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This Month in Archives of Neurology
Arch Neurol. 2001;58:21-22.
Multiple Sclerosis: New Strategies
Gilden and colleagues (SEE ARTICLE) describe new, sophisticated molecular immunological techniques that will enhance our ability to identify putative antigen targets in multiple sclerosis (MS). Multiple sclerosis antigens have been elusive, and this review offers new ideas to track them down.
Urinary Clues in MS
Whitaker and colleagues (SEE ARTICLE) describe how urinary myelin basic protein–like material may serve as an indicator of failed remission and axonal damage in patients with advanced secondary progressive MS. Perspective is provided in an editorial comment by J. Theodore Phillips, MD, PhD. (SEE ARTICLE)
MRI and MS
Leist and colleagues (SEE ARTICLE) have examined the relationship between the frequency of enhancing magnetic resonance imaging (MRI) lesions and atrophy in patients with relapsing MS. In general, patients with a high proportion of lesions with a central contrast pallor have a higher rate of atrophic changes. Both enhancing lesions and atrophy have a predictive value, especially for patients with early disease. An editorial comment by Michael K. Racke, MD, Kathleen Hawker, MD, and Elliott M. Frohman, MD, PhD, is included. (SEE ARTICLE)
Axonal Damage in MS
De Stefano et al (SEE ARTICLE) describe the finding of axonal damage in the earliest stages of MS using magnetic resonance spectroscopy. Axonal and demyelinating disease may move forward together from day 1, and these observations are critical in appreciating the pathogenesis of this complex disease. An editorial comment on the role of axonal injury is provided by Carl Bjartmar, MD, PhD, Grahame Kidd, PhD, and Richard M. Ransohoff (SEE ARTICLE) .
Imaging MS
Van Walderveen and colleagues (SEE ARTICLE) have studied clinical characteristics of patients with MS in relation to lesion volume size on T1-weighted MRI. A more destructive type of lesion in certain subgroups of patients with MS is discussed. As the authors point out, these findings in subgroups of patients with MS may have implications for the selection of such patients for specific clinical trials.
Augmenting Suppressor Cells in MS
Qu et al (SEE ARTICLE) studied etretinate treatment in patients with MS receiving interferon beta-1b and found that it augments suppressor cell function. There were no meaningful changes in Expanded Disability Status Scale rating scores. The role of retinoids in the treatment of MS remains unclear, but further clinical trials are warranted.
Apoptosis of Blood Leukocytes in MS
Leussink and colleagues (SEE ARTICLE) from Germany define the degree of apoptosis contributing to the elimination of T cells in MS. They find that steroid pulse therapy is a strong inducer of leukocyte apoptosis, which may contribute to the down-regulation of T cell activity, and thereby terminate inflammation in patients with MS. This is an elegant neuroimmunologic study providing insight into one phase of disease pathogenesis.
Trigeminal Root Lesions in MS
Nakashima and colleagues (SEE ARTICLE) describe linear pontine trigeminal root lesions associated with facial sensory symptoms in patients with MS. These lesions are rare but important in defining facial sensory disturbances.
Callosal Atrophy in MS
Pelletier and colleagues (SEE ARTICLE) show significant callosal atrophy during the course of MS with associated specific functional impairment of interhemispheric information transfer. This is an elegant anatomical-functional correlation study and confirms the potential value of using callosal dysfunction as a surrogate marker of disease progression.
MRI Lesion Burden and Cognitive Loss in MS
Sperling and colleagues (SEE ARTICLE) have demonstrated a strong association between cognitive impairment for specific functions and MRI lesion burden in frontal and parietal white matter. Their findings indicate that frontoparietal subcortical networks underlie the pattern of neuropsychological impairment seen in patients with MS.
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