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The neuroscience of formal thought disorder - the state of the art
- E. Dornelles, D. Telles-Correia
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, pp. S133-S134
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Introduction
Even though the construct of Formal Thought Disorder (FTD) is an ambiguous and disputed one, it has endured as a fundamental psychopathological concept in the clinical coalface of Psychiatry. FTD can be summarized as a multidimensional concept, which reflects difficulties or idiosyncrasies in thought, language, and communication in general. It is usually subdivided into positive versus negative and objective versus subjective, and it can be a major challenge for both mental health professionals and patients themselves.
ObjectivesIn this presentation, we aim to explore the latest neuroscientific findings regarding FTD and its putative neurobiological substrate, ranging from the synaptic and neurotransmitter level to the structural and functional one, briefly considering some of the linguistic and neuropsychological implications.
MethodsWe conducted a thorough narrative review by researching the Pubmed database using the following search string: “formal thought disorder”[Title/Abstract] and selecting only those articles published after 2010. Afterwards, we summarized the main findings from the gathered information.
ResultsSome of the most consistent findings in current meta- and mega-analyses of structural MRI studies in patients with schizophrenia and FTD are volume reductions of regional grey matter in the frontal operculum and the language-related lateral temporal cortices, namely the left superior temporal gyrus and middle temporal gyrus. Another consistent finding is the so-called reversed lateralization of the temporal cortices. Regarding functional MRI studies of FTD, amongst the most common implicated regions are the bilateral superior and middle temporal gyri, the fusiform gyrus and the inferior frontal gyrus. Alterations in the glutamatergic, dopaminergic and serotoninergic neurotransmitter systems have also been linked to FTD.
ConclusionsMany areas of the brain have been implicated in the pathogenesis of FTD, though some more consistently than others. The superior temporal, middle temporal and inferior frontal gyri in particular have repeatedly revealed both structural and functional alterations in patients with FTD. A reversed lateralization has also been observed at both structural and functional levels. The different neurotransmitter systems have also been connected with FTD, with the glutamate system being the one more thoroughly explored. However, the direction of causality between changes in the brain and FTD, and the influence of potential mediators remain largely unknown.
Disclosure of InterestNone Declared
The pathogenesis of formal thought disorder – towards an integrative view
- E. Dornelles, D. Telles-Correia
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- Journal:
- European Psychiatry / Volume 66 / Issue S1 / March 2023
- Published online by Cambridge University Press:
- 19 July 2023, p. S623
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Introduction
Formal Thought Disorder (FTD) is a cluster of symptoms and signs, and can be summarized as a multidimensional construct, reflecting idiosyncrasies in thought, language, and communication in general. The inquiry into its etiology is complicated by the ambiguity of the construct itself, and many theories regarding its pathogenesis have been put forward. Two main neurocognitive models, however, have been garnering attention in mainstream FTD research: the “dyssemantic” and the “dysexecutive” hypotheses. These concepts have been classically pitted out against each other as mutually exclusive, but recent studies have proposed a more integrative view.
ObjectivesIn this presentation, we aim to explore the two main models for explaining FTD pathogenesis, and to show how an integrative model which accounts for both the dyssemantic and dysexecutive deficits seen in patients with FTD might be better at explaining its etiology.
MethodsWe conducted a systematic review of the available literature according the PRISMA 2020 statement. We began by researching the Pubmed and Cochrane databases using the following search string: ((“Formal thought disorder*”[Title/Abstract]) AND (dysexecutive[Title/Abstract])) OR ((“Formal thought disorder*”[Title/Abstract]) AND (dyssemantic[Title/Abstract])) OR ((“Formal thought disorder*”[Title/Abstract]) AND (pathogenesis[Title/Abstract])) OR ((“Formal thought disorder*”[Title/Abstract]) AND (etiology[Title/Abstract])). 20 articles were retrieved, along with 2 ongoing trials. We screen for a total of 12 included articles. We also included 17 articles from citation searching, resulting in a final count of 29 included articles. We then summarized the main findings.
ResultsTwo influential hypotheses explaining the neurocognitive pathogenesis of different FTD symptom are the “dyssemantic” and “dysexecutive” hypotheses. The “dyssemantic” model emphasizes abnormalities in language-processing related brain regions and functional networks. Some studies suggest that the dysfunctions might involve higher-order semantics and the syntactic component. The “dysexecutive” hypothesis suggests that impaired planning and monitoring might lead to poorly formulated or prone-to-error speech. Recent studies, however, have suggested that FTD might be related to a combination of both executive dysfunction and impaired semantic processing, which would then combine in different proportions and yield the different FTD manifestations.
ConclusionsWhile disfunctions in both semantic and executive cognitive faculties have been independently explored as potential explanations for the pathogenesis of FTD, a more integrative picture has surfaced in recent research. It proposes that FTD might actually be the reflections of a combination of different proportions of disfunctions in the executive and/or linguistic processes. More research is needed, with better defined FTD dimensions, in order to further explore this model.
Disclosure of InterestNone Declared
What is the Pisa Syndrome? A review
- H. Santos, E. Dornelles, J. Pereira, A. Vieira
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, p. S725
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Introduction
Pisa syndrome (PS) is a type of dystonia of rare occurrence, first described in 1972 as an adverse effect of neuroleptic agents. It is used to describe a postural abnormality that includes trunk flexion in the coronal plane and axial rotation, which improves in the supine position.
ObjectivesIn this work, we aim to conduct a brief review of Pisa Syndrome aetiology, pathophysiology and treatment.
MethodsA non-systematic search was conducted through the PubMed database for “pisa syndrome”. Articles were screened for relevant information on PS aetiology, pathophysiology and treatment.
ResultsPisa syndrome has been associated as an adverse effect of multiple drugs from different classes, mainly antipsychotics, dopaminergic agents and cholinesterase inhibitors. The underlying mechanisms are not yet fully understood. Nevertheless, one of the most consensual hypothesis considers PS as a consequence of a cholinergic-dopaminergic imbalance that can be caused by antipsychotic treatment. Some factors have been associated with increased risk for developing PS such as old age and polypharmacy. PS appears to be better treated with the reduction or interruption of the agent(s) associated with its onset.
ConclusionsDespite its low incidence, Pisa syndrome can occur as a side effect of a number of different medications and the identification of the trigger-drug is fundamental so it can be reduced or interrupted in order to treat this condition.
DisclosureNo significant relationships.
Cannabis use and cognitive impairment in schizophrenia
- M. Gonçalves, J. Romão, R. André, F. Félix, G. Andrade, R. Saraiva, E. Dornelles, E. Fernandes, M. Abreu, I. Chendo, F. Ismail
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- Journal:
- European Psychiatry / Volume 65 / Issue S1 / June 2022
- Published online by Cambridge University Press:
- 01 September 2022, pp. S456-S457
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Introduction
Neurocognitive deficits amongst patients with schizophrenia are considered one of schizophrenia’s central features. These deficits appear to be present from the first episode of psychosis (FEP) and certain cognitive impairments could be components of a genetic vulnerability to schizophrenia. Regarding research on cannabis and cognition in schizophrenia, different studies have assessed neurocognitive functions: memory, attention/vigilance, processing speed, verbal learning, executive functions, and verbal fluency.
ObjectivesThe aim is to do a review of recent findings concerning the association of cannabis use with cognition in schizophrenia.
MethodsA literature review was conducted using the PubMed search database.
ResultsPatients with schizophrenia and concomitant cannabis use are associated with worse performance in immediate verbal learning, and in some studies with worse working memory performance. There is an improvement of verbal memory when they cease the cannabis’ consumption. Regarding attention capacity and memory types assessed, the results are controversial. In FEP, heavy cannabis use during the previous year correlates with slower processing speed. Also, FEP-patients with cannabis use but no family history of psychosis perform worse in executive functions, while those with a family history of psychosis perform better.
ConclusionsThe studies of psychosis, cannabis and cognition differ in relevant aspects, which might be connected to the result variability. Therefore, before solid conclusions can be reached, it is important to carry out longitudinal studies to understand the changes in the cognitive variables, which can depend on the pattern of cannabis’ use (concurrent or prior to the FEP). Possible confounding variables that might be present should be acknowledged.
DisclosureNo significant relationships.