J. Pelletier et al., A longitudinal study of callosal atrophy and interhemispheric dysfunction in relapsing-remitting multiple sclerosis, ARCH NEUROL, 58(1), 2001, pp. 105-111
Objectives: To determine if callosal atrophy and interhemispheric dysfuncti
on can be detected in the early stages of relapsing-remitting, multiple scl
erosis (MS) and to evaluate their progression in relation to the disability
and evolution of lesions seen on magnetic resonance imaging during a 5-yea
r period.
Methods: We compared 30 patients who had clinically definite early-onset re
plasing-remitting MS and mild disability with control subjects. Regional an
d segmental callosal size and extent of white matter abnormalities on magne
tic resonance imaging, as well as performance on tasks exploring interhemis
pheric transfer of motor, auditory, and sensory information were assessed.
Patients with MS were evaluated at baseline and after 5 years. Physical dis
ability was determined at both rimes using the Expanded Disability Status S
cale score.
Results: Patients with MS were seen with significant callosal atrophy and f
unctional impairment of interhemispheric transfer at baseline that worsened
during the 5-year study. A significant correlation was found between the m
ag nitude of disability and the severity of morphological and functional ca
llosal involvement at baseline. This association persisted at rear 5. Basel
ine clinical characteristics such as age and prestudy relapse rate were unr
elated to callosal size or interhemispheric performance. However, the numbe
r 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 p
rogressed over time. The relationship between disability, T2-weighted lesio
ns load, and degree of morphological and functional callosal impairment con
firm the potential value of using callosal dysfunction as a surrogate marke
r of disease progression in MS.