Browse by author
Lookup NU author(s): Dr Richard Quinton
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Objective: To investigate the etiology of mirror movements in patients with X-linked Kallmann’s syndrome (xKS) through statistical analysis of pooled white matter data from structural MR images. Background: Mirror movements occur in 85% of xKS patients. Previous electrophysiologic studies have suggested an abnormal ipsilateral corticospinal tract projection in xKS patients exhibiting mirror movements. However, an alternative hypothesis has proposed a functional lack of transcallosal inhibitory fibers. Methods: T1-weighted brain scans were normalized into stereotaxic space with segregation of gray and white matter to allow comparison of pooled white matter data on a voxel-by-voxel basis using SPM-96 software. Nine xKS patients were compared with two age-matched groups of nonmirroring individuals: nine patients with autosomal Kallmann’s syndrome (aKS) and nine age-matched normal (healthy) men. Results: Hypertrophy of the corpus callosum was found in both Kallmann’s syndrome groups: the anterior and midsection in xKS, and the genu and posterior section in aKS. Bilateral hypertrophy of the corticospinal tract was found only in the group of xKS patients exhibiting mirror movements. SPM analysis was validated by an independent region of interest analysis of corpus callosum size. Conclusion: Although morphometry on its own cannot determine the cause of mirror movements, the specific finding of a hypertrophied corticospinal tract in xKS is consistent with electrophysiologic evidence suggesting that mirror movements in xKS result from abnormal development of the ipsilateral corticospinal tract fibers.
Author(s): Krams M, Quinton R, Ashburner J, Friston KJ, Bouloux P-MG, Frackowiak RSJ, Passingham JE
Publication type: Article
Publication status: Published
Journal: Neurology
Year: 1999
Volume: 52
Pages: 816-822
Print publication date: 01/03/1999
ISSN (print): 0028-3878
ISSN (electronic): 1526-632X
Publisher: Lippincott Williams & Wilkins
URL: http://dx.doi.org/10.1212/WNL.52.4.816
DOI: 10.1212/WNL.52.4.816
PubMed id: 10078733
Altmetrics provided by Altmetric
