Skip Navigation



Brain Advance Access published online on September 23, 2008

Brain, doi:10.1093/brain/awn228
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
131/11/3051    most recent
awn228v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Sevilla, T.
Right arrow Articles by Palau, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sevilla, T.
Right arrow Articles by Palau, F.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author (2008). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Vocal cord paresis and diaphragmatic dysfunction are severe and frequent symptoms of GDAP1-associated neuropathy

Teresa Sevilla1,2, Teresa Jaijo3,4, Dolores Nauffal5, Diego Collado6, María José Chumillas7, Juan J. Vilchez1,2, Nuria Muelas1, Luis Bataller1,2, Rosalía Domenech5, Carmen Espinós3,4 and Francesc Palau3,4

1Department of Neurology, University Hospital La Fe, 2CIBER de Enfermedades Neurodegenerativas (CIBERNED), 3Laboratory of Genetics and Molecular Medicine, Instituto de Biomedicina de Valencia, CSIC, 4CIBER de Enfermedades Raras (CIBERER), 5Department of Pneumology, 6Department of Otolaryngology and 7Department of Clinical Neurophysiology, University Hospital La Fe, Valencia, Spain

Correspondence to: Teresa Sevilla, Hospital Universitari La Fe, Avda. Campanar 21, 46009-Valencia, Spain E-mail: sevilla_ter{at}gva.es

Cranial nerve involvement in Charcot-Marie-Tooth disease (CMT) is rare, though there are a number of CMT syndromes in which vocal cord paralysis is a characteristic feature. CMT disease due to mutations in the ganglioside-induced differentiation-associated protein 1 gene (GDAP1) has been reported to be associated with vocal cord and diaphragmatic palsy. In order to address the prevalence of these complications in patients with GDAP1 mutations we evaluated vocal cord and respiratory function in nine patients from eight unrelated families with this disorder. Hoarseness of the voice and inability to speak loudly were reported by eight patients and one had associated symptoms of respiratory insufficiency. Patients were investigated by means of peripheral and phrenic nerve conduction studies, flexible laryngoscopy, pulmonary function studies and polysomnography. Nerve conduction velocities and pathological studies were compatible with axonal CMT (CMT2). Flexible laryngoscopy showed left vocal cord palsy in four cases, bilateral cord palsies in four cases and was normal in one case. Restrictive respiratory dysfunction was seen in the eight patients with vocal cord paresis who were all chair-bound. These eight had confirmed phrenic nerve dysfunction on neurophysiology evaluation. The patient with normal vocal cord and pulmonary function had a less severe clinical course.This study shows that CMT patients with GDAP1 mutations develop severe disability due to weakness of limb muscles and that laryngeal and respiratory muscle involvement occurs late in the disease process when significant proximal upper limb weakness has developed. The early and predominant involvement of the left vocal cord innervated by the longer left recurrent laryngeal nerve suggests a length dependent pattern of nerve degeneration. In GDAP1 neuropathy, respiratory function should be thoroughly investigated because life expectancy can be compromised due to respiratory failure.

Key Words: Charcot-Marie-Tooth disease; CMT 2K; ARCMT; Vocal cord paralysis; GDAP1 mutations

Received May 1, 2008. Revised August 23, 2008. Accepted August 26, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.