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.

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.

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.

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The findings suggest that schizophrenia affects language production in deaf patients with schizophrenia in a unique way not seen in hearing patients.