Myrna Gopnik

Familial aggregation of a developmental language disorder

This paper investigates the etiology of developmental dysphasia and its linguistic properties. Data are presented that suggest that at least some cases of dysphasia are associated with an abnormality in a single dominant gene. The results of a series of tests on a large three-generation family, in which half of the members have dysphasia, are reported. These results show that abstract morphology is impaired in these subjects. It is argued further that the data are consistent with the hypothesis that the dysphasics learn the feature-marked lexical items of language as unanalyzed lexical items. They do not have the underlying capacity to learn language by constructing paradigms.

Inflectional morphology in a family with inherited specific language impairment

The production of regular and irregular past tense forms was investigated among the members of an English-speaking family with a hereditary disorder of language. Unlike the control subjects, the family members affected by the disorder failed to generate overregularizations (e.g., digged )o r novel regular forms (plammed, crived), whereas they did produce novel irregularizations (crive‐ crove). They showed word frequency effects for regular past tense forms (looked) and had trouble producing regulars and irregulars (looked, dug). This pattern cannot be easily explained by deficits of articulation or of perceptual processing, by previous simulations of impairments to a singlemechanism system, or by the extended optional infinitive hypothesis. We argue that the pattern is consistent with a three-level explanation. First, we posit a grammatical deficit of rules or morphological paradigms. This may be caused by a dysfunction of a frontal/basal-ganglia “procedural memory” system previously implicated in the implicit learning and use of motor and cognitive skills. Second, in contexts requiring inflection in the normal adult grammar, the affected subjects appear to retrieve word forms as a function of their accessibility and conceptual appropriateness (“conceptual selection”). Their acquisition and use of these word forms may rely on a “declarative memory” system previously implicated in the explicit learning and use of facts and events. Third, a compensatory strategy may be at work. Some family members may have explicitly learned a strategy of adding suffix-like endings to forms retrieved by conceptual selection. The morphological errors of young normal children appear to be similar to those of the affected family members, who may have been left stranded with conceptual selection by a specific developmental arrest. The same underlying deficit may also explain the impaired subjects’ difficulties with derivational morphology.

Impairments of tense in a familial language disorder

Abstract This paper reports an in-depth analysis of one particular aspect of familial language impairment: tense. The subjects in this study are all adults from a family in which half of the members exhibit severe difficulties in acquiring language while the other members of the family are not language impaired. Though these language impaired adult native speakers of English routinely produce sentences such as “The people in the house called the ambulance and the boy went to hospital,” which appear to be correctly marked for tense, they also produce sentences like, “She remembered when she hurts herself the other day,” in which the tense marking on the second verb does not agree with either the tense marking on the first verb or the semantic idea of “pastness” established by the temporal phrase. Data from tests of tense production, grammaticality ratings and spontaneous speech converge to suggest that the language impaired subjects do not have an intact underlying obligatory syntactic rule for tense, though they appear to have the semantic notion of “pastness.” The patterns of impairment include a willingness to produce and accept unmarked forms in obligatory contexts, an advantage in producing irregular verbs compared to regular ones, errors in selecting the correct tense for the context, and a tendency to learn regular past forms as individual lexical items. This suggests that there is a deficit in their knowledge of the syntactic requirements for tense marking and agreement. The subjects seem to compensate in part by relying to a greater extent on general learning and reasoning abilities, including memorization of regular inflected forms in a manner similar to the one in which non-impaired language learners are thought to learn irregular forms.

Compensatory strategies in genetic dysphasia: Declarative memory

There does not appear to be a consensus in the developmental dysphasia literature as to the characteristics of Specific Language Impairment (SLI). This may be because there are likely to be several different types of developmental dysphasias of widely different etiologies. Converging evidence from epidemiological and twin studies of SLI [ 1, 21 has shown a pattern of occurrence typical of any genetically transmitted trait. Even though at the time this paper goes to press the gene (or genes) associated with the pattern of linguistic deficits discussed here has not yet been isolated, we call the deficit we describe genetic dysphasia and predict that the gene, or genes, involved will eventually be found, as no other explanation is compatible with the data. This is not to claim that there is a gene for morphology or even for grammar. The only claim that we make here is that there is a genetic component in this developmental condition. The expression of a particular gene or set of genes is constrained by a number of environmental factors during fetal development. It (or they) may also affect functions other than language subserved by different parts of the brain [3]. Nevertheless, its manifestations, when expressed, are fairly systematic and predictable, specifically affecting the ability to acquire some types of implicit linguistic competence, particularly the incidental internalization of those aspects of phonology and morphology which are described by linguists as implicit rules. Should the gene(s) never be found, the descriptions of the deficit and of the compensatory strategies that follow would nevertheless remain valid for this population. Equivalent cross-linguistic impairments have been found in speakers of languages other than English as morphologically different as Greek and Japanese. The individuals’ impairment can hardly be attributed to social causes since many of the members of families intensively studied so far (in one case fraternal twins) do not exhibit the impairment and yet are raised in the same environment, eat the same foods, live in the same neighbourhood, are exposed to the same dialect from parents and siblings. Many of the children with a parent with genetic dysphasia do not show signs of abnormal language acquisition despite the fact that they get the same (possibly impaired) language input as their siblings who do demonstrate language impairment. Non-linguistic causes such as specific hearing deficits have been ruled out since it has ben shown that these individuals were perfectly able to make the required phonemic distinctions in discrimination tasks on lexical items involving the same phonemic properties as the deficient morphology [4]. Because there are likely to be several types of SLI with corresponding different etiologies, we shall refer to our subjects as individuals with genetic dysphasia to distinguish them as a

What underlies inflectional error patterns in genetic dysphasia

Abstract We compare linguistic and non-linguistic explanations which attempt to account for the difficulties that individuals with genetic dysphasia experience with inflectional morphology. The non-linguistic explanations that we focus on are low performance IQ and performance deficits which are manifested at the level of auditory processing or at the mapping between representation and articulatory output. We argue that none of these hypotheses can account for the patterns observed; the impairment lies in the construction of the grammar itself. We hypothesise that the dysphasic grammar lacks sublexical (morphological) features which mark inflectional information in languages. Consequently, the grammar does not contain the morphological rules which introduce these features and, following from this, there is no structure internal to ‘inflected’ words. We summarise the experimental evidence which supports this hypothesis.

The inheritance and innateness of grammars

This volume, the sixth in the Vancouver series based on an annual conference at Simon Fraser University, collects papers that discuss the evidence and arguments regarding the inheritability and innateness of grammars. The evidence - which ranges from babies who are just beginning to learn the properties of their native language, to language-impaired adults who will never learn it - converges to show that whole precursors of language exist in other creatures, the abilities necessary for constructing fully fledged grammars are part of the biological endowment of human beings.

Familial Language Impairment:More English Evidence

Subjects between the ages of 9 and 22 with a history of familial language impairment were tested on a wide range of linguistic tasks. The data show that they are not different from the non-impaired members of their family or from external controls in their ability to hear and understand the morphological marker for plural or to understand a narrative, but they are significantly different in recognizing or correcting grammatical errors, in producing tense or number marking, and in understanding sentences with non-canonical word order. This pattern of deficits is similar to that which occurs cross-linguistically and in on-line processing tasks. These data support the hypothesis that these subjects do not build normal representations in their grammar nor construct productive grammatical rules. However, they are able to use other means such as memory and explicit rules to simulate grammar.

Neuroanatomical correlates of familial language impairment: A preliminary report

Language impairment is not always associated with other cognitive and neurological disorders. Individuals identified with Specific Language Impairment (SLI) but normal cognition/intellect and an associated family history are classified as subjects with familial language impairment (FLI). In this preliminary report, we identified five families with FLI and selected six children (FLI-children) and five adults (FLI-adults) for magnetic resonance imaging (MRI) scan of brain volumes. Four out of five adults from these families had generalized cortical atrophy, mostly in the anterior region. Using a tissue-classification method, the volume occupied by grey matter, white matter and cerebro-spinal fluid (CSF) was calculated. The results indicated that compared to the controls, the CSF/grey and CSF (grey+white) ratios were significantly high in FLI-adults, being P < 0.003 and P < 0.02, respectively, whereas the grey/ white ratio was significantly low (P < 0.06) in FLI-adults. The only significant difference observed between FLI-children and controls was in the grey/white ratio (P < 0.0001) with this ratio being higher in affected children. These initial findings suggest that FLI in adults may be associated with cortical atrophy. In future studies, we plan to acquire additional morphological data and perform localized analyses for various brain regions especially those associated with language in order to better understand the neuroanatomical correlates of FLI in both children and adults.

Familial language impairment: The evidence

Muller argues that general cognitive skills and linguistic skills are not necessarily independent. However, cross-linguistic evidence from an inherited specific language disorder affecting productive rules suggests significant degrees of modularity, innateness, and universality of language. Confident claims about the overall nature of such a complex system still await more interdisciplinary research.

Sibling resemblance for specific components of linguistic competence in families of speech/language impaired children

Abstract We examined performance on specific linguistic tests in 23 English and French speaking families, recruited from clinical and other sources, of children who met the following criteria for specific language impairment (SLI): clinically diagnosed language impairment without peripheral hearing loss, mental retardation (non-verbal IQ≥70), neurological disorder, schizophrenia or autism. Subjects, at least 9 years old, completed a battery of French or English language tests, including derivational morphology, verb tense morphology, grammaticality judgement, syntactic comprehension, and pointing. listening comprehension and WUG pluralization test were analyzed only in the English group. The verb tense morphology (real words) and verb tense morphology (non-real words), respectively, showed non-parametric sibling correlations of 0.39 and 0.35 ( p p =0.05). Impaired grammatical morphology is a predominant aspect of SLI, and the present study, which requires independent replication, suggests that verb tense morphology and derivational morphology warrant particular attention in future familial and genetic studies.