Patient-empowerment and self-management have many benefits; self-compassion being just one of them. #ClinicSpeak #ThinkHand #MSBlog
The study below shows that when pwMS, or other chronic diseases, can self-manage your disease, your physical health depends strongly on the expectancy of a positive outcome (realistic thinking). The corollary is that when options for self-management in controlling your disease are limited (no DMTs, no prevention of infections, no lifestyle modifications, etc.) then your physical health depends more strongly on unrealistic thinking, or dare I say beliefs and/or pseudoscience.
When some pwMS are told that they have passed from the so called ‘relapsing phase‘ to the more ‘advanced phase‘ (formerly called SPMS) they shift from an having an expectancy of a positive outcome to either a ‘sense of hopelessness‘ or in some cases to a phase of ‘unrealistic thinking‘. For example, several of my patients with more advanced MS have gone onto to explore risky therapies abroad, contrary to my advice, in the hope of curing their MS and reversing their disability. Unfortunately, this phenomenon is fuelled by dogma that states MS is a two-staged disease, the first stage driven by inflammation and the second stage being due to neurodegeneration, and that there is a ‘window of opportunity‘ to treat MS. Many experts in the field simply don’t accept the possibility that MS can be modified through-out its course, which perpetuates the problem.
Fournier et al. Optimism and adaptation to chronic disease: The role of optimism in relation to self-care options of type 1 diabetes mellitus, rheumatoid arthritis and multiple sclerosis. Br J Health Psychol. 2002 Nov;7(Part 4):409-432.
DESIGN: The cross-sectional design involved 104 patients with type 1 diabetes, 95 patients with rheumatoid arthritis and 98 patients with multiple sclerosis, recruited via their physician at the out-patient department of five hospitals.
METHOD: Confirmatory Factor Analysis (LISREL) was employed to confirm a three-dimensional approach of optimism: outcome expectancies, efficacy expectancies and unrealistic thinking. Multi-sample analysis by path modelling was used to examine whether the relationship of the three optimistic beliefs with coping (CISS-21), depression and anxiety (HADS), and physical functioning (SF-36) differs with the controllability based on the self-care options of chronic disease.
RESULTS: These show that when chronic disease must be controlled by self-care, physical health depends more strongly on positive efficacy expectancies. In contrast, when self-care options for controlling chronic disease are limited, physical health depends more strongly on positive unrealistic thinking and relates negatively to positive efficacy expectancies. The impact of the three optimistic beliefs on mental health is independent of the controllability by self-care.
CONCLUSION: Optimistic beliefs are differently beneficial for physical health dependent on the controllability of chronic disease. Unrealistic beliefs are helpful when patients are confronted with moderately to largely uncontrollable disease where self-care options are limited, in contrast to positive efficacy expectancies that are helpful when patients deal with largely controllable disease where self-care is required.
At Barts-MS we actively promote patient-empowerment and self-management of MS. It is clear that by doing this pwMS learn ‘self-compassion‘. We also make it clear that we subscribe to the hypothesis that MS is potentially modifiable throughout its course, which is why we have launched our #ThinkHand campaign and explains why we want to do a trial in pwMS with more advanced MS. We want to test whether, or not, a highly-effective anti-inflammatory drug, with CNS penetration, is able to delay worsening of disability in the upper limbs and beyond. We are not deliberately promoting unrealistic expectations; our strategy won’t reverse existing disability it is simply being designed on the expectation that we may be able to keep pwMS with more advanced disease independent a little longer.
Patient-empowerment and self-management have many benefits; they improve anxiety and mood and make pwMS feel the have something to offer. They also teach pwMS to have self-compassion; i.e. extending compassion to one’s self in instances of perceived inadequacy, failure, or general suffering (Wikipedia).
Fournier et al. Optimism and adaptation to chronic disease: The role of optimism in relation to self-care options of type 1 diabetes mellitus, rheumatoid arthritis and multiple sclerosis. Br J Health Psychol. 2002 Nov;7(Part 4):409-432.
OBJECTIVES: To determine the role of optimistic beliefs in adaptation processes of three chronic diseases different in controllability by self-care. It was expected that optimism towards the future would relate to adaptation independently of the controllability of disease. Optimism regarding one’s coping ability should be beneficial in controllable diseases. Unrealistic optimism was expected to be beneficial in uncontrollable disease.
DESIGN: The cross-sectional design involved 104 patients with type 1 diabetes, 95 patients with rheumatoid arthritis and 98 patients with multiple sclerosis, recruited via their physician at the out-patient department of five hospitals.
METHOD: Confirmatory Factor Analysis (LISREL) was employed to confirm a three-dimensional approach of optimism: outcome expectancies, efficacy expectancies and unrealistic thinking. Multi-sample analysis by path modelling was used to examine whether the relationship of the three optimistic beliefs with coping (CISS-21), depression and anxiety (HADS), and physical functioning (SF-36) differs with the controllability based on the self-care options of chronic disease.
RESULTS: These show that when chronic disease must be controlled by self-care, physical health depends more strongly on positive efficacy expectancies. In contrast, when self-care options for controlling chronic disease are limited, physical health depends more strongly on positive unrealistic thinking and relates negatively to positive efficacy expectancies. The impact of the three optimistic beliefs on mental health is independent of the controllability by self-care.
CONCLUSION: Optimistic beliefs are differently beneficial for physical health dependent on the controllability of chronic disease. Unrealistic beliefs are helpful when patients are confronted with moderately to largely uncontrollable disease where self-care options are limited, in contrast to positive efficacy expectancies that are helpful when patients deal with largely controllable disease where self-care is required.
I don't have any “sense of positive outcome'' from the beginning, because it seems there is no such.What am I doing wrong?
Re: `sense of positive outcome'If diagnosed early and treated her the short- and intermediate-term outcomes are remarkably good with some MSers behaving as if they are normal.
Vasy, you're not practicing mindfulness, are you. Sheesh.
The sense of falling off a cliff and no-one trying to stop you is pervasive. I mean this in the sense that there are so many unknowns ahead that no-one is able to help you prepare for. Hope for the best and prepare for the worst seems to be the best way forward.
Prof G you may be interested to know that Caroline Wyatt has gone to Mexico for HSCT. Is this 'unrealistic thinking' on her part? https://carolinewyatt.com/2017/01/20/puebla-day-5-of-hair-loss-liberty-and-marie-antoinette/
Thanks for this. Yes, I was aware of her going to Mexico for HSCT. My thoughts are with her and I sincerely hope she does not develop any complications.
Lol what a funny thing to say to people… MS patient: "I would like take Lemtrada doctor". Doctor: "Ok, we will arrange your first infusion".MS patient: "Thanks doc."Doctor: "My thoughts are with you and I sincerely hope you do not develop any complications."
When I was diagnosed a decade ago there was lots of fundraising activity for projects to cure MS, roll back the ravages of MS, repair the damage… 10 years later we seem to be going backward. Now we have one disease and, one the relapses have stopped, all we can hope for is that our ability to hold something or write might be extended by a few months. Wow! To say I'm underwhelmed is an under-statement. I hope you never experience a disease which is devastating, but where the so called experts and researchers throw you a few bed crumbs and kill your hope.
Isn't trying to modify more advanced disease, better than admitting defeat under the banner of we 'missed the boat' or 'the therapeutic window has closed'?
My sons, Happy New Christmas to you all!I was in the Big Smoke this week to see a screening of T2: Trainspotting. The film made me feel old as I was merely a sprightly teenager when the first part came out in 1996. Coincidently, I was in Edinburgh that summer because of something I wrote at school got me a delegate role at the television festival. That summer Scotland was basking in the glory of culture and science, firstly for Trainspotting, secondly for Dolly the Sheep: the latter promising to advance genetic understandings and to usher in restorative medical breakthroughs.Here we are in 2017, and Don Giovannoni remains disappointingly clueless, nowadays pushing 9-hole cardboard peg tests over expensive toxic drugs. If Kate is disappointed, then imagine how Don Giovannoni feels? He has gone from 'esteemed' scientist to a novelty market seller on Amazon. That's a tough fall.Truth is, Kate, Don Giovannoni et al have failed you. Whilst they deliberate over T cells vs. B cells, you suffer, all the while reading this pointless blog in the hope that it may prove worthwhile. It won't. These guys are desperately shooting hoops over unattainable fairground prizes because, well, it pays the mortgage. They do not know why MS happens, launching myriad projects, acquiring money for them, then seeing them all fail. It is embarrassing.Read this article (http://www.bbc.co.uk/news/health-38669588) because this is where our NHS is headed. I myself am gonna invest in developing a 10-hole cardboard box test. It'll make me wealthy and get purchasers' their money's worth, with an extra hole thrown in for fun. Bargin, bruv.
It seems like trying to "modify advanced disease" through our current immunotherapies is like trying to "rearrange deck chairs on the Titanic". I completely agree with Kate's comments and understand her frustration.You may well be right Dr. G. that starting current immunotherapies (excluding CRAB drugs) "might" stop the disease from moving into a progressive phase, which is great for the early diagnosed, but does not appreciably help those in later RRMS or progressive phases in the long term.Yes, Tysabri may improve patient hand function but how long can patients stay on this drug without harm-2 years, maybe slightly more? Then what? Pray another immunotherapy, like Cladribine or anti-plasma cell therapy, is approved in 5-10 years after phase III trials are completed? I think the T- and B-cell may be a small part of the answer, even taking into account your therapeutic lag theory, in progressive disease (about 23-25% based on current trials by Siponimod and Ocrezulimab) but is far from anything that halts progression completely or addresses remyelination and neurorestoration. Here is hoping current stem cell therapy, neuronal support, astrocyte and microglial research pan out. I wish researchers and Pharma would treat Dr. G's treatment pyramid of MS like a rectangle but this is not currently embraced, probably because it is not lucrative. Would like to know MD hypothesis on progressive phase of MS?
Just checked on Amazon, the cardboard 9-hole peg test is not available, only the expensive plastic version. Am I mistaken? When can I buy one?
"Would like to know MD hypothesis on progressive phase of MS?"See education posts.. we need combination aproaches one agent will not do it all
Dre how good is your hand function? I hope keeping you independent and able to write and/or type. Or are you using voice activated software? I am about to invest in the necessary time and training for the latter; my hand function is going downhill fast and I want to be prepared for when I can't use a keyboard anymore.
Can't comment
MD, Re: "we need combination aproaches one agent will not do it all"I assume you mean neuroprotective therapies as an example..when can we expect these combination therapies to be available?
MD, if you could, please review the new ground-breaking publication in Nature that states MS progression/nerve damage is 2nd to angry A1 astrocytes triggered by APC activated microglia:"Neurotoxic reactive astrocytes are induced by activated microglia"Where does this leave T and B-cell theories in progressive disease or how do they fit together or do they fit at all? Is this the beginning of a revolution in treatment of progressive MS world? I look forward to your team's review. Would this explain why T and B-cell immunotherapies have been relatively ineffective in halting progressive MS?
I will have a look I have just read the abstract but they call their angry astrocytes A1. I think I would have called then gliotic astrocytes which have been known for yeares. The T and B cell theroy is still alive and kicking, because you have to ask what makes them angry. In this case activated microglia. What made the microglial activated then this is where T and B cells will come in, they trigger/create the environment to activate microglial, but this is why there are aspects of progression that do not respond to certain anti-inflammatory drugs. That astrocytes contribute to nerve survival is well known and they do such things as control the lactate that impinges on energy levels of the nerve. But lets have a look and break some ground.We have been saying for some time that you have to control the glial inflammation to control progression so, this is a new part of a jigsaw, but this does not change my world view. If it thrusts the astrocyte into the limelight great…it is an underestimated cell. We know that astrocytes control the glutamate-glutamine cycle and we know how important this may be in glutamate excitotixicity killing nerves.
So you are saying that I should take on the side effects of a DMT for my PPMS in the hope that the inflammation that threatens to degrade my hand function will respond to the DMT? Do we know that the inflammation in PPMS is not a different kind? A kind that will not respond to the DMTs on offer?
There is more than one type of inflammation and they all dont response to curret DMT
I really do not know why you insist that refering to "worsening", "advanced" MS makes anything better. With PPMS then, I never had this mysterious "relapsing phase" and I was just "worsening" going on "advanced" from the start. So much for optimistic belief.
RE: "PPMS"We think pwPPMS simply did not have an early lesion in an eloquent site to cause a relapse. They present after the reserve in a particular pathway has been lost; usually the lower limbs. About 10% of pwMS will go onto have relapses and even more on MRI (~25%). All the data supports PPMS as being the same as relapsing MS.
So why don't the DMTs work in PPMS? I have lesions in my spine which are probably progressing, causing me issues with my limbs. I don't see how any current DMT would help with that.
I actually get really upset reading this, thinking, is my neuro just fobbing me off then? Lying to me? They could be giving me something to fend off the damage of my PPMS, but they don't, because they'd rather I just degrade slowly, to some crisis point.But I think – this doesn't make sense in terms of everything I've read – we don't know that progressive MS is not driven by a different kind of inflammation, a kind of inflammation that does not respond well to the current drugs; we don't even know that this inflammation isn't the core of the disease (inside-out hypothesis).But here I'm being told that it's all one hotch potch. And on the basis of no firm, proven knowledge of the pathology of this heinous disease, you are muddying the waters still more with trying to simplify the terminology.
Prof G, you wisely ignored my & anon question in unrelated comments.If PPMS is the same disease as relapsing, then RRMS long term outcomes should be unmodifiable with that “hard and early'' approach. Whats the point then
Hi Vasy,I don't quite understand the train of thought that if PP and RR are the same disease, RRMS long term outcomes are going to be unmodifiable… can you clarify?
Your comment will be visible after approval.How many replies are not approved?
AnonymousSunday, January 22, 2017 4:38:00 pm – the change in terminology helps those cases like my partner… sent home without meds on diagnosis due to a premature and incorrect PPMS diagnosis. A change of neuro 2 months later led to an offer of Tysabri or Lemtrada – nothing else had changed (cept a new enhancing lesion that perhaps could have been avoided had the meds been started earlier). AnonymousSunday, January 22, 2017 6:19:00 pm – because "They present after the reserve in a particular pathway has been lost; usually the lower limbs…" In other words, the theory (and that's all it is at this stage) is that by the time you realise there is a problem, treatment is likely to be less effective.AnonymousSunday, January 22, 2017 6:44:00 pm – until they get their class 1 evidence, and then have another 5 years to actually catch up and update their knowledge with that evidence, most neuros are going to continue to fob off people with PPMS. Cept in countries where ocrelizumab becomes available- there, they'll have something to offer. But it's all theories theories theories.I had understood that "true" PPMS is (perhaps) made of those people who have very few observable lesions but lots of disability (of course, their grey matter could be riddled with lesions we don't see so it's all a bit speculative anyway). As my partner likes to say, MS is a disease of "everyone is very individual and we don't know much at all".
Yes please explain the hard and early approach not working it certainily works in beasties where you have the same disease different of damage occurring.
Ok, I’ll try to explain.It’s postulated that RRMS and PPMS is the same disease,It’s assumed that progressive worsening in PPMS is due to earlier focal damage, that went unnoticed to patient.It’s assumed that RRMS to SPMS transition is due to the same as above.For me as a layperson who know nothing about medicine or biology (well, at least I know something about complex systems, reliability and redundancy as an engineer) it is obvious that if early focal damage in PPMS went unnoticed, that thare is far less damage than in relapsing phase of RRMS. Both quantitatively and qualitatively. If damage in important pathway is severe, patient notices it. If it is neligible, than it went unnoticed, or pathway is not so important. And it went unnoticed in most PPMSers. Yes, I know about equivocal sites, reserve capacity and so on. But Also I know that if objective symptoms do appear then most of the reserve in that pathway already exhausted, didn’t you posted on this, Prof B? So PPMSers must have either more reserve in important pathways, less focal damage, or both, then RRMSers have.Ok, you can mellow down relapsing phase early by highly active therapies. But most of those people would still have focal events, on a smaller scale probably. But still noticeable for most of them.The damage is already done and continues. Please correct me if I’m wrong, Prof B, but for me it looks like you can reduce focal inflammatory activity of RRMSer to probably that seen in PPMS, or probably RRMSers will still have more of it, as they still notice relapses from time to time, and PPMSers usually don’t untill progression kicks in. But whats then? PPMSers still progress with a little focal damage, isnt it absurd to wait progression not to kick in in RRMSers treated with HSCT/alemtuzumab/whastsoever in 10-20 years who accumulated much more damage?Hope my question is clear now..
Anon 5:32 am"Your comment will be visible after approval.How many replies are not approved?"A few. Some are spam "miracle herbal cures" etc and a minority are abusive usually written in capital letters (you know who you are) that are tiresome and offensive. The vast majority of comments are approved.
Person using the TROLL font. MD2 says "You know who you are" and I say "we know who you are". Please stop, you are wasting both your own and our time. We know what you think of us, but the rest of the readers are never going to see your views as every thing you write is spammed.
Prof Mouse, as Prof G ignores me…Am I right in that you don't have adequate model of primary progressive disease in mice? E.g. there is no EAE flavour in which progression kicks in without clinically obvious prior attack ?
There is primary progressive/chronic disease in the C57Bl/6 mouse but this is after a primary immune attack.
Don't worry, he ignores me too:-). As MD2 says we have models that goes progressive from one attack
For every attack in MS (RRMS) there are ten or more brain lesions that go unnoticed. Also there is perhaps age issue that younger people early disease onset is RR where as onset of PPMS/SPMS occurs in older people
The question is does RRMS element create the progression if so early treatment with effect DMT should take the lesion level to or below that in PPMS. Will those people still get SPMS in ten years or will it be delayed. In animals I would say it will be delayed and may stop if done early enough. For MS the experiment is in progress..hoefully someone is collecting the data
Also I was forgetting that cannabinoid receptor knockout mice CB1KO)on the ABH background (that normally shows a relapsing remitting phenotype) become progressive after one attack.
I see mice left severely disabled after very first attack so the question is it that adequate..
I really liked reading your thoughts Vasy. I think the clarity of thought and logic of engineers should perhaps be employed more often in MS research!But MD – "onset of PPMS/SPMS occurs in older people" – not in me. PPMS started in me in my early twenties, and any notion of "relapses" remained elusive to me for over a decade thereafter. Strange disease.
Yes, I believe so. Maybe I'm not best placed to comment having a diagnosis of less than 2years, but after the ThinkHand was highlighted on this site, I gave more attention to the sheer amount of daily activities that requires hand and arm to complete. Sounds silly, but I was gobsmacked, especially when thinking about the fact that the public's perception of MS is a wheelchair and that was my first concern! As I've learned more about the disease I'm now living with, I cannot comprehend how it has been reduced to one solitary aspect of the disability and pain and fatigue it can inflict!Anything that is facilitative of our bodies, or parts of our bodies, continuing to function – bring it on I say!Btw – what happened to Wednesday's tutorial – thought the response from some PwMS were potentially beneficial to the day – if it went ahead???
Thre wednesday tutorial went ahead…the feedback has been very positiveThe speaker wMS gave an amazing account of their journey
Wasn't clear that I'm responding to Prof G query about modifying more advanced disease
Re: ".. about modifying more advanced MS."We have to do the studies; at present we hypothesise that we can modify the course, but our targets are set much lower than early in the course of the disease. We are focusing on hand/arm and bulbar (swallowing and speech) function. By the time you have advanced MS most of the reserve is lost in the legs and therefore it becomes very difficult to modify. Please note we are not saying we can necessarily modify the more advanced stages, however, recent data suggests we can. Let's do the trial and then we can all discuss the results.
"Please note we are not saying we can necessarily modify the more advanced stages, however, recent data suggests we can. Let's do the trial and then we can all discuss the results."Realistically, if the trial was to start tomorrow, results are some 10 to 20 years away. I'm not trying to kill us early (and I suspect I'm younger than you): but are you and I still going to be around to discuss the results?lol.
As I have been diagnosing for 3 years I still try to have a positive thinking about everything, but the future is "an uncertain place", this uncertain place is for everyone, but when you go to live with uncertainty daily when having to deal with a "hidden villain" the future becomes even more of an unknown, and the questions "when will I go to the wheelchair, when will I ever lose the functions of my hands, legs, etc.?" become constant, even when you would not want this constant sense of the fleetingness of life to become present.Now I know a recent case of a physically active middle-aged man, he's even a bodybuilder, and he's supposedly dealing with what would be "stem cell replacement" and just had a relapse. So I think there really is an active, constant inflammation that drives the future death of neurons and nerves, otherwise stem cells would be "the answer to the solution of everything in MS" and so far nothing concrete has been defined.
No one knows what the future holds. That includes tomorrow. I feel with having been diagnosed with MS a year ago, that I have another piece of the jigsaw puzzle that is my life. It's not a good piece. But I know about it. No one knows what will come to them… in a way we are all in the same boat, wondering what the future holds. Keep the chin up! I know, I know. It's not easy. Life isn't easy for anyone. We have to be as strong and as positive as we can. Peace out!