Neuroimaging Advances in Brain Function of Laryngeal Dystonia: A Systematic Review.

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Bibliographic Details
Title:	Neuroimaging Advances in Brain Function of Laryngeal Dystonia: A Systematic Review.
Authors:	Hu, Yuanjia¹, Xing, Lu^1,2, Wu, Shengtao³, Zhuang, Peiyun^1,2 peiyunzhuang@163.com
Source:	Journal of Speech, Language & Hearing Research. Apr2026, Vol. 69 Issue 4, p1631-1642. 12p.
Subject Terms:	*Brain, Brain physiology, Brain anatomy, Research funding, Sensorimotor integration, Magnetic resonance imaging, Systematic reviews, MEDLINE, Gray matter (Nerve tissue), Thalamus, White matter (Nerve tissue), Neuroradiology, Online information services, Cerebellum, Data analysis software, Spasmodic dysphonia
Abstract:	Purpose: This study aims to review neuroimaging research on brain function in laryngeal dystonia (LD), summarize current evidence on its pathophysiological mechanisms, and highlight directions for future investigation. Method: PubMed, Scopus, and Web of Science Core Collection were searched from database inception to November 2025. Two reviewers independently screened studies, extracted data, and assessed study quality using the Newcastle--Ottawa Scale. Eligible studies were synthesized through systematic review and visual analysis. Results: A total of 33 studies were included. These studies employed imaging techniques such as functional magnetic resonance imaging and voxel-based morphometry to identify abnormalities in patients with LD. Structurally, key findings include gray matter alterations in sensorimotor areas, reduced thalamic volume, and impaired white matter integrity. Functionally, this manifests as sensorimotor integration dysfunction (characterized by M1/S1 and cerebellar hypoactivation alongside pallidal and thalamic hyperactivation) and network decoupling (e.g., weakened M1-S1 connectivity). Conclusions: The pathological mechanism of LD is a complex network imbalance involving the core "cortico-basal ganglia-thalamo-cerebellar" loop, driven primarily by sensorimotor integration dysfunction. Current research is limited in quantity and suffers from significant methodological heterogeneity. Future studies should further clarify the functional interactions among brain regions and their relationship with clinical symptoms, thereby providing a theoretical basis for the development of targeted therapies. Supplemental Material: https://doi.org/10.23641/asha.31329103 [ABSTRACT FROM AUTHOR]
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Database:	Education Research Complete

Description
Abstract:	Purpose: This study aims to review neuroimaging research on brain function in laryngeal dystonia (LD), summarize current evidence on its pathophysiological mechanisms, and highlight directions for future investigation. Method: PubMed, Scopus, and Web of Science Core Collection were searched from database inception to November 2025. Two reviewers independently screened studies, extracted data, and assessed study quality using the Newcastle--Ottawa Scale. Eligible studies were synthesized through systematic review and visual analysis. Results: A total of 33 studies were included. These studies employed imaging techniques such as functional magnetic resonance imaging and voxel-based morphometry to identify abnormalities in patients with LD. Structurally, key findings include gray matter alterations in sensorimotor areas, reduced thalamic volume, and impaired white matter integrity. Functionally, this manifests as sensorimotor integration dysfunction (characterized by M1/S1 and cerebellar hypoactivation alongside pallidal and thalamic hyperactivation) and network decoupling (e.g., weakened M1-S1 connectivity). Conclusions: The pathological mechanism of LD is a complex network imbalance involving the core "cortico-basal ganglia-thalamo-cerebellar" loop, driven primarily by sensorimotor integration dysfunction. Current research is limited in quantity and suffers from significant methodological heterogeneity. Future studies should further clarify the functional interactions among brain regions and their relationship with clinical symptoms, thereby providing a theoretical basis for the development of targeted therapies. Supplemental Material: https://doi.org/10.23641/asha.31329103 [ABSTRACT FROM AUTHOR]
ISSN:	10924388
DOI:	10.1044/2025_JSLHR-25-00663