Linguistic markers of autism spectrum conditions in narratives: A comprehensive analysis.

Background & Aims: Narratives are regularly elicited as part of standardized assessments for autism spectrum conditions (ASC) such as the ADOS, but have rarely been utilized as linguistic data in their own right. We here aimed for a specific and comprehensive quantitative linguistic profile of such narratives across nominal, verbal, and clausal domains of grammatical organization, and error patterns. Methods: We manually transcribed and annotated narratives elicited from the ADOS from a sample of bilingual autistic Spanish-Catalan children (n = 18), matched with typically developing controls (n = 18) on vocabulary-based verbal IQ. Results: Results revealed fewer relative clauses and more frequent errors in referential specificity and non-relational content-word choice in ASC. Frequent error types are also discussed qualitatively. Conclusions & Implications: These findings, based on more finegrained linguistically defined variables, help to disentangle previous inconsistencies in the literature, and to better situate language changes in the spectrum of neurocognitive changes in this population.

Language disintegration in spontaneous speech in Huntington's disease: a more fine-grained analysis.

Huntington's disease (HD) is a neurodegenerative disease causing motor symptoms along with cognitive and affective problems. Recent evidence suggests that HD also affects language across core levels of linguistic organization, including at stages of the disease when standardized neuropsychological test profiles are still normal and motor symptoms do not yet reach clinical thresholds ('pre-manifest HD'). The present study aimed to subject spontaneous speech to a more fine-grained linguistic analysis in a sample of 20 identified HD gene-carriers, 10 with pre-manifest and 10 with early manifest HD. We further explored how language performance related to non-linguistic cognitive impairment, using standardized neuropsychological measures. A distinctive pattern of linguistic impairments marked off participants with both pre-manifest and manifest HD from healthy controls and each other. Fluency patterns in premanifest HD were marked by prolongations, filled pauses, and repetitions, which shifted to a pattern marked by empty (unfilled) pauses, re-phrasings, and truncations in manifest HD. Both HD groups also significantly differed from controls and each other in how they grammatically connected clauses and used noun phrases referentially. Functional deficits in language occurred in pre-manifest HD in the absence of any non-linguistic neuropsychological impairment and did largely not correlate with standardized neuropsychological measures in manifest HD. These results further corroborate that language can act as a fine-grained clinical marker in HD, which can track disease progression from the pre-manifest stage, define critical remediation targets, and inform the role of the basal ganglia in language processing.

Deficits in nominal reference identify thought disordered speech in a narrative production task.

Formal thought disorder (TD) is a neuropathology manifest in formal language dysfunction, but few behavioural linguistic studies exist. These have highlighted problems in the domain of semantics and more specifically of reference. Here we aimed for a more complete and systematic linguistic model of TD, focused on (i) a more in-depth analysis of anomalies of reference as depending on the grammatical construction type in which they occur, and (ii) measures of formal grammatical complexity and errors. Narrative speech obtained from 40 patients with schizophrenia, 20 with TD and 20 without, and from 14 healthy controls matched on pre-morbid IQ, was rated blindly. Results showed that of 10 linguistic variables annotated, 4 showed significant differences between groups, including the two patient groups. These all concerned mis-uses of noun phrases (NPs) for purposes of reference, but showed sensitivity to how NPs were classed: definite and pronominal forms of reference were more affected than indefinite and non-pronominal (lexical) NPs. None of the measures of formal grammatical complexity and errors distinguished groups. We conclude that TD exhibits a specific and differentiated linguistic profile, which can illuminate TD neuro-cognitively and inform future neuroimaging studies, and can have clinical utility as a linguistic biomarker.

A systematic linguistic profile of spontaneous narrative speech in pre-symptomatic and early stage Huntington's disease.

Cognitive decline accompanying the clinically more salient motor symptoms of Huntington's disease (HD) has been widely noted and can precede motor symptoms onset. Less clear is how such decline bears on language functions in everyday life, though a small number of experimental studies have revealed difficulties with the application of rule-based aspects of language in early stages of the disease. Here we aimed to determine whether there is a systematic linguistic profile that characterizes spontaneous narrative speech in both pre-manifest and/or early manifest HD, and how it is related to striatal degeneration and neuropsychological profiles. Twenty-eight early-stage patients (19 manifest and 9 gene-carriers in the pre-manifest stage), matched with 28 controls, participated in a story-telling task. Speech was blindly scored by independent raters according to fine-grained linguistic variables distributed over 5 domains for which composite scores were computed (Quantitative, Fluency, Reference, Connectivity, and Concordance). Voxel-based morphometry (VBM) was used to link specific brain degeneration patterns to loci of linguistic decline. In all of these domains, significant differences were observed between groups. Deficits in Reference and Connectivity were seen in the pre-manifest stage, where no other neuropsychological impairment was detected. Among HD patients, there was a significant positive correlation only between the values in the Quantitative domain and gray matter volume bilaterally in the putamen and pallidum. These results fill the gap of qualitative data of spontaneous narrative speech in HD and reveal that HD is characterized by systematic linguistic impairments leading to dysfluencies and disorganization in core domains of grammatical organization. This includes the referential use of noun phrases and the embedding of clauses, which mediate crucial dimensions of meaning in language in its normal social use. Moreover, such impairment is seen prior to motor symptoms onset and when standardized neuropsychological test profiles are otherwise normal.

Toward true integration.

Whether in sign or speech, language is more integrative than the target article suggests. A more integrative view embraces not only sign/speech and co-sign/speech gesture, but also indicative gestures irrespective of modality, and locations along with movements in the signed modality, as suggested by both linguistic acquisition and pathologies. An extended integrative view also proves advantageous in terms of conceptual coherence.

Can delusions be understood linguistically?

Delusions are widely believed to reflect disturbed cognitive function, but the nature of this remains elusive. The "un-Cartesian" cognitive-linguistic hypothesis maintains (a) that there is no thought separate from language, that is, there is no distinct mental space removed from language where "thinking" takes place; and (b) that a somewhat broadened concept of grammar is responsible for bestowing meaning on propositions, and this among other things gives them their quality of being true or false. It is argued that a loss of propositional meaning explains why delusions are false, impossible and sometimes fantastic. A closely related abnormality, failure of linguistic embedding, can additionally account for why delusions are held with fixed conviction and are not adequately justified by the patient. The un-Cartesian linguistic approach to delusions has points of contact with Frith's theory that inability to form meta-representations underlies a range of schizophrenic symptoms. It may also be relevant to the nature of the "second factor" in monothematic delusions in neurological disease. Finally, it can inform the current debate about whether or not delusions really are beliefs.

The linguistics of schizophrenia: thought disturbance as language pathology across positive symptoms.

We hypothesize that linguistic (dis-)organization in the schizophrenic brain plays a more central role in the pathogenesis of this disease than commonly supposed. Against the standard view, that schizophrenia is a disturbance of thought or selfhood, we argue that the origins of the relevant forms of thought and selfhood at least partially depend on language. The view that they do not is premised by a theoretical conception of language that we here identify as 'Cartesian' and contrast with a recent 'un-Cartesian' model. This linguistic model empirically argues for both (i) a one-to-one correlation between human-specific thought or meaning and forms of grammatical organization, and (ii) an integrative and co-dependent view of linguistic cognition and its sensory-motor dimensions. Core dimensions of meaning mediated by grammar on this model specifically concern forms of referential and propositional meaning. A breakdown of these is virtually definitional of core symptoms. Within this model the three main positive symptoms of schizophrenia fall into place as failures in language-mediated forms of meaning, manifest either as a disorder of speech perception (Auditory Verbal Hallucinations), abnormal speech production running without feedback control (Formal Thought Disorder), or production of abnormal linguistic content (Delusions). Our hypothesis makes testable predictions for the language profile of schizophrenia across symptoms; it simplifies the cognitive neuropsychology of schizophrenia while not being inconsistent with a pattern of neurocognitive deficits and their correlations with symptoms; and it predicts persistent findings on disturbances of language-related circuitry in the schizophrenic brain.