http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15177777

Clin Neurol Neurosurg. 2004 Jun;106(3):246-8
Compston A.
School of Clinical Medicine, University of Cambridge Neurology, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.

The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myelin.

The phases of symptom onset, recovery, persistence and progression in multiple sclerosis can be summarized as

• functional impairment with intact structure due to direct effects of inflammatory mediators,
• demyelination and axonal injury with recovery through plasticity and remyelination, and
• chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage.