This Is MS Multiple Sclerosis Community: Knowledge & Support

Many of these people used to belong to this website, but have moved on because of the "hype" behind CCSVI as well as all of the other mis-information that is being spread.

(Scared--we're "sure" because his new MRI taken last month showed normal looking gray matter (atrophy has reversed), and he's had no MS relapses or progression in the last 3 years.)
cheer

where are the current failures of HSCT ? there were deaths initially when they used TBI, which they no longer use today. if the procedure, whether myeloablative or non-myeloablative, is done properly, i am not aware of any issues. all i have seen are people that are not longer using a CRAB drug and their MS is in remission. Sandi had her HSCT 12 years ago and she is still MS free today. certainly, some have not recovered from some of their disabilities, but the underlying disease is not attacking them anymore...they are not getting worse. on the other hand, many people have improved their EDSS score.

once the third trial is complete odds are this will be approved by the fda and most put it around the yr 2020-2022 in the US.

Initial trials tended to select patients for secondary progressive disease with an increase in permanent disability of 0.5–1.0 Expanded Disability Status Scale (EDSS) steps within the prior 12 months. Despite using intense regimens, the patients’ disability did not improve and even continued to progress at a rate not convincingly different than the natural history of progressive MS.6,7 Immune analysis of samples collected before and after HSCT demonstrated an immune reset with a surge in recent thymic emigrants (naïve T cells) and change in T-cell receptor (CDR3) repertoire skewing.23 Therefore, in progressive MS, despite aggressive immune ablative therapy resulting in a post-transplant immune reset, patients did not improve and disability progressed within the post-transplant follow-up reported.
The initial HSCT clinical outcomes reaffirmed that progressive MS is an axonal degenerative disease and not primarily immune mediated.24 Transplant results also suggest that the relatively common and often unchallenged clinical practice of treating progressive MS with FDA-approved therapies, all of which are immune-based interventions, should be viewed as an ineffective and costly expenditure of limited financial resources.

Here is a recent analysis from this year, Harry and shaight. HCST does nothing for progressive or secondary disease. This is from one of the inventors of this therapy--Dr. Richard Burt of Northwestern, who now states that secondary progressive MS is NOT about the immune system, but about axonal degeneration. There is no inflammation or immune involvement in SPMS. He has been studying HCST treatment for a decade.

Multiple sclerosis (MS) is a chronic disease that is characterized by central nervous system (CNS) inflammation, demyelination, and neurodegeneration. Although the pathophysiology of MS is not completely understood, it is clear that much of the underlying disease process is clinically silent and continues even when patients are not experiencing symptoms. Most patients initially present with relapsing/remitting MS, in which acute disease episodes are separated by a return to normal or near-normal neurologic function. Eventually, most patients transition to secondary progressive MS, which is defined by the gradual accumulation of irreversible neurologic impairment. A consensus has recently begun to emerge that the long-term progressive disability in patients with MS is due to irreversible neurodegeneration, and that inflammation is less prominent in the later stage of the disorder. MS lesions exhibit extensive axonal transection and degeneration, and may involve both gray matter and white matter. 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. The gradualaccumulation of axonal injury probably contributes to the long-term atrophy of the CNS that is often observed in patients with chronic MS, and to the eventual progression of neurologic impairment. Early initiation of disease-modifying therapy may therefore help to slow long-term neurodegeneration and disease progression in patients with MS. (Adv Stud Med. 2009;9(2):37-41)

So, it looks like it would be best in my view to have the HSCT procedure before the transistion to the secondary progressive phase.

Pathology studies conducted as early as the 19th century have already recognized that MS affects not only the WM but also the gray matter (GM), which somehow got neglected over the years [1]. However, in the last decade, substantial pathological, immunological and imaging evidence confirmed that tissue damage in the GM is a key component of the disease process in MS and that it occurs from the earliest clinical stages [2-5]. During the past few years, the number of studies investigating GM damage in MS has increased exponentially.
In the last 5 years, numerous cross-sectional and longitudinal studies established that GM damage is a better predictor of physical disability and cognitive impairment than WM damage [5]. Most studies examining this argument used novel imaging techniques that can indirectly assess the extent of GM damage, the most important being a measurement of GM atrophy [2,5].

Here is a recent analysis from this year, Harry and shaight. HCST does nothing for progressive or secondary disease. This is from one of the inventors of this therapy--Dr. Richard Burt of Northwestern, who now states that secondary progressive MS is NOT about the immune system, but about axonal degeneration. There is no inflammation or immune involvement in SPMS. He has been studying HCST treatment for a decade.

Professor Shimon Slavin heads a clinic in Tel Aviv, Israel, which performs stem cell transplants for cancer patients and various auto immune diseases, among them MS. He has been working in the field of HSCT since the 1980s and worked at the National Institute of Health at the same time as Dr. Burt. Professor Slavin has developed a more gentle method of ablating the immune system, known as RIC (reduced intensity conditioning) which is the protocol which is also used by Dr. Burt in his studies at Northwestern.

Immune-based treatment, including HSCT, is not effective in progressive MS. Patients with a long disease duration, older age, or high EDSS scores without active inflammation on MRI, until proven otherwise, should have their diagnosis of relapsing–remitting MS questioned.