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Art posted an interesting study (http://www.neurology.org/cgi/content/abstract/65/2/280) on the Boston Cure site finding that Grey Matter (GM) atrophy (axonal death) is the biggest factor in MS disibility. This raises an interesting question:
if axonal death is responsible for most of the disability in MS, then how do we explain the appearent reversal of disability in patients whose progression has been halted (such as with drugs - tovaxin, campath, etc.; or even during long remissions)? This recovery has so far been attributed to re-mylination (a known capability). But if disibility is mostly due to dead axons, and not de-mylination, then do we conclude that disibility reveral is due to re-growth of dead axons - not a known capability!

Hi Bill,

The loss of axons is certainly the cause of long term disability in MS patients, however short term loss of function can be caused by the improper conduction of denuded axons. If left to a toxic environment the axons themselves will eventually die.

The theory behind the functional recovery that follows treatment with drugs such as Campath is that the axons are remyelinated and therefore do not continue to die.

In addition the Brain is capable of rewiring itself past injured areas, a feature known as plasticity. It may be that this plays a part in functional recovery.

Finally some axon regeneration may be occurring (although not proven). The following is an extract from Alasdair Coles talking about Campath.

We imagined that Campath-1H treatment of multiple sclerosis would prevent further deterioration but would do nothing for damage already acquired. Quite unexpectedly however, most patients treated using a single dose of Campath-1H show a steady improvement in their disability over the next 12-24 months. This was encouraging but difficult to understand. The brain was being encouraged to repair itself; but why?

This project tests one possible explanation: that cells of the immune system are altered after Campath-1H treatment and they travel to the brain to release factors that encourage repair of nerve fibres.

Regards
Robin