Relapse of first-episode schizophrenia patients and neurocognitive impairment: the role of dopaminergic and anticholinergic burden

Background: the prevention of relapse may be a key factor to diminish the cognitive impairment of first-episode schizophrenia (FES) patients. We aimed to ascertain the effects of relapse, and dopaminergic and anticholinergic treatment burdens on cognitive functioning in the follow-up. Methods: ninet...

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Detalles Bibliográficos
Autores: Cuesta, Manuel J., Ballesteros, Alejandro, Sánchez Torres, Ana María, Amoretti, Silvia, López-Ilundain, José M., Merchán-Naranjo, Jessica, González-Ortega, Itxaso, Salgado, Purificación, Rodríguez-Jiménez, Roberto, Roldán-Bejarano, Alexandra, Sarró, Salvador, Ibáñez, Ángela, Usall, Judith, Escartí, Maria José, Moreno-Izco, Lucía, Mezquida, Gisela, Parellada, Mara, González Pinto, Ana, Berrocoso, Esther, Bernardo, Miguel, 2EPs Group
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2022
País:España
Institución:Universidad Pública de Navarra
Repositorio:Academica-e. Repositorio Institucional de la Universidad Pública de Navarra
OAI Identifier:oai:academica-e.unavarra.es:2454/54642
Acceso en línea:https://hdl.handle.net/2454/54642
Access Level:acceso abierto
Palabra clave:Antipsychotics
Cognition
Dopamine burden
Anticholinergic burden
First episode psychosis
Relapse
Descripción
Sumario:Background: the prevention of relapse may be a key factor to diminish the cognitive impairment of first-episode schizophrenia (FES) patients. We aimed to ascertain the effects of relapse, and dopaminergic and anticholinergic treatment burdens on cognitive functioning in the follow-up. Methods: ninety-nine FES patients participated in this study. Cognitive assessments were performed at baseline and after 3 years of follow-up or, in those patients who relapsed, after >2 months of stabilization of the new acute psychotic episode. The primary outcomes were final cognitive dimensions. Results: repeated measures MANOVA analyses showed improvements in the whole sample on the end-point assessments in processing speed and social cognition. However, only impairment in social cognition showed a significant interaction with relapse by time in this sample. Relapse in FES patients was significantly associated with poor performance on end-point assessments of working memory, social cognition and global cognitive score. Anticholinergic burden, but not dopaminergic burden, was associated with verbal memory impairment. These significant associations resulted after controlling for baseline cognitive functioning, relapse and dopaminergic burden. Conclusions: the relationship between relapse and cognitive impairment in recovered FES patients seems to be particularly complex at the short-term follow-up of these patients. While relapse was associated with working memory, social cognition impairments and global cognitive score, anticholinergic burden might play an additional worsening effect on verbal memory. Thus, tailoring or changing antipsychotics and other drugs to reduce their anticholinergic burden may be a potential modifiable factor to diminish cognitive impairment at this stage of the illness.