Multiple Sclerosis Associated With
Peripheral DeMyelinating Neuropathy
Di Trapani G, Carnevale A, Cioffi RP, Massaro AR, Profice P
Clin Neuropathol 1996 May-Jun;15(3):135-8
Catholic University, Institute of Neurology, Policlinico A. Gemelli, Rome, Italy
PMID# 8793246; UI# 96385388
We report clinical, ElectroPhysiological, Magnetic Resonance Imaging, and Nerve Biopsy findings of 2 patients with definite Multiple Sclerosis and Peripheral DeMyelinating Disease.
Although it is not easy to assess the real incidence of Peripheral Neuropathy in patients with Multiple Sclerosis, this association seems to be rare.
The combination of Central and Peripheral DeMyelination may be a fortuitous coincidence, but it appears improbable.
Alternatively, these patients may represent a specific subpopulation and common ImmunoPathoGenetic mechanisms such as (Immunological factors, Endothelial alterations, and abnormal expression of Adhesion Molecules) may underly both Central and Peripheral Myelin involvement.
The study of these cases might clarify specific mechanisms of PathoGenetic significance in DeMyelinating Diseases.
Experimental Strategies To Promote CNS ReMyelination In Multiple Sclerosis
Insights gained from the Theiler's virus model system.
Miller DJ, Asakura K, Rodriguez M
J NeuroSci Res 1995 Jun 15;41(3):291-6
Mayo Clinic and Foundation, Dept of Immunology, Rochester, Minnesota 55905, US
PMID# 7563222; UI# 96028306
The destruction of Central Nervous System (CNS) Myelin, the lipid-rich insulator surrounding Axons in the mammalian Brain and Spinal Cord, is the primary pathological finding in Multiple Sclerosis.
Myelin loss can result in a significant clinical deficit, and was originally thought to be permanent, similar to Axonal destruction.
However, Myelin regeneration is now an established phenomenon in both human disease and animal models of CNS DeMyelination.
In this review, the concept of ReMyelination in DeMyelinating Diseases such as Multiple Sclerosis is discussed.
And the usefulness of animal models of CNS DeMyelination in developing experimental strategies to promote ReMyelination is examined.
Special emphasis is given to the Theiler's Murine EncephaloMyelitis model, which has been the primary animal model used to investigate therapies designed specifically to stimulate Myelin repair.
Multiple Sclerosis: Role Of Growth Factors And ReMyelination
Presse Med 1994 Nov 5;23(34):1577-81
Hopital de la Salpetriere, INSERM U-134, Paris, France
PMID# 7824494; UI# 95124957
Multiple Sclerosis is a frequent and often disabling Neurological Disease. Its Etiology and treatment remain to be discovered.
It has been demonstrated in Multiple Sclerosis Brains that ReMyelination can occur after the Myelin damage.
This Myelin repair is achieved by Oligodendrocytes, which are the Myelinating Cells of the Central Nervous System or by Oligodendrocytes precursors still present in adult Central Nervous System.
Several recently discovered Growth Factors can stimulate Oligodendrocytes precursors migration and proliferation, or act as survival factors for mature Oligodendrocytes.
These Glial Growth Factors may represent a new therapeutic approach in Multiple Sclerosis, aiming at the stimulation of the endogenous capacities of ReMyelination.