Email: "In some cases (mine, for example), no oligoclonal bands detected in CSF. What does this indicate?"
Not much. The 2001 McDonald diagnostic criteria mandated that you had to have abnormal CSF, i.e. local synthesis of IgG OCBs, to be diagnosed with PPMS. In 2005 this criterion was dropped without much scientific evidence to allow people with negative CSF to be diagnosed with PPMS. So you can be labelled as having PPMS with a negative CSF.
Interestingly, in the ORATORIO study (ocrelizumab in PPMS) you had to have an abnormal CSF to participate in the study. Therefore we don't know if OCB-ve PPMS will respond to ocrelizumab. Saying this the OCB-status never made it into the label. So OCB-ve PPMS can be treated with ocrelizumab despite no evidence to support it efficacy in this subgroup of patients with PPMS.
My very belated diagnosis is relapsing/remitting MS. Honestly, all I care about is how I feel, how my symptoms are, so I'm ambivalent about 'activity'. It doesn't make me feel worse, and I'm scared of being relabelled secondary progressive, because then treatment options disappear. And some treatments could, theoretically, make me feel a bit better. I think that's the main reason AHSCT has become so desired by a lot of people with MS, because some people say it makes one feel better. But so can Lemtrada, possibly. That's the hope.
This happened in the Autism world too (I'm also autistic). It used to be split up into autism, Asperger's, etc, but it was changed so now we're all just on the Autism Spectrum. I prefer that, not dividing us along false lines that encourage misconceptions. I'd prefer it if MS also just becomes the 'MS spectrum'; MS is also incredibly different for everyone. It confuses doctors, but that doesn't matter, they can just do some research.
Brilliant. Dogma 1 summarises it so well. It should be mandatory reading for all euros and they should repeat it daily. I am so fed up of being told that my MRI results are 'clearly encouraging' as they show no signs of active inflammatory activity, whilst ignoring the fact that my leg mobility is inexorably declining and I have gone from EDSS 1 to EDSS 6.5 in 10-years with no signs of any slow down
Thank you so much for this! I’m forwarding this to my neuro at UCSF as I’m ‘relapsing with progression’. I’m 50, diagnosed two years ago and sure I’ve had it for decades. In the last five years it’s hit me like a sledgehammer cognitively with episodic amnesia (seizures), visually, and now w increased mobility concerns. My neuro acknowledges that it’s one disease but the lack of characterization means exemption from studies.
Dr Aaron Bolster does a YouTube channel that isn’t quite as research focused but something akin to this might be a resolve to the funding challenges you are experiencing? Also, might provide a larger audience which Id think would be better so researchers here and abroad aren’t operating in a silo.
Sep 20, 2022·edited Sep 20, 2022Liked by Gavin Giovannoni
Thank you for the information.
I agree that all MS is one disease. MS Spectrum Disorder makes sense to me.
As for the higher number of women vs men with MS. To me it seems it is due to chronic stress and our ability to cope or escape such stresses. Stress hormones effect every cell in our bodies. Women experience more chronic stress in our patriarchal societies and it continues to get worse. I feel that the books “The Body Keeps the Score” by Bessel Van der Kolk, and “ When the Body Says No” by Gabor Mate explain autoimmune diseases very well. Even when EBV is shown to be the cause of MS, there is a reason why almost everyone has had EBV, yet only very few develop MS. I feel it isn’t due to Genetics, but it’s because of our society and our genetic sensitivity to the stress our society causes.
He mentioned he thinks it's an outdated form to label MS and mainly used in the US as to classify which treatment you get put on
His thoughts where basically one works better for you than others and if you limit treatment due to "MS type" youre doing more bad than good.
Eg Tysabri might work better for me than ocrevus, or visa versa same with Lemtrada. And even to your point about responders of interferons where some people just do well on these for whatever reason
For my understanding if inflammation in RRMS > SPMS > PPMS making it all 1 disease with simply different levels of inflammation, how come Siponimod works in stage 2 but not stage 1?
Email: "In some cases (mine, for example), no oligoclonal bands detected in CSF. What does this indicate?"
Not much. The 2001 McDonald diagnostic criteria mandated that you had to have abnormal CSF, i.e. local synthesis of IgG OCBs, to be diagnosed with PPMS. In 2005 this criterion was dropped without much scientific evidence to allow people with negative CSF to be diagnosed with PPMS. So you can be labelled as having PPMS with a negative CSF.
Interestingly, in the ORATORIO study (ocrelizumab in PPMS) you had to have an abnormal CSF to participate in the study. Therefore we don't know if OCB-ve PPMS will respond to ocrelizumab. Saying this the OCB-status never made it into the label. So OCB-ve PPMS can be treated with ocrelizumab despite no evidence to support it efficacy in this subgroup of patients with PPMS.
My very belated diagnosis is relapsing/remitting MS. Honestly, all I care about is how I feel, how my symptoms are, so I'm ambivalent about 'activity'. It doesn't make me feel worse, and I'm scared of being relabelled secondary progressive, because then treatment options disappear. And some treatments could, theoretically, make me feel a bit better. I think that's the main reason AHSCT has become so desired by a lot of people with MS, because some people say it makes one feel better. But so can Lemtrada, possibly. That's the hope.
This happened in the Autism world too (I'm also autistic). It used to be split up into autism, Asperger's, etc, but it was changed so now we're all just on the Autism Spectrum. I prefer that, not dividing us along false lines that encourage misconceptions. I'd prefer it if MS also just becomes the 'MS spectrum'; MS is also incredibly different for everyone. It confuses doctors, but that doesn't matter, they can just do some research.
Brilliant. Dogma 1 summarises it so well. It should be mandatory reading for all euros and they should repeat it daily. I am so fed up of being told that my MRI results are 'clearly encouraging' as they show no signs of active inflammatory activity, whilst ignoring the fact that my leg mobility is inexorably declining and I have gone from EDSS 1 to EDSS 6.5 in 10-years with no signs of any slow down
Thank you so much for this! I’m forwarding this to my neuro at UCSF as I’m ‘relapsing with progression’. I’m 50, diagnosed two years ago and sure I’ve had it for decades. In the last five years it’s hit me like a sledgehammer cognitively with episodic amnesia (seizures), visually, and now w increased mobility concerns. My neuro acknowledges that it’s one disease but the lack of characterization means exemption from studies.
Dr Aaron Bolster does a YouTube channel that isn’t quite as research focused but something akin to this might be a resolve to the funding challenges you are experiencing? Also, might provide a larger audience which Id think would be better so researchers here and abroad aren’t operating in a silo.
Thank you for the information.
I agree that all MS is one disease. MS Spectrum Disorder makes sense to me.
As for the higher number of women vs men with MS. To me it seems it is due to chronic stress and our ability to cope or escape such stresses. Stress hormones effect every cell in our bodies. Women experience more chronic stress in our patriarchal societies and it continues to get worse. I feel that the books “The Body Keeps the Score” by Bessel Van der Kolk, and “ When the Body Says No” by Gabor Mate explain autoimmune diseases very well. Even when EBV is shown to be the cause of MS, there is a reason why almost everyone has had EBV, yet only very few develop MS. I feel it isn’t due to Genetics, but it’s because of our society and our genetic sensitivity to the stress our society causes.
My neuro believes the same.
He mentioned he thinks it's an outdated form to label MS and mainly used in the US as to classify which treatment you get put on
His thoughts where basically one works better for you than others and if you limit treatment due to "MS type" youre doing more bad than good.
Eg Tysabri might work better for me than ocrevus, or visa versa same with Lemtrada. And even to your point about responders of interferons where some people just do well on these for whatever reason
Thank you! As an MS patient your voice of wisdom and practical thinking is so appreciated. As patients we deserve the truth.
For my understanding if inflammation in RRMS > SPMS > PPMS making it all 1 disease with simply different levels of inflammation, how come Siponimod works in stage 2 but not stage 1?
The subtypes have sabotaged treatment and CT.
How about NFL screening in young people who are susceptible to getting MS.
Could this lead to discovering PPMS early? Will raised NFL be enough to grand a MRI or an LP?
So, you speak of a sentinel event that people seek a doctors advice. Could this be a sensory event like muscle twitches?
I believe this is how I started, followed by a bought of face paint and headache several years later.
Thanks for another great one which I will print out and have handy when I visit the neurologist!