Abstract

Grammatical markers are not uniformly impaired across speakers of different languages, even when speakers share a diagnosis and the marker in question is grammaticalized in a similar way in these languages. The aim of this work is to demarcate, from a cross-linguistic perspective, the linguistic phenotype of three genetically heterogeneous developmental disorders: specific language impairment, Down syndrome, and autism spectrum disorder. After a systematic review of linguistic profiles targeting mainly English-, Greek-, Catalan-, and Spanish-speaking populations with developmental disorders (n = 880), shared loci of impairment are identified and certain domains of grammar are shown to be more vulnerable than others. The distribution of impaired loci is captured by the Locus Preservation Hypothesis which suggests that specific parts of the language faculty are immune to impairment across developmental disorders. Through the Locus Preservation Hypothesis, a classical chicken and egg question can be addressed: Do poor conceptual resources and memory limitations result in an atypical grammar or does a grammatical breakdown lead to conceptual and memory limitations? Overall, certain morphological markers reveal themselves as highly susceptible to impairment, while syntactic operations are preserved, granting support to the first scenario. The origin of resilient syntax is explained from a phylogenetic perspective in connection to the “syntax-before-phonology” hypothesis.

Highlights

  • In his seminal book The Biological Foundations of Language, Eric Lenneberg made the following observation when comparing different states of verbal behavior: Some aphasic symptoms bear certain similarities to the common derangements of speech and language seen in individuals in good health under conditions of mental exhaustion or states of drowsiness [...]

  • The case reports presented in the following are the result of extensive database searching through PubMed, SCOPUS, ScienceDirect, and Google Scholar, as well as probing individual journals for results retrieved by searches for any combination of the terms “primary/specific language impairment,” “autism spectrum disorder(s),” “Down(’s) syndrome,” “linguistic phenotype,” “impaired/atypical phonology/morphology/syntax/semantics/pragmatics,” “word retrieval in SLI/ASD/Down Syndrome (DS),” and “linguistic impairment/disorder.”

  • Omissions of (i) infinitival to, (ii) relative markers and pronouns, (iii) wh-pronouns in embedded wh-clauses Errors in tense marking and agreement Intact case marking and A-movement 90% accuracy in question comprehension Failure to disambiguate when prosody is required to interact with syntax/discourse Ability to imitate or discriminate prosodic structures without reference to meaning Errors on the more complex object relative clauses

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Summary

Introduction

In his seminal book The Biological Foundations of Language, Eric Lenneberg made the following observation when comparing different states of verbal behavior: Some aphasic symptoms bear certain similarities to the common derangements of speech and language seen in individuals in good health under conditions of mental exhaustion or states of drowsiness [...]. Overlaps in the behavioral profile of populations with different diagnoses have led to the claim that variation across phenotypes (i.e., breakdowns) is constrained in a way that renders some aspects of language processing—or more generally, cognition—more vulnerable in all pathological conditions, while others are consistently spared across individuals and conditions, both acquired and developmental (Phillips, 2005; Glisky, 2007; Kambanaros and van Steenbrugge, 2013; Benítez-Burraco and Boeckx, 2014; Leivada, 2014, 2015; Kambanaros and Grohmann, 2015; Tsimpli et al, 2017a) This high vulnerability of certain aspects of language is possibly the result of brain network organization. Multiple theoretical perspectives and neuroimaging research are addressing outstand ing questions about the nature and extent of brain connectivity aberrations in SLI vs. autism (Verhoeven et al, 2012) and DS (Anderson et al, 2013)

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