Deep brain stimulation and psychosis: A case series and two candidate causal brain circuits
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Le résumé fourni par la source
Schizophrenia and psychosis are debilitating conditions with suboptimal treatment options. Deep brain stimulation (DBS) offers promise, but effective treatment targets remain undefined. Examining cases in which DBS either induced or alleviated psychotic symptoms may help identify circuits causally involved in psychosis and suggest candidate targets for intervention. We systematically reviewed the literature to identify all published cases in which DBS modulated (i.e., caused or improved) psychotic symptoms, regardless of target and indication. Authors of original publications were contacted to gather individual case data, allowing DBS electrode reconstruction and stimulation volume modeling. This data was aggregated into standard space and used to characterize anatomical structures most consistently associated with change in symptoms. After screening 332 studies, 36 cases were retained. This included 16 patients who received DBS for treatment-resistant schizophrenia or psychosis (nucleus accumbens, N=7; subgenual cingulate, N=4; substantia nigra pars reticulata, N=3; habenula, N=2) and 18 patients who received DBS for treatment of other conditions and experienced psychotic symptoms as a side effect (anterior nucleus of the thalamus, N=7; centromedian nucleus, N=1; subthalamic nucleus, N=6; nucleus accumbens, N=2; globus pallidus pars interna, N=1; amygdala, N=1). Finally, DBS of the nucleus basalis of Meynert improved visual hallucinations in two additional cases. Although stimulation sites were anatomically heterogeneous, qualitative integration of the empirical anatomical findings with current neurobiological models of schizophrenia revealed two circuits potentially implicated in psychotic symptoms: one centered on the mediodorsal nucleus of the thalamus and its main subcortical afferents, and one involving the nucleus accumbens - ventral tegmental area loop. We propose a preliminary theoretical framework linking these circuits to the emergence and improvement of psychotic symptoms, thereby generating testable hypotheses for future mechanistic and clinical studies. We suggest that disruption of these circuits may respectively relate to impaired filtering of cognitive and limbic representations, and aberrant salience processing.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Deep brain stimulation and psychosis: A case series and two candidate causal brain circuits
- Date Crossref
- 22/11/2025
- Éditeur
- openRxiv
- Type
- posted-content
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Circuit Therapeutics (United States) pays non établi dans la noticeEntreprise
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Hospital de Sant Pau pays non établi dans la noticeÉtablissement de santé
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Charité - Universitätsmedizin Berlin pays non établi dans la noticeÉtablissement de santé
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Mass General Brigham pays non établi dans la noticeÉtablissement de santé
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Tampere University Hospital Department of Neurosciences pays non établi dans la noticeÉtablissement de santé
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Tampere University pays non établi dans la noticeUniversité ou école supérieure
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Juntendo University pays non établi dans la noticeUniversité ou école supérieure
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Fondazione IRCCS Istituto Neurologico Carlo Besta pays non établi dans la noticeÉtablissement de santé
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University of Pennsylvania Department of Neurosurgery pays non établi dans la noticeUniversité ou école supérieure
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Düsseldorf University Hospital pays non établi dans la noticeÉtablissement de santé
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Heinrich Heine University Düsseldorf pays non établi dans la noticeUniversité ou école supérieure
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QIMR Berghofer Medical Research Institute pays non établi dans la noticeStructure de recherche
Circuit Therapeutics (United States), Hospital de Sant Pau et Charité - Universitätsmedizin Berlin, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.