Zoologist, 30, 629 - 705.
Elman, J. (1990). Finding structure in time. Cognitive
Science, 14, 179 - 211.
Elman, J. (1991). Incremental learning, or the importance
of starting small. Proceedings of the Thirteenth Annual Conference of the
Cognitive Science Society. Hillsdale, NJ: Erlbaum, 443 - 448.
Fletcher, P. (1990). Speech and language defects. Nature,
Frazier, L. & Friederici, A. (1991). On deriving the
properties of agrammatic comprehension. Brain and Language, 40, 51-66.
Fodor, J. (1983). Modularity of mind. Cambridge, Mass.:
Fodor, J.A. (1985). Multiple book review of 'The modularity
of mind'. Behavioral and Brain Sciences, 8, 1-42.
Freud, A. (1953). On aphasia: A critical study. New York:
International Universities Press. (Original work published in 1891).
Gazzaniga, M. (1993, April). Language and the cerebral
hemispheres. Paper presented at the FESN Study Group on Evolution and Neurology
of Language, Geneva.
Gold, E. (1967). Language identification in the limit.
Information and Control, 16, 447 - 474.
Goldman-Rakic, P.S. (1987). Development of cortical circuitry
and cognitive function. Child Development, 58, 601-622.
Gopnik, M. (1990). Feature-blind grammar and dysphasia.
Nature, 344, 715.
Gopnik, M. and Crago, M. (1991). Familial aggregation
of a developmental language disorder. Cognition, 39:1, 1 - 50.
Greenfield, P. and Savage-Rumbaugh, E. (1991). Imitation,
grammatical development and the invention of protogrammar by an ape. In
N. Krasnegor, D. Rumbaugh, R. Schiefelbusch and M. Studdert-Kennedy (Eds.),
Biological and behavioral determinants of language development. Hillsdale,
NJ: Erlbaum, 235 - 262.
Heilman, K.M. & Scholes, R.J. (1976). The nature of
comprehension errors in Broca's, conduction and Wernicke's aphasics. Cortex,
Hubel, D.H., & Wiesel, T.N. (1963). Receptive fields
of cells in striate cortex of very young, visually inexperienced kittens.
Journal of Neurophysiology, 26, 944-1002.
Huttenlocher, P. R. (1990). Morphometric study of human
cerebral cortex development. Neuropsychologia 28:6, 517 - 527.
Jernigan, T. & Bellugi, U. (1990). Anomalous brain
morphology on magnetic resonance images in Williams Syndrome and Down Syndrome.
Archives of Neurology, 47, 429-533.
Johnson, M. (Ed.). (1993). Brain development and cognition:
A reader. Oxford: Blackwell Publishers.
Kandel, E.R., Schwartz, J.H., & Jessell, T.H. (1991).
Principles of neural science (3rd ed.). New York: Elsevier.
Karmiloff-Smith, A. (1993). Beyond modularity: A developmental
perspective on cognitive science. Cambridge, MA: MIT Press.
Kim, J., Pinker, S., Prince, A. and Sandup, P. (1991).
Why no mere mortal has ever flown out to center field. Cognitive Science,
15:2, 173 - 218.
Klima, E. & Bellugi, U. (1988). The signs of language.
Harvard University Press.
Kutas, M. & Kluender, R. (1991). What is who violating?
A reconsideration of linguistic violations in light of event-related potentials.
Center for Research in Language Newsletter, 6:1. La Jolla: University of
California, San Diego, Center for Research in Language.
Lashley, K.S. (1950). In search of the engram. In Symposia
of the Society for Experimental Biology, No. 4. Physiological mechanisms
and animal behaviour. New York: Academic Press,
Leonard, L., Bortolini, U., Caselli, M., McGregor, K.
and Sabbadini, L. (in press). Two accounts of morphological deficits in
children with Specific Language Impairment. Language Acquisition.
Lettvin, J.Y., Maturana, H.R., McCulloch, W.S., &
Pitts, W.H. (1959). What the frog's eye tells the frog's brain. Proceedings
of the Institute of Radio Engineering of New York, 47, 1940-1951.
Lightfoot, D. (1991). The child's trigger experience --
Degree-0 learnability. Behavioral Brain Sciences, 14:2, 364.
Linebarger, M., Schwartz, M., & Saffran, E. (1983).
Sensitivity to grammatical structure in so-called agrammatic aphasics. Cognition,
Lüders, H., Lesser, R., Dinner, D., Morris, H., Wyllie,
E., and Godoy, J. (1991). Localization of cortical function: New information
from extraoperative monitoring of patients with epilepsy. Epilepsia, 29
(Suppl. 2), S56-S65.
Lüders, H., Lesser, R., Hahn, J., Dinner, D., Morris,
H., Resor, S., and Harrison, M. (1986). Basal temporal language area demonstrated
by electrical stimulation. Neurology, 36, 505-509.
Lüders, H., Lesser, R., Hahn, J., Dinner, D., Morris,
H., Wyllie, E., and Godoy, J. (1991). Basal temporal language area. Brain,
MacWhinney, B. (1991). Implementations are not conceptualizations:
Revising the verb-learning model. Cognition, 40, 121 - 157.
MacWhinney, B. & Bates, E. (Eds.) (1989). The crosslinguistic
study of sentence processing. New York: Cambridge University Press.
Marchman, V. (1993). Constraints on plasticity in a connectionist
model of the English past tense. Journal of Cognitive Neuroscience , 5:2,
Marchman, V., Miller, R. and Bates, E. (1991). Babble
and first words in children with focal brain injury. Applied Psycholinguistics,
Menn, L. & Obler, L.K. (Eds.). (1990). Agrammatic
aphasia: Cross-language narrative sourcebook. Amsterdam/Philadelphia: John
Merzenich, M., Nelson, R., Stryker, M., Cynader, M., Schoppmann,
A. & Zook, J. (1984). Somatosensory cortical map changes following digit
amputation in adult monkeys. Journal of Comparative Neurology, 224, 591-605.
Milberg, W. & Albert, M. (1991). The speed of constituent
mental operations and its relationship to neuronal representation: An hypothesis.
In R.G. Lister & H.J. Weingartner (Eds.), Perspectives on cognitive
neuroscience. New York: Oxford University Press.
Milner, B. (1993, April). Carotid-amytal studies of speech
lateralization and gesture control. Paper presented at the FESN Study Group
on Evolution and Neurology of Language, Geneva.
Newport, E. (1990). Maturational constraints on language
learning. Cognitive Science, 14, 11 - 28.
Norman, D.A., & Shallice, T. (1980). Attention to
action: Willed and automatic control of behavior. Center for Human Information
Processing (Technical Report No. 99). (Reprinted in revised form in R.J.
Davidson, G.E. Schwartz & D. Shapiro [Eds.] , Consciousness and
self-regulation [Vol. 4]. New York: Plenum Press.)
Ojemann, G.A. (1991). Cortical organization of language.
Journal of Neuroscience, 11:8, 2281-2287.
Petersen, S.E., Fiez, J.A. & Corbetta, M. (1992).
Neuroimaging. Current Opinion in Neurobiology - Special Issue on Cognitive
Neuroscience, 2, 217-222.
Petitto, L. and Marentette, P.F. (1991). Babbling in the
manual mode: Evidence for the ontogeny of language. Science, 251, 1493-1499.
Pinker, S. (1991). Rules of language. Science, 253, 530
Pinker, S. and Prince, A. (1988). On language and connectionism:
An analysis of a parallel distributed processing model of language acquisition.
Cognition, 28, 73 - 193.
Plunkett, K. and Marchman, V. (1991). U-shaped learning
and frequency effects in a multi-layered perceptron: Implications for child
language acquisition. Cognition, 38:1, 43 - 102.
Plunkett, K., & Marchman, V. (1993). From rote learning
to system building: Acquiring verb morphology in children and connectionist
nets. Cognition, 48, 21-69.
Posner, M.I. & Driver, J. (1992). The neurobiology
of selective attention. Current Opinion in Neurobiology - Special Issue
on Cognitive Neuroscience, 2, 165-169.
Rakic, P. (1975). Timing of major ontogenetic events in
the visual cortex of the rhesus monkey. In N. Buchwald & M. Brazier
(Eds.), Brain mechanisms in mental retardation. New York: Academic Press.
Rasmussen, T., & Milner, B. (1977). The role of early
left-brain injury in determining lateralization of cerebral speech functions.
Annals of the New York Academy of Sciences, 299, 355-369.
Reilly, J., Stiles, J., Larsen, J., & Trauner, D.
(1994). Affective facial expression in infants with focal brain damage.
Manuscript submitted for publica-tion.
Rom, A. and Leonard, L. (1990). Interpreting deficits
in grammatical morphology in specifically language-impaired children: Preliminary
evidence from Hebrew. Clinical Linguistics and Phonetics, 4:2, 93 - 105.
Rumelhart, D., McClelland, J. and the PDP Research Group
(1986). Parallel distributed processing: Explorations in the microstructure
of cognition, Vol. 1. Cambridge, MA.: MIT/Bradford Books.
Savage-Rumbaugh, S., Murphy, J., Sevcik, R., Brakke, K.,
Williams, S., & Rumbaugh, D. (1993). Language comprehension in ape and
child. Monographs of the Society for Research in Child Development, Serial
#233, Volume 58, 3-4, 222-242.
Schneider, W., & Shiffrin, R. (1977). Controlled and
automatic human information processing: 1. Detection, search and attention.
Psychological Review, 84, 321-330.
Sereno, M. (1990). Language and the primate brain. Center
for Research in Language Newsletter, 4:4. La Jolla: University of California,
San Diego, Center for Research in Language.
Shankweiler, D., Crain, S., Gorrell, P., & Tuller,
B. (1989). Reception of language in Broca's aphasia. Language and Cognitive
Processes, 4:1, 1 - 33.
Stiles-Davis, J. (1988). Spatial dysfunctions in young
children with right cerebral hemisphere injury. In J. Stiles-Davis, M. Kritchevsky
& U. Bellugi (Eds.), Spatial cognition: Brain bases and development.
Hillsdale, NJ: Erlbaum.
Stiles-Davis, J., Janowsky, J., Engel, M., & Nass,
R. (1988). Drawing ability in four young children with congenital unilateral
brain lesions. Neuropsychologia, 26, 359-371.
Stiles, J. & Nass, R. (1991). Spatial grouping activity
in young children with congenital right- or left-hemisphere brain injury.
Brain & Cognition, 15, 201-222.
Stiles, J. & Thal, D. (1993). Linguistic and spatial
cognitive development following early focal brain injury: Patterns of deficit
and recovery. In M. Johnson (Ed.), Brain development and cognition: A reader.
Oxford: Blackwell Publishers.
Tallal, P., Stark, R. and Mellits, D. (1985). Identification
of language-impaired children on the basis of rapid perception and production
skills. Brain and Language, 25, 314 - 322.
Tallal, P., Townsend, J., Curtiss, S. and Wulfeck, B.
(1991). Phenotypic profiles of language-impaired children based on genetic/family
history. Brain and Language, 41, 81 - 95.
Thal, D., Bates, E., & Bellugi, U. (1989). Language
and cognition in two children with Williams Syndrome. Journal of Speech
and Hearing Research, 3, 489-500.
Thal, D., Marchman, V., Stiles, J., Aram, D., Trauner,
D., Nass, R. and Bates, E. (1991). Early lexical development in children
with focal brain injury. Brain and Language, 40, 491-527.
Thal, D., Tobias, S. and Morrison, D. (1991). Language
and gesture in late talkers: A one-year follow-up. Journal of Speech and
Hearing Research, 34, 604 - 612.
Vargha-Khadem, F. and Passingham, R. (1990). Speech and
language defects. Nature, 346, 226.
Vargha-Khadem, F., Isaacs, E., Papaleloudi, H., Polkey,
C. and Wilson, J. (1991). Development of language in six hemispherectomized
patients. Brain, 114, 473 - 495.
Wulfeck, B. (1987). Sensitivity to grammaticality in agrammatic
aphasia: Processing of word order and agreement violations. Doctoral dissertation,
Wulfeck, B., & Bates, E. (1991). Differential sensitivity
to errors of agreement and word order in Broca's aphasia. Journal of Cognitive
Neuroscience, 3, 258-272.
Wurm, S.A. (1993, April). Language contact and unusual
semantic features: Some ideas on language and thought. Paper presented at
the FESN Study Group on Evolution and Neurology of Language, Geneva.
Zurif, E. & Caramazza, A. (1976). Psycholinguistic
structures in aphasia: Studies in syntax and semantics. In H. & H.A.
Whitaker (Eds.), Studies in neurolinguistics (Vol. I). New York: Academic
Zurif, E., Swinney, D., & Garrett, M. (1990). Lexical
processing and sentence comprehension in aphasia. In A. Caramazza (Ed.),
Cognitive neuropsychology and neuro-linguistics: Advances in models of cognitive
function and impairment. Hillsdale, NJ: Erlbaum.