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A Longitudinal Study of Callosal Atrophy and Interhemispheric Dysfunction in Relapsing-Remitting Multiple Sclerosis
J. Pelletier, MD, PhD;
L. Suchet, MD;
T. Witjas, MD;
M. Habib, MD;
C. R. G. Guttmann, MD, PhD;
G. Salamon, MD;
O. Lyon-Caen, MD;
A. Ali Chérif, MD
Arch Neurol. 2001;58:105-111.
Objectives To determine if callosal atrophy and interhemispheric dysfunction can
be detected in the early stages of relapsing-remitting multiple sclerosis
(MS) and to evaluate their progression in relation to the disability and evolution
of lesions seen on magnetic resonance imaging during a 5-year period.
Methods We compared 30 patients who had clinically definite early-onset replasing-remitting
MS and mild disability with control subjects. Regional and segmental callosal
size and extent of white matter abnormalities on magnetic resonance imaging,
as well as performance on tasks exploring interhemispheric transfer of motor,
auditory, and sensory information were assessed. Patients with MS were evaluated
at baseline and after 5 years. Physical disability was determined at both
times using the Expanded Disability Status Scale score.
Results Patients with MS were seen with significant callosal atrophy and functional
impairment of interhemispheric transfer at baseline that worsened during the
5-year study. A significant correlation was found between the magnitude of
disability and the severity of morphological and functional callosal involvement
at baseline. This association persisted at year 5. Baseline clinical characteristics
such as age and prestudy relapse rate were unrelated to callosal size or interhemispheric
performance. However, the number of baseline T2-weighted lesions was correlated
with callosal involvement and this relation persisted at year 5.
Conclusion Patients who had relapsing-remitting MS in the early stages of the disease
and mild disability had significant callosal involvement that progressed over
time. The relationship between disability, T2-weighted lesions load, and degree
of morphological and functional callosal impairment confirm the potential
value of using callosal dysfunction as a surrogate marker of disease progression
in MS.
From the Department of Neurology (Drs Pelletier, Suchet, Witjas, Habib,
and Ali Chérif) and Neuroradiology (Dr Salamon) University Hospital
of Marseilles, Marseilles, France, and Centre Hospitalo-Universitaire, Timone;
the Neurophysiology and Neuropsychology Unit, INSERM E 9926, University of
Marseilles, (Drs Pelletier, Habib, and Ali Chérif); the Federation
of Neurology, University Hospital La Salpétrière of Paris, Paris,
France (Dr Lyon-Caen); and the Department of Radiology, Brigham and Womens
Hospital, Harvard Medical School, Boston, Mass (Dr Guttmann).
Corresponding author: J. Pelletier, MD, PhD, Department of Neurology,
CHU Timone, F-13385 Marseilles 5, France (e-mail: jpelletier{at}ap-hm.fr).
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