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Language, Logic, and Concepts.

Ray S. Jackendoff, Paul Bloom and Karen Wynn, editors.
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Chapter

11

Some Evidence
Grammars

for Impaired

Myrna

Gopnik

Over the last few years, specific language impairment (SLI ) has become a
hot topic because it may have the potential to tell us something about the
biological basis of language . I am afraid that comments about this
research, on both sides, have often generated more heat than light . If we
are really interested in the science of it all , then it is important to get the
issues out on the table and seewhich ones we can agree about , which ones
are still outstanding , and how we could resolve them . This chapter is
intended to make a stab at clarifying some of the issues.
The fact that we would even be discussing language and biology in the
same breath would have been unimaginable when I was an undergraduate
in 1955 (though Darwin , himself , did suggest that learning language might
be an instinct ). Over the last 40 years the picture has changed radically .
Research has shown that all languages, despite their seeming differences,
are built on the same general plan and that most children acquire their
native language as easily as they learn to walk upright , without explicit
teaching and with no apparent effort . Newborns can't do it , but it appears
in the first year of life , and the necessary precursors for this achievement
seem to be there at birth . Experiments with very young babies have shown
that humans come equipped with special abilities to selectively pay
attention to and process language ( KuhI1991 ; Kuhl and Meltzoff 1997) .
These data suggest that there is a biological basis to language . It follows
that if language is part of the biological endowment of humans , then
humans must have some genetic properties that build the particular kinds
of brain circuitry that are specialized for human language . If this is true ,
then it would not be surprising to find that some change in this genetic
endowment can interfere with the way brain circuitry is built and thereby
impair the ability to acquire or use language in the normal way . And in
fact this does happen . Though most children do acquire language without

264

Gopnik

any consciouseffort, there are some children who have real trouble with
language, and their linguistic problems persist into adulthood. What
makes this population particularly interesting is that this disorder seems
to be associatedwith some geneticfactors and neurological anomalies. If
this is true, then this situation provides a ready-made natural experiment
to investigatevarious hypothesesabout the biology of language.
This " ready-made" looks easier than it is, however. There are lots of
piecesto the argument that have to be put together, linguistic, psycholinguistic, genetic, and neurological, before we can be sure about what we
are seeing. The first problem is to show that at least some casesof this
disorder are really genetic.

11.1 Genetics
Several epidemiological studies have shown that an individual with a
developmentallanguagedisorder is significantly more likely to have a relative who is also affectedthan is an unaffectedindividual (Tomblin 1989,
1996). Data from the ongoing Genetic Language Impairment Project
conducted at McGill University confirms this pattern of familial clustering of SLI (Palmour 1997). In this study, we looked at subjectswho had a
clinical history of language impairment, but no history of any other
exclusionarycriteria, suchasimpaired auditory acuity, mental retardation,
or autism. Then we took detailed family histories. Of the 95 subjectsin this
initial study, 53 (55.8%) had at least one affected first- or second-degree
relative. In 21 of the families there was a clear pattern of multigenerational impairment. Our researchteam has also found evidenceof familial
aggregation in language-impaired subjects in England (Gopnik 1990),1
Greece(Dalalakis 1994), and Japan (Fukuda and Fukuda 1994).
So we have convergingevidencefrom a number of independentstudies
that show that languageimpairment clustersin families. The question is,
" Is this pattern the result of somegeneticfactors or is it the result of social
or linguistic factors that prevail in this family?" The latter seemsextremely
unlikely becausesome membersof the family have perfectly normal languageand other individuals in the samefamily appear to have grammars
that violate the universal properties that are found in language. Within
genetics, the way to distinguish betweenthe influence of the environment
and the influence of genesis to compare the pattern of impairment in
monozygotic (identical) with that in dizygotic (fraternal) twins. If the
crucial factors for clustering are social, then both kinds of twins should

Evidencefor Impaired Grammars

265

look similar. If , on the other hand, the pattern is due to genetic factors,
then the twins with the samegenesshould be more alike than those who
are merely siblings genetically but have shared a similar social context.
Severalindependentstudieshave shown that this disorder is significantly
more concordant in monozygotic twins than in dizygotic twins (Bishop,
North , and Donlan 1995; Tomblin 1997; Tomblin and Buckwalter 1998).
Therefore, both the epidemiological data and the twin studiesstrongly
suggestthat genetic factors are associatedwith this disorder. But genes
do not code for behavior such as language. They code for proteins that
control developmentthat, in turn, may have consequences
for the way in
which languagedevelops. To really understandwhat is going on, then, we
have to find somelikely consequences
that the geneticfactors could have
for development; and sincelanguagehappensin the brain, the most likely
place to look is neurology.

11.2 Neurology
Previous studieshave documentedneurological anomaliesin the brains of
subjectswith familial languageimpairment (Plante et al. 1991). Our team
has examinedmagneticresonanceimages(MRIs ) from five of the affected
adult membersof the families we have been studying and has found that
" comparedto controls, the CSF (cerebro-spinal fluid)/ grey and CSF/ grey
+ white ratios were significantly high in FLI -adults [familial language
impaiffilent] . . . whereas the grey/white ratio was significantly low. . . .
Thesefindings suggestthat FLI in adults may be associatedwith cortical
atrophy" (Kabani et al. 1997). Though thesedata are all very interesting
and go in the right direction, they are far from the end of the story. The
global patterns documentedin these studies do not provide the kind of
fine-grained picture that we needif we are to really understandthe details
of how the neurological anomalies interact with the linguistic problems.
Our imaging team, headedby Alan Evans, is now developing procedures
that can look at the MRI data in much finer detail, and this has the
potential for clarifying someof thesequestions.
One interesting question is how these neuroanatomical anomalies
arise. We are just beginning to get somehints of how this might happen.
Current evidenceseemsto suggestthat this geneticimpairment interferes
with normal brain developmentin the fetus. Gallagher and Watkin (1997)
used 3D ultrasonic neuroimaging to study in utero brain development
from 24 to 32 weeks of gestational age. Three of the fetuseswere from

266

Gopnik

families that had no history of languageimpairment (- FLI ). The fourth

fetus was from a family that did have a clear history of languageimpairment (+ FLI ). Gallagher and Watkin found that though all the fetuses
had overall brain volumes within the normal range, their patterns of
growth were significantly different. In particular, the + FLI fetus showed
limited growth in those regions of the brain that are associatedwith language performance. This evidencefrom fetal development is consistent
with the evidencefrom older subjects.
11.3

Neuropsychology

The data given above suggestthat the geneticfactors associatedwith this

disorder have consequencesfor the development of the brain and that
theseneuroanatomical anomalieshave direct consequences
for the acquisition of language. Since we know that genescan have many different
effects, it is to be expectedthat somegenesthat affect languagemay have
pleiotropic effects and so not be " specific" to language. Moreover, the
extensive anomalies that have been observed in brain structure would
make it surprising if these subjects had no other deficits. And , indeed,
clinicians report that some of these language-impaired subjectsdo have
other problems including low performance IQ, dyslexia, spatial rotation
difficulties, depression, and apraxias; however, none of theseother specific
deficits reliably occurs with the language disorder, and there are many
individuals who have one of these other problems without having any
languagedisorder. The question is whether the languageimpairment that
we seein theseindividuals comesfrom a separateand special " language
faculty" that is out of order, or whether somemore general cognitive or
perceptual processingsystemis not functioning and the purported " language" problems are merely a result of a breakdown in a much more
general system.
In our own project, Dr . H . Chertkow, a neurologist, has examined 30
of our Canadian subjectsand finds that some, but not all, of the individ uals with this languagedisorder do have other nonlinguistic problems and
that some of the membersof thesefamilies who are not impaired on our
diagnostic languagetest also have other problems.
F or example, as shown in table 11.1, in a sample of 12 subjectsfrom
these families, 6 were clearly impaired by our diagnostic language test
and 6 were not. Neurological testing revealedthat 3 of the 6 languageimpaired subjectshad mild impairment in left and right hemispheresen-

268

Gopnik

sorimotor function, but then so did 1 subject who showed no language

impairment by our tests. Two of the language-impaired subjectsexhibited
some impairment in mental calculation, as did 1 non-language-impaired
subject. In general, the language-impaired subjects appear to be more
vulnerable to having other disorders in addition to their language disorder, but there seemsto be no necessarypattern to theseother problems.
And , as we have shown, it is by no means the casethat theseother disorders always co-occur with languageproblems. The fact that this disorder affects neuroanatomy makes it not surprising that other areasmight
also be implicated in somecases. This doesnot mean, however, that these
other disorders causethe languageimpairment.
The evidence indicates that this linguistic disorder has some genetic
foundation and that the genetic factors produce anomalous neuroanatomical structures. If we want to know how this affects language, we
must have a detailed and extensivepicture of preciselywhat goeswrong
with thesesubjects' language.

11.4 Linguistics
Our research goals in linguistics over the years have been clear: to
describethe grammatical systemthat producesthe pattern of errors that
are observed. After 10 years and almost 100 language-impaired subjects
and well more than 100 controls representingfour different native languages(English, French, Greek, and Japanese
), the data convergeto tell
us that the language-impaired subjects cannot construct normal representations for grammatically complex words and they therefore cannot
use rules that depend on the content of theserepresentations. For example, though they appear to have no problems with the larger grammatical
categoriesof languagelike noun and verb, they are unable to recognize
that words can be composedof roots and affixes. They therefore do not
construct abstract linguistic features such as tense, number, aspect, case,
or gender, and they do not recognizethat there are linguistic rules that
operate on these features. But this does not mean that they cannot use
words that, from the point of view of the nonnal grammar, have these
features. For example, in spontaneousspeechthey usually use the correct
forms such as " books" or " walked." They can do this becausethey
memorize theseforms as unanalyzed chunks that in their lexicon simply
encodethe semanticmeaning of " more than one" or " in the past" rather
than the sublexicalfeatures" plural" or " past." They are more accuratein

Evidencefor Impaired Grammars

269

using the " more than one" forms than the " in the past" forms. This is
probably becausein English the relationship between the form with the
plural marker and the semanticcontext of " more than one" is very regular
and direct and therefore is easy to memorize. However, the relationship
between the past-marked forms and temporal past context is extremely
complicated and not at all regular or direct (Shaer 1996), and therefore it
is more difficult to assign a consistentmeaning relationship between the
inflected foffi1 and the meaning of pastnessby any rote means.
How do we know that theseindividuals do not construct complex representations? We have two sourcesof evidence, linguistic and psycholinguistic. The linguistic evidencecomesboth from spontaneousspeechand
from a wide seriesof linguistic tests. One of the things that makesparents
notice that their children have difficulties with languageis that they make
mistakes in spontaneousspeechin foffi1s like past tensesand pronouns
long after their playmates and siblings have got the systemfigured out.
And these problems persist into adulthood. But as these individuals get
older, they do not make theseerrors very often. Many of them get tense
right over 80% of the time. This is in contrast to the control subjects, who
get tense right virtually all of the time. Marking tense in your native
language is an automatic, unconsciousprocess, not something that you
get wrong. And this leads us to a very interesting problem. Is someone
who gets tenseright 80% of the time impaired, or simply absent-minded?
Let's put it another way. Generally speaking, people get their own name
right all of the time. If someonegot his or her name right 80% of the time,
we might begin to wonder. What our model suggestsis that the languageimpaired subjects, in fact, never get tense right . They do not have the
category " tense" in their grammar. What they do 80% of the time is
produce a word that has the samesurfaceform as the marked foffi1 in the
normal grammar. It looks like they get tensemarking right most of the
time, but they get there by a very different route- by memorization or by
explicit rule (Paradis and Gopnik 1997).
The only way to figure out what these individuals really know about
language is to give them linguistically significant tests. The data from
thesediagnostic testsconvergeto tell us that the pattern of what they can
do and what they cannot do is strikingly similar in all of the five populations- speakersof English from Canada and England, and speakersof
French, Greek, and Japanese
- that we have looked at (seefigure 11.1).
These tests show that the language-impaired speakershave significant
problems with grammaticality judgments, tense production, and deriva-

271

Evidencefor Impaired Grammars

Table 11.2
Ability to produce tense marking (% correct). Subjects were given items like
" Every day I walk to school. Just like every day, yesterday I
." This task
requiresthe subject to recognizethat the temporal context specifiedin the second
sentencerequires a particular verb form .

Language-impaired

subjects
Controls

English
(England)

English
(Canada
)

French
(Canada
)

Japanese

Greek

38.3
91.7

52.3
93.5

46.7
96.4

48.1
97.9

20.0
87.1

tional morphology.2 They have fewer problems with a pointing task that
requires them to auditorily distinguish between words like " book" and
" books" or " books" and " cooks." These general diagnostic tests have
beensupplementedby much more detailed testsdesignedto test particular
hypotheses. For example, we have data about tense from spontaneous
speech, grammaticality judgment tasks, grammaticality rating tasks,
storytelling, and tenseproduction; and theseresults are consistentover a
wide range of types of stimuli and responses
- oral, aural, written, pointing, and so on (Gopnik 1994). We also have results that show that these
speakershave problems with plurals and comparatives.
One question was whether theseproblems with tensein English could
be accountedfor by the fact that regular past tensein English is encoded
by a form that has been described as " phonologically vulnerable"
(Fletcher 1990) or by somespecialand particular problems with our first
set of English-speaking subjects, who all came from one particularly
interesting family . In order to resolvethis question, we decidedto look at
more English-speaking subjects and at subjects whose native language
was not English. These data show that the problem with tenseis unique
neither to our first subjectsnor to English. It showsup in every population we have looked at (seetable 11.2; seealso Fukuda 1994; Dalalakis
1996; Gopnik et al. 1996; Royle 1996; Gopnik 1998; Ullman and Gopnik ,
to appear) . All of thesepopulations have similar problems with producing correct tense forms, no matter how tense is encoded in their native
language- in a final stressedsyllable as in French or in a three-syllable
element like " mashita" in Japanese
. Interestingly, both the Greek control and language-impaired subjects have lower scores than the other
subjects; this happens becauseeach verb in Greek has more than 60

272
Table

Gopnik
11 .3

Forms of Greek " lik -os" (" wolf " )

Singular

Plural

Nominative

Iik

os

Iik

Genitive

Iik

Iik

on

Accusative

Iik

Iik

us

Vocative

Iik e (!)

Iik i

different inflected forms, as opposed to 4 in English, so there are simply many more ways to go wrong and it is harder to be right just by
chance.
The next question that we had to addresswas whether the subjects'
problem with language was confined to tense, as has been suggested
(Rice, Wexler, and Cleave 1995), or whether they made similar errors in
other parts of the inflectional system. Tests show that across the four
languagesthey make errors in number, case, and gender.3
All of this led us to think that these individuals had a particular
problem with inflectional rules, but Jenny Dalalakis's innovative work on
compounds and diminutives in Greek made it clear that the languageimpaired subjectshave just as much difficulty with finding the root of a
complex word as they have with adding an inflection (Dalalakis 1996). It
is not merely that they cannot add an inflection to a root; they do not
even recognize that there are roots and inflections. There is no way to
check this in English becausethere are words in English like ' 'walk" and
" book" that do not have any overt inflectional marking. In Greek, however, all nouns and verbs are inflected. For example, the word for " wolf "
has eight different forms (seetable 11.3). It would seemto be child's play
to figure out that " lik " is the root and all of the rest are inflectional forms.
But not for these children. They make serious errors in tasks like compounding and diminutivization that depend upon the manipulation of
roots. They seemto know that they are supposedto take part of the word,
but they are not sensitiveto the boundariesbetweenroots and inflections
so sometimesthey take a part that is shorter than the root and sometimes
they take a part that is longer than the root . The rule for compounding in
Greek requires that the two roots be conjoined (la ), in some caseswith
the insertion of an " 0" that marks the morphemeboundary (lb ); then the
inflection is added to the end of the conjoined roots.

273

Evidencefor Impaired Grammars

( 1) a. lik
wolf

-anthrop
man

-os
masc.sing.
nom

b . lik

wolf

- t

titan thropos
werewolf

-+

likofola

-0

- fol

-a

compound
morpheme

nest

fem .sing.
nom .

wolfnest

(A similar rule holds for forming diminutives . For the details , seeDalalakis
1996.) The subjects were shown pictures and told (in Greek ), for example, " This is a mouse (pondikos ) and this is a man (anthropos ) that becomes a mouse. We would call him a 'mouseman ' (pondikanthropos ) ."
They were asked to form similar compounds in response to other pictures .
The language -impaired subjects had significantly more difficulty with this
task than did the controls (see table 11.4) . Sometimes the language impaired subjects produced fonDs in which the first root was shorter
than required (2a), and sometimes they produced forms in which it was
longer (2b).
(2) a. anthrop
man

-fagh
eater

-os
masc.sing.
nom

b. lot

* anthrofaghos
man -eater

-+

* loto ~faghos

-fagh

-os

eater

masc .smg .

perSImmon

-+

nom

persImmon

- eater

It is clear then that these subjects' problem with inflectional rules is an

epiphenomenon of their problem with knowing that there are roots and
inflections

at all .

N ow we are back to one of the problems that we discussed at the

beginning : where do the " inflected " forms that these speakers do produce
come from ? One of the compensatory mechanisms that we have suggested
is memorization - they simply learn inflected words one at a time as

Table

11 .4

Greek compounding and diminutivization

(% correct )

Language impaired
sub,jects
Compounding

16

Diminutivization

38

Young
controls
95
100

Age-matched
controls
99
100

274

Gopnik

everyonehas to do for irregulars. If this is true, then they should be more

successfulwith regularly inflected words that they have heard frequently
than with those that are rare. And that is precisely what we find: frequency is a more robust predictor of problems than regular versusirregular inflection (Fukuda and Fukuda 1994; Gopnik 1994; Gopnik and
Goad 1997; Ullman and Gopnik , to appear) .
This is precisely the opposite from what we seewith normal controls,
for whom regularly inflected forms do not show any frequency effects.
This strongly suggeststhat memory and not rules are producing the
inflected forms used by language-impaired subjects. To clinch this argument, we looked at the absolute endpoint of the frequency scale, novel
words that these individuals could never have seenbefore. If they were
using a rule, they should have had no problem with this task. If they were
producing actual forms from memory, then it should have been impossible for them. We testedsuch forms in all four languagesand over a wide
range of different kinds of rules (for results, seetable 11.5). These data
clearly and convincingly show that the language-impaired subjectsperform significantly worse than non-language-impaired subjects on every
grammatical task and for every languagepopulation that we have tested.
One might then ask, " If thesespeakersdo not have the rule, how do they
ever get it right at all?" The answerseemsto be that they do not ever get
the unconscious, automatic rule for inflection right . What they can do is
use an explicit rule- in the caseof the English speakers, for example, a
rule that tells them to add an " -s" for plurals or an " -ed" for past. And
there is clear evidencethat this is what they are doing. In our original
scoring of thesetests, we were very generousand gave the subjectscredit
for producing an inflected form even if it did not sound preciselylike the
normal form . In a very detailed phonological analysis of these subjects'
attempts at producing plurals, Goad and Rebellati (1995) found that even
when the English-speakinglanguage-impaired subjectsdo produce a kind
of sibilant at the end of the word given in the stimulus sentence
, they do
not obey the normal rules in English that govern the incorporation of the
affix into the word. For example, they do not have voicing assimilation
and say " wug-s" instead of " wug-z." The plural does not behavelike an
affix in the grammar of the language-impaired subjects. It is as if they
were producing a kind of compound by adding a wordlike " s" that means
" more than one." This careful analysis showsthat only 9% of the forms
that they produce phonologically resemblethe " correct" form . A similar
analysis of the novel verbs shows the same pattern. Apparently, then,

Evidence
forImpaired
Grammars

275

Table 11.5
Ability to mark novel words grammatically (% correct). In each of these tests
the subjects were given a context, usually in pictures, which required that a
grammatical rule be applied to a novel word: " This pencil is weff. This pencil is
even
."
Controls

Language-impaired
subjects

English (in England)

English (in Canada)
French (in Canada)
Greek

95.4
93.5
92.6
87.1

38.0
52.3
33.3
20.0

Japanese
Plurals
English (in England)
English (in Canada)
Greek

89.1

37.0

95.7
99.2
79.8

57.0
58~3
42.1

Comparatives
English (in England)

74.0

21.0

Compounds
Greek

93.6

12.8

80.5

20.2

83.9

40.2

Past tense

Japanese
Diminutives
Greek

these speakers produce forms that look " inflected " by very different
means than the normal grammar .
So far , all of our hypotheses about the way that the language-impaired
subjects must be representing words in their grammar have been inferred
from their performance on linguistic tests. But there is another , more direct
way to look at their mental lexicon . Eva Kehayia conducted a series of
on-line psycholinguistic tests to probe the way in which languageimpaired subjects were processing complex words . It might be the case
that these subjects have normal representations for the inflected forms ,
but some processing difficulties make these forms unavailable to them in
spontaneous speech or elicited production tasks. Psycholinguistic research
on aphasics shows that though they make errors in spontaneous speech
and in linguistic tests, their mental representations appear to be intact
( Kehayia and Jarema 1994; Kehayia , in press) . The language-impaired

276

Gopnik

subjectsin thesetestswere 12 speakersof Canadian English, 7 speakersof

French, and 4 speakersof Greek (in Greece). They were compared with
24 controls in each language. The general form of the tests required the
subjectsto look at a single word that appearedon a computer screenand
decide whether it was a real word in their language or not. The word
stayed on the screen until the subject pushed the button to register a
decision. Half of the testswere simple lexical decisiontasks and half were
primed lexical decision tasks. The experimental model assumesthat the
amount of time that it takes a subject to make a decision is a measureof
the way in which the subject is processingthe item. Though the subjects
thought that we were interestedin their ability to judge whether a word
was a real word or a novel word, the real experimental variables investigated inflection, compounding, and derivation. The results are consistent acrossall of the tests and all of the languages(seetable 11.6). Both
groups are above 90% accurate in judging whether a sequenceis or is
not a word; however, they are very different in the way that they process
the words and nonwords. In the processingexperiments, the English-,
French-, and Greek-speaking control subjectsall show a significant differencein reaction times, more than 30 milliseconds, for inflected versus
uninflected words and nonwords. Affected individuals show no such difference. This indicates that the language-impaired subjects, crosslinguistically, are building mental representationsthat differ in nature from those
of non-language-impaired individuals.
These results suggestthat these subjectsare insensitive to the internal
structure of words. They treat all words as if they were simple unanalyzed chunks. They are good at knowing if a word is a real word or not:
they simply look it up in their mental lexicon. In some cases, this takes
them longer than controls becausethey have more items to search, but in
other cases(e.g., Greek compounds), where the rules for forming the
complex word are intricate, their whole-word strategy is actually more
efficient. This result is illustrated in table 11.7. Notice that the languageimpaired individuals process all three forms in the same way, whereas
the controls processthem significantly differently. The controls perform
fasteston the existing compoundsand sloweston the compoundsthat are
made up of real words but that do not exist in the language. What is
particularly interesting is that the language-impaired subjects' wholeword lookup strategy makes them perform significantly faster than
the controls on nonword compounds and especially faster on novel
compounds.

Evidencefor Impaired Grammars

278
Table

Gopnik
11 .7

Reaction time (in ms)

Language-impaired
subjects(Greek)

Controls (Greek)

817

870

N onword compounds
kigofaghos
(" kigoeater " ; like
English " wugeater " )
Navel compounds
migofaghos
(' 'flyeater " )
Existing compounds
hortofaghos
(" vegetable eater" ==
" vegetarian " )

(3) a. V [+ past]
walked
" move on foot" (+ past)
b. V
walked
" move on foot in the past"

111111111I1

1111111111

The results of the experimentsin this study clearly show that the performance pattern of the language-impaired subjects is significantly different from that of the control subjects on word and nonword targets
for inflection, derivation, and compounding. The controls in this study
behavejust as reported elsewherein the literature (Taft and Forster 1975;
Laudanna, Badecker, and Caramazza 1989; Kehayia and Jarema 1994).
They processproductively formed complex words by meansof decomposition, and they processsimple and idiosyncratic complex words by means
of whole-word access
. The language-impaired subjectsappear to process
all of the items by means of whole-word access(Kehayia 1994, in press;
Dalalakis 1996). The results of these on-line studies are consistent with
what the off-line linguistic tests have shown: the language-impaired subjects do not build complex representationsfor words; instead, they treat
both complex and simple words in the same way- as if they were
unanalyzedchunks.
The question then is, " What do their representationslook like?" There
are two possibilities for representingwords with no internal structure.

Evidence
for ImpairedGrammars

279

The difference betweentheserepresentationsis that in (3a) the information that this word refers to something that happened in the past is
expressedby a morphological feature (+ past) and in (3b) the concept of
pastnessis expressedas part of the meaning of the word.
As I have argued, the data from a wide range of grammaticality judgment tasks, production tasks, novel-form tasks, and reaction time experiments indicate that these subjects show no sensitivity to the internal
structure of words. These data strongly suggestthere is no evidencethat
the lexical entries of language-impaired speakers contain sublexical
(morphological) featuresfor tense, number, and perhapsother inflectional
properties. Sincethere is no evidencefor such featuresfrom the linguistic
behavior of thesespeakers, we have no grounds for introducing such features into their representations. Given that regular pastsend in a coronal
stop in English, and given that language-impaired individuals can sometimes add a pastlike ending to novel words, we assumethat these individuals store such forms in family resemblanceclassesand that they can
thus perform " wug" -type tasksthrough analogy (Gopnik and Goad 1997).
We therefore have a broad range of crosslinguisticevidence, both on-line
and off-line, that all tells the samestory: that the language-impaired subjects, though they get the same linguistic input as their siblings, do not
build the samesort of grammar. The grammarsthat they do build appear
to rely on memory and analogy and not productive rules for handling the
morphological aspectsof language. The spontaneousspeechof the older
subjects, and even their performance on some linguistic tests, demonstrates that a reasonablesimulacrum of morphology can be constructed
by using memory and analogy instead of productive rules. They do not
perform perfectly, but they are not terrible either. It is only when the
subjectsare given teststhat dependon productivity or when their internal
processesare monitored that the full extent of their inabilities can be
detected.
All of this would be interesting evenif it only provided a description of
the difficulties that a small group of language-impaired subjectshave. But
if it is all true, and if this disorder is related to somegeneticfactors that in
turn have consequencesfor neurological development, then apparently
there are some genetic and neurological precursorsthat are required for
the normal courseof theseaspectsof languagedevelopmentto take place.
This does not mean that we think that there is a gene for morphology!
From the point of view of linguistics, there is good evidencethat though
morphology is one of the striking aspectsof languagethat seemsto stump

280

Gopnik

these individuals
The question
ficulties

, it is by no means the only one they have trouble

that is still open is whether

are directly

causes their
problems

their prosodic

in morphology

are an independent

or whether

are . And

were found , it would

there is abundant

even if the genes associated

not follow

genes would be the ones that guide the normal

the factors

of neurologi -

is associated with some genetic factors , no one

what these factors

this disorder

language

shed light on the relative

of the three levels of grammar . Though

evidence that this disorder

yet knows

would

dif -

system that

these other

result of their general pattern

cal damage . The answer to this question

independence

and syntactic

related to the same out -of -order linguistic

problems

with .

that make a system function

necessarily
linguistic

in the normal

with

that these same

system to develop ;
case might

not be

the same as those that can cause the system to break down . Of course ,
there is much
intellectual

more

to find

out . Weare

only

at the beginning

of this

journey , but it does appear that it will turn out that Darwin

was right that language is part of the biological

nature of humans .

Notes
1 . This family has been the subject of much debate ( Fletcher 1990; Vargha Khadem et al . 1995) . For a d'etailed discussion of some of these disputes , see
Gopnik and Goad 1997. From the data , it is clear that the language impair ment seen in this family is not caused by oral apraxia or low performance IQ .
Moreover , as I will show , the same pattern of impairment is found in English speaking subjects in Canada as well as in French -, Greek -, and Japanese-speaking
subjects.
2. Since Japanese does not have a rich , productive system of derivational
phology , we did not test the Japanese-speaking subjects on this task .

mor -

3. They also make errors in syntax and in some phonological processes such as
prosody , but discussing these in detail would take us too far afield here (van der
Lely and Harris 1990; van der Lely 1997; Clahsen 1992; Piggott and Kessler 1994;
Rice , Wexler , and Cleave 1995; Goad , in press) .
References
Bishop , D . V ., North , T ., and Donlan , C . ( 1995) . Genetic basis of specific
language impairment : Evidence from a twin study . Developmental Medicine and
Child Neurology , 37, 56- 71.
Clahsen , H . ( 1992) . Linguistic perspectives on specific language impairment
( Theorie des Lexikons Arbeitspapier 37) . Dusseldorf : Heinrich Heine Universitat .
Dalalakis , J. ( 1994). Familial language impairment
Papers in Linguistics , 10, 216- 227.

in Greek . McGill

Working

Evidencefor Impaired Grammars

281

Dalalakis , J. ( 1996) . Developmental language impairment : Evidence from Greek

and its implications for morphological representation . Unpublished doctoral dissertation , McGill University .
Fletcher , P. ( 1990) . Untitled scientific correspondence . Nature , 346, 226.
Fukuda , S. ( 1994) . Lexical representation of Japanese complex verbs : A theoreti cal model and implication from dysphasic children . McGill Working Papers in
Linguistics , 10, 194- 205.
Fukuda , S. E ., and Fukuda , S. ( 1994) . Developmental language impairment in
Japanese: A linguistic investigation . Mc ~ ill Working Papers in Linguistics , 10,
150 - 177 .

Gallagher , T ., and Watkin , K . ( 1997) . 3D ultrasonic fetal neuroimaging and

familial language disorders : In utero brain development . Journal of Neuro linguistics , 10, 187- 201.
Goad , H . (in press) . Plurals in SLL . Prosodic deficit or morphological deficit ?
Language Acquisition .
Goad , H ., and Rebellati , C . (1995) . Pluralization is compounding in SLI . In
P. Koshinen ( Ed .), Proceedings of the Annual Meeting of the Canadian Linguistic
Association . Toronto : University of Toronto , Department of Linguistics .
Gopnik , M . ( 1990). Feature -blindness : A case study . Language Acquisition , 1,
139 - 164 .

Gopnik , M . ( 1994) . Impairments of tense in a familial language disorder . Journal

of Neurolinguistics , 8, 109- 133.
Gopnik , M ., Dalalakis , J., Fukuda , S. E ., Fukuda , S., and Kehayia , E . ( 1996) .
Genetic language impairment : Unruly grammars . In W . G . Runciman , J. Maynard
Smith , and R . I . M . Dunbar ( Eds .), Evolution of social behaviour patterns in pri mates and man. Oxford : Oxford University Press.
Gopnik , M ., and Goad , H . ( 1997) . What underlies inflectional error patterns in
genetic dysphasia ? Journal of Neurolinguistics , 10, 109- 137.
Gopnik , M . ( 1998). Familial language impairment : More English evidence. Folia
Phoniatrica et Logopaedica .
Kabani , N ., MacDonald , D ., Math , M ., Evans , A ., and Gopnik , M . ( 1997) .
Neuroanatomical
correlates of familial language impairment : A preliminary
report . Journal of Neurolinguistics , 10, 203- 214.
Kehayia , E . (1994) . Whole -word access or decomposition in word recognition in
familial language impairment : A psycholinguistic study . McGill Working Papers
in Linguistics , 10, 123- 128.
Kehayia , E . (in press) . Morphological representation and processing of inflected
and derived words in Greek -speaking individuals . In Proceedings of the 2nd
International Conference on Greek Linguistics .
Kehayia , E., and Jarema , G . ( 1994) . Morphological priming (or Prim # ing ) on
inflected verb forms : A comparative study . Journal ofNeurolinguistics , 2, 83- 94.

282

Gopnik

Kuhl

effect

"

for

1991

Kuhl

. ,

of

Palmour

. ,

10

and

. ,

Plante

16

with

. ,

Rice

. ,

850

Royle

thesis

Shaer

863

1996

1996

. ,

Verb

ni

. ,

. ,

language

Mahwah

Tomblin

Gopnik

NJ

in

der

SLI

boy

Perception

&

Ed

28

. )

Press

531

specific

learning

in

the

inheritance

and

1989

546

and

The

Priming

homographic

linguistic

impairment

Journal

of

Compensatory

strategies

Neurolinguistics

1994

in

10

173

Prosodic

genetic

185

dyspha

constraints

McGill

in

Working

Papers

familial

in

Linguis

. ,

and

Rapcsak

Brain

Cleave

and

1991

Language

1995

Specific

Journal

41

MRI

findings

52

66

language

of

Speech

in

boys

impairment

and

as

Hearing

Research

in

of

tense

1996

Tense

subjects

Unpublished

Master

' s

In

of

and

and

14

linking

638

of

647

54

287

Ed

. )

prefixed

language

295

impair

to

Toward

contributions

Rice

theory

retrieval

developmental

environmental

' " ence

storage

Behavior

Disorders

and

refel

Lexical

Verbal

Hearing

Genetic

time

University

concentration

and

and

Familial

DLI

McGill

1975

Learning

French

the

genetics

risk

of

for

language

1997

The

Epidemiology

of

inheritance

and

specific

language

innateness

of

impairment

grammars

New

York

In

Oxford

. ,

and

Buckwalter

twins

Journal

of

1998

Speech

Heritability

Language

of

&

poor

Hearing

language

Research

41

phology

van

magnet

among

Ullman

sense

Erlbaum

. )

achievement

199

1997

production

ty

Speech

Press

infinitive

ersi

1989

Ed

report

impairment

University

Tomblin

perceptual

not

nativism

Gopnik

University

of

and

Verbal

of

specific

Vance

Forster

Journal

Tomblin

"

do

Oxford

preliminary

Making

of

Evolution

in

dissertation

and

Journal

Tomblin

ment

optional

In

Caramazza

Robb

doctoral

words

and

impairment

Wexler

Unpublished

Taft

monkeys

Journal

Kessler

McGill

show

extended

1997

Language

230

Swisher

of

language

infants

specific

period

studies

215

and

York

. ,

and

23

Genetic

human

categories

speech

mory

impairment

lO

New

Gopnik

and

memory

Piggott

188

1997

tics

and

speech

Badecker

Declarative

107

. ,

is

Meltzoff

ofM

language

38

lingu

Paradis

90

language

Journal

Neuro

adults

grammars

stems

Human

of

of

innateness

tics

50

and

development

Laudanna

prototypes

Psychophysics

sia

the

. ,

Lely

and

Gopnik

hereditary

Modularity

specific

1997

and

to

appear

language

Language

innateness

The

impairment

and

cognitive

Journal

production

of

Applied

Ps

inflectional

development

oj

Neurolinguistics

mor

' cholinguistics

in

10

grammatical

75

107

20

Evidencefor Impaired Grammars

283

van der Lely, H ., and Harris, M . (1990). Comprehensionof reversiblesentencesin

specificallylanguageimpaired children. Journal of Speechand Hearing Disorders,
55 , 101 - 117 .

Vargha -Khadem , F ., Watkins , K ., Alcock , K ., Fletcher , P., and Passingham , R .

( 1995) . Praxic and nonverbal cognitive deficits in a large family with a genetically
transmitted speech and language disorder . Proceedings of the National Academy of
Sciences

, 92 , 930 - 933 .

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Language, Logic, and Concepts.
Ray S. Jackendoff, Paul Bloom and Karen Wynn, editors.
2002 The MIT Press.
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