Dissecting the neurobiology of linguistic disorganisation and impoverishment in schizophrenia

Palaniyappan, Lena

doi:10.1016/j.semcdb.2021.08.015

Cited by 29 publications

(22 citation statements)

References 262 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…D2blockers may reduce error-induced shifts in the discourse plan, correcting the positive FTD features, but cannot improve the (nondopaminergically mediated) precision of the higherorder discourse plan per se, and the eventual gravitation toward reduced speech output (negative FTD), as seen in the long term. More broadly, neuromodulatory aberrations in the higher-level association cortex result in excitation/inhibition imbalance that underwrites precision modulation 38 as well as FTD 59 in schizophrenia. Specific brain regions, such as anterior insula, 60 dorsal anterior cingulate cortex 61 and hippocampus, 62 appear to play a key part in precision-weighting mechanisms; the course of FTD may relate to the volumetric 63 and connectivity 64,65 changes of these regions in schizophrenia.…”

Section: E51mentioning

confidence: 99%

The Bayesian brain and cooperative communication in schizophrenia

Palaniyappan

Venkatasubramanian

2022

jpn

Self Cite

View full text Add to dashboard Cite

The act of will and the action of the body are not two different states…; they do not stand in the relation of cause and effect but are one and the same thing…. The action of the body is nothing but the act of will …. translated into perception. -Arthur Schopenhauer, 1819 1 Our social world is an ever-changing milieu in which boundless verbal and nonverbal signals are generated by fellow humans. To ensure our survival, we must perceive certain regularities from the complexity that surrounds us. A failure to meet this daily challenge may prove costly for some; social encounters trigger several psychiatric symptoms, while social withdrawal reduces their intensity, at least temporarily. 2 For example, disorganization (or formal thought disorder), one of the central features of schizophrenia, presents primarily as a disruption in cooperative communication that occurs in a social context. Though many technical advances now allow us to study "socially" interacting agents in the laboratory (for example, see Kingsbury and colleagues 3 ), psychiatric symptoms are rarely studied in the context of neural mechanisms of social encounters. To tackle this challenge, we need empirical tools to study the dynamic neural framework of social interaction, starting from a 2-person perspective. In this editorial, we first present such a tool: an emerging "active inference" perspective of cooperative communication between 2 individuals. We then introduce the 2-brain problem of formal thought disorder in schizophrenia as an exemplar case of its utility and map resulting theoretical expectations to known signs of this construct. Lastly, we highlight several experimental opportunities that arise from casting of formal thought disorder in the active inference framework.

show abstract

Section: E51mentioning

confidence: 99%

The Bayesian brain and cooperative communication in schizophrenia

Palaniyappan

Venkatasubramanian

2022

jpn

Self Cite

View full text Add to dashboard Cite

show abstract

“…Abnormal cortical thickness in schizophrenia has been previously linked to dysregulated glutamate levels (Plitman et al, 2014(Plitman et al, , 2016Shah et al, 2020) and glutamatergic dysfunction had been considered to contribute to the "FTD" burden in schizophrenia (Kircher et al, 2018). We select dACC as our region of interest for glutamate measurement as it constitutes the core hub of the large-scale brain network called the Salience Network that appears to play a key role in the neurocognitive dysfunction in schizophrenia (Palaniyappan, 2021). Finally, we used a picture description task to study computational linguistic measures that are reflective of a "negative" FTD, first described by Fish (Casey and Kelly, 2019) and later reported by Andreasen (1979) and others (Kircher et al, 2018) as being more characteristic of established schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Widespread cortical thinning, excessive glutamate and impaired linguistic functioning in schizophrenia: A cluster analytic approach

Liang

Silva

Jeon

et al. 2022

Front. Hum. Neurosci.

Self Cite

View full text Add to dashboard Cite

IntroductionSymptoms of schizophrenia are closely related to aberrant language comprehension and production. Macroscopic brain changes seen in some patients with schizophrenia are suspected to relate to impaired language production, but this is yet to be reliably characterized. Since heterogeneity in language dysfunctions, as well as brain structure, is suspected in schizophrenia, we aimed to first seek patient subgroups with different neurobiological signatures and then quantify linguistic indices that capture the symptoms of “negative formal thought disorder” (i.e., fluency, cohesion, and complexity of language production).MethodsAtlas-based cortical thickness values (obtained with a 7T MRI scanner) of 66 patients with first-episode psychosis and 36 healthy controls were analyzed with hierarchical clustering algorithms to produce neuroanatomical subtypes. We then examined the generated subtypes and investigated the quantitative differences in MRS-based glutamate levels [in the dorsal anterior cingulate cortex (dACC)] as well as in three aspects of language production features: fluency, syntactic complexity, and lexical cohesion.ResultsTwo neuroanatomical subtypes among patients were observed, one with near-normal cortical thickness patterns while the other with widespread cortical thinning. Compared to the subgroup of patients with relatively normal cortical thickness patterns, the subgroup with widespread cortical thinning was older, with higher glutamate concentration in dACC and produced speech with reduced mean length of T-units (complexity) and lower repeats of content words (lexical cohesion), despite being equally fluent (number of words).ConclusionWe characterized a patient subgroup with thinner cortex in first-episode psychosis. This subgroup, identifiable through macroscopic changes, is also distinguishable in terms of neurochemistry (frontal glutamate) and language behavior (complexity and cohesion of speech). This study supports the hypothesis that glutamate-mediated cortical thinning may contribute to a phenotype that is detectable using the tools of computational linguistics in schizophrenia.

show abstract

“…In acute stages of illness, positive FTD is more prominent, and appears to be a transdiagnostic feature [40,43], though the later persistence of positive [28] as well as negative FTD [49] is more likely to occur in schizophrenia. Furthermore, pharmacological manipulations with dopaminergic agents recover the state-like features more reliably than trait-like features (see [50] for a review). Taken together, the neural correlates of persistent trait-like features may map on to the vulnerability (or diathesis) for FTD and the construct of schizophrenia more broadly, unlike the correlates of acute FTD (time-varying symptoms issue).…”

Section: Issue 2: the Varying Course Of Ftdmentioning

confidence: 99%

Language Network Dysfunction and Formal Thought Disorder in Schizophrenia

Palaniyappan

Homan

Alonso-Sánchez

2022

Schizophrenia Bulletin

View full text Add to dashboard Cite

Background Pathophysiological inquiries into schizophrenia require a consideration of one of its most defining features: disorganization and impoverishment in verbal behavior. This feature, often captured using the term Formal Thought Disorder (FTD), still remains to be one of the most poorly understood and understudied dimensions of schizophrenia. In particular, the large-scale network level dysfunction that contributes to FTD remains obscure to date. Study Design In this narrative review, we consider the various challenges that need to be addressed for us to move towards mapping FTD (construct) to a brain network level account (circuit). Study Results The construct-to-circuit mapping goal is now becoming more plausible than it ever was, given the parallel advent of brain stimulation and the tools providing objective readouts of human speech. Notwithstanding this, several challenges remain to be overcome before we can decisively map the neural basis of FTD. We highlight the need for phenotype refinement, robust experimental designs, informed analytical choices, and present plausible targets in and beyond the Language Network for brain stimulation studies in FTD. Conclusions Developing a therapeutically beneficial pathophysiological model of FTD is a challenging endeavor, but holds the promise of improving interpersonal communication and reducing social disability in schizophrenia. Addressing the issues raised in this review will be a decisive step in this direction.

show abstract

Dissecting the neurobiology of linguistic disorganisation and impoverishment in schizophrenia

Cited by 29 publications

References 262 publications

The Bayesian brain and cooperative communication in schizophrenia

The Bayesian brain and cooperative communication in schizophrenia

Widespread cortical thinning, excessive glutamate and impaired linguistic functioning in schizophrenia: A cluster analytic approach

Language Network Dysfunction and Formal Thought Disorder in Schizophrenia

Contact Info

Product

Resources

About