A connectivity-based approach to the pathophysiology of hemiballism

• Autor(a) principal: Rozanski,VE
• Data de Publicação: 2016
• Outros Autores: Wick,F, Nádia Moreira Silva, Ahmadi,SA, Kammermeier,S, João Paulo Cunha, Boetzel,K, Vollmar,C
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://repositorio.inesctec.pt/handle/123456789/6420; http://dx.doi.org/10.1016/j.baga.2016.02.002

Background: Hemiballism may arise as a rare consequence of focal basal ganglia lesions. Pathophysiologically, there is a controversy between the role of the STN as the exclusive lesion localization as opposed to several brain regions in which lesions may induce hemiballism. This is most likely due to a motor circuit affection. Objectives: To study the affection of neural networks in the pathogenesis of hemiballism. Methods: We analysed focal vascular lesions inducing hemiballism (n = 8), their localizations and connectivity profiles. Probabilistic tractography (FSL: http://fsl.fmrib.ox.ac.uk/fsl/) was used to study connectivity. Results: Lesions inducing hemiballism were distributed across several anatomic regions (basal ganglia, thalamus, caudate, internal capsule) without a clear predilection. However, we detected increased connectivity for these lesions toward the STN and mesial cortical motor regions (pre-SMA/SMA). These regions are interconnected via subthalamo-pallido-thalamo-cortical networks. Conclusions: We provide evidence for the involvement of the subthalamo-pallido-thalamic pathways in the pathogenesis of hemiballism, which is consistent with data on experimental hemiballism in animals. Electrophysiological basal ganglia recordings and functional MRI would complement our findings to assess the activation patters within these circuits.