georgegoss wrote: "sometimes" (a small minority of cases) treated patients with RRMS have a MS-relapse following treatment which is then quickly put into remission with additional doses of cyclophosphamide infusions post-HSCT.
George, I'm curious about this relapse. Does it always happen immediately after the HSCT treatment or do they monitor the patient over a long period of time and then give more cyclophosphamide when the patient relapses some time in the future?
I guess one indication if it did not work on a person with SPMS is that if you did not have any improvements over time as you and Asher seem to be experiencing.
But, I have been doing a lot of research on the causes of MS and the different phases of disease. One new theory is that during the relapsing phase, the meylin sheath is targeted. The sheath can be damaged but remeylination can occur.
Durring the secondary progressive phase of the disease the theory is that when the meylin sheath is damaged beyond repair, the axon is exposed and thus permanent damage can begin to occur to the axon.
Demyelination alone does not appear to cause axonal injury, and most axons survive transitory demyelination. However, axons that are chronically demyelinated are at substantial risk of degeneration. This may reflect the loss of important nerve growth factors that are produced by surrounding oligodendrocytes and that are essential for axonal survival.
I'm not sure this also holds true for primary progressive MS because this seems to cause axonal loss at the onset, similiar to ADEM but maybe not as aggresively. However, I believe the theory for secondary progressive MS as described above could explain why there is a better succes rate with HSCT the sooner it is administered.