Visual dysfunction of superior colliculus and lateral geniculate nucleus in idiopathic blepharospasm.

Brainstem Dystonia Eye-blinking Human vision Neuroimaging

Journal

Journal of the neurological sciences
ISSN: 1878-5883
Titre abrégé: J Neurol Sci
Pays: Netherlands
ID NLM: 0375403

Informations de publication

Date de publication:
15 Oct 2024
Historique:
received: 30 04 2024
revised: 06 09 2024
accepted: 13 10 2024
medline: 20 10 2024
pubmed: 20 10 2024
entrez: 19 10 2024
Statut: aheadofprint

Résumé

The etiology and pathophysiology of idiopathic blepharospasm (BP) are still largely unknown. It has been hypothesized that BP is the consequence of a dysfunction of the basal ganglia loop, although cortical areas, cerebellum, and other brainstem structures may be involved. There is some evidence that the superior colliculus (SC), a sensorimotor brainstem structure, is involved in another adult-onset focal dystonia, the cervical dystonia. To date, there is no data concerning the implication of the SC in BP. Our study aims to investigate the role of the SC in people with idiopathic BP compared to controls using fMRI and a visual stimulation paradigm based on luminance contrast variations. People with idiopathic BP and controls underwent brain fMRI using a standardized protocol, allowing modulation of visual activity in the SC, the lateral geniculate nucleus (LGN), and the primary visual cortex (V1), at increasing luminance levels (1 %, 3 %, 5 %, 9 %). Ten BP women and ten sex- and age-matched controls were enrolled. Compared to controls, the BP group showed no modulation of visual responses at all luminance levels (p < 0.05) in both SC and LGN. In BP, BOLD responses in V1 were significantly lower at 5 % (p = 0.001), and 9 % (p = 0.002) luminance level. Our findings support the concept of SC and LGN dysfunction in idiopathic BP. Brain fMRI, targeting these sub-cortical visual structures, could play a future important role both as a biomarker and in our understanding of the pathophysiology of adult-onset focal dystonias.

Sections du résumé

BACKGROUND BACKGROUND
The etiology and pathophysiology of idiopathic blepharospasm (BP) are still largely unknown. It has been hypothesized that BP is the consequence of a dysfunction of the basal ganglia loop, although cortical areas, cerebellum, and other brainstem structures may be involved. There is some evidence that the superior colliculus (SC), a sensorimotor brainstem structure, is involved in another adult-onset focal dystonia, the cervical dystonia. To date, there is no data concerning the implication of the SC in BP.
OBJECTIVES OBJECTIVE
Our study aims to investigate the role of the SC in people with idiopathic BP compared to controls using fMRI and a visual stimulation paradigm based on luminance contrast variations.
METHODS METHODS
People with idiopathic BP and controls underwent brain fMRI using a standardized protocol, allowing modulation of visual activity in the SC, the lateral geniculate nucleus (LGN), and the primary visual cortex (V1), at increasing luminance levels (1 %, 3 %, 5 %, 9 %).
RESULTS RESULTS
Ten BP women and ten sex- and age-matched controls were enrolled. Compared to controls, the BP group showed no modulation of visual responses at all luminance levels (p < 0.05) in both SC and LGN. In BP, BOLD responses in V1 were significantly lower at 5 % (p = 0.001), and 9 % (p = 0.002) luminance level.
CONCLUSIONS CONCLUSIONS
Our findings support the concept of SC and LGN dysfunction in idiopathic BP. Brain fMRI, targeting these sub-cortical visual structures, could play a future important role both as a biomarker and in our understanding of the pathophysiology of adult-onset focal dystonias.

Identifiants

pubmed: 39426359
pii: S0022-510X(24)00408-8
doi: 10.1016/j.jns.2024.123272
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

123272

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

Auteurs

Sara Meoni (S)

Grenoble-Alpes University, INSERM, U1216, University Hospital of Grenoble-Alpes, Grenoble Institut Neurosciences, Grenoble, France; Movement Disorders Unit, Department of Neurology, University Hospital of Grenoble-Alpes, Grenoble, France. Electronic address: smeoni@chu-grenoble.fr.

Michel Dojat (M)

Grenoble-Alpes University, INSERM, U1216, University Hospital of Grenoble-Alpes, Grenoble Institut Neurosciences, Grenoble, France.

Michael Hutchinson (M)

Department of Neurology, St. Vincent's University Hospital, Dublin, Ireland; School of Medicine and Medical Science, University College Dublin, Dublin, Ireland.

Pierre Pelissier (P)

Movement Disorders Unit, Department of Neurology, University Hospital of Grenoble-Alpes, Grenoble, France.

Christophe Chiquet (C)

Department of Ophthalmology, University Hospital of Grenoble-Alpes, HP2 Laboratory, INSERM U1300, Grenoble, France.

Elena Moro (E)

Grenoble-Alpes University, INSERM, U1216, University Hospital of Grenoble-Alpes, Grenoble Institut Neurosciences, Grenoble, France; Movement Disorders Unit, Department of Neurology, University Hospital of Grenoble-Alpes, Grenoble, France.

Classifications MeSH