Barts-MS rose-tinted-odometer: ★
After my clinic last week I was emotionally drained and probably more than usual. Patient after patient was telling me the same story and asking the same questions.
“Since lockdown last year things have gotten worse, what can I do about it?”
My superficial interpretation is that most of these patients had gotten worse because of relative physical and mental inactivity. Working from home or not working, self-isolation to prevent getting COVID-19 and less physical exercise are taking their toll. I am increasingly making the point that unless you use it you will lose it (#UseItOrLoseIt). Put simply less physical exercise (self-isolation), less mental exercise (reduced work or no work) and less emotional exercise (social interactions) are having a devastating impact on people with MS. Then there is the shredder, i.e. ongoing MS disease activity be it new focal inflammatory lesions or the dreaded smouldering MS. As we have not been able to monitor pwMS with regular MRIs and change and escalate treatments a large number of pwMS are paying the price of having their MS undertreated.
One of the patients I spoke to via a video consult wanted to know why she was getting worse and why she was not eligible for siponimod treatment. She had not had a relapse in over 10 years and had no new lesions when we imaged her last year January 2020. She has gone from EDSS 6.0, i.e. being able to walk several hundred metres with a cane, to being wheelchair-bound in just 12 months. This rapidity of her secondary progression is faster than what we usually see. Most people spend at least 3 to 4 years at EDSS 6.0 and EDSS 6.5. The question I have is there be another reason for the rapid progression? Had she developed a new lesion in the spinal cord? The only way to sort this out is with an MRI and possible lumbar puncture and CSF analysis to measure neurofilament levels. The problem we have is that we are not doing non-urgent MRIs or lumbar punctures at present. However, I suspect the repeat MRI and CSF analysis will show no obvious new inflammation, which will make her ineligble for siponimod.
Many of these patients don’t understand that beyond relapses and focal MRI activity the real MS lurks. I explain why disease worsening or disability progression occurs in MS under 4 headings:
1. SS (scissors and stripper): The acute focal inflammatory lesion acts like molecular scissors and strippers, cutting axons and stripping myelin off axons. The cut and naked axons are blocked from conducting signals and result in a neurological deficit. The neurological deficit from this acute conduction block will vary depending on the pathway affected, for example, if the lesions affect the optic nerves it will cause loss of vision. The way to prevent the SS from causing conduction block is to prevent new lesions from forming. If this patient has a new lesion it would offer her hope and make her eligible for siponimod.
2. EF (energy failure): The demyelinated axons may recover function by a process called axonal plasticity or remyelination. Axonal plasticity is the process by which the neuron inserts new ion channels into the demyelinated axonal segments and restores conduction. Remyelination may also occur, but the new myelin is never as thick and as efficient as the old myelin and is susceptible to intermittent failure. These demyelinated and thinly remyelinated sections of axons are susceptible to temperature and fatigue. If the temperature rises these sections block and if the axons are used too much, for example with exercise, they run out of energy and also block. Sometimes the type of ion channel that is inserted into the axons fire spontaneously can cause intermittent symptoms, for example, pins and needles, pain, neuralgia and muscle spasms. As these ion channels are sodium channels it explains why these intermittent symptoms respond to drugs that block sodium channels, for example, carbamazepine, oxcarbazepine, phenytoin and lamotrigine.
I suspect a large amount of progressive disability in this patient is due to these mechanisms; sadly, we don’t have any add-on treatments we can offer her at present.
Another process that helps with recovery is that the surviving axons form sprouts to reconnect disconnected pathways and create new synapses, which are the connections between nerve fibres. All these processes increase the energy requirements of the axon, which makes it vulnerable to die-off later. At the same time the ‘MS lesion’ remains inflamed and some of the chemicals produced as part of the inflammation poison the mitochondria, which are energy factories of the axons. A further reduction in energy production puts further stress on the system. As a result of these processes, there is a delayed dying off of axons that takes place over months to years after the initial MS lesion has formed. This delayed dying off of axons explains why despite effective treatments stopping new MS lesions from forming some people with MS still notice a slow deterioration in their functioning. This is why we have added this patient to our prescreening log for the upcoming Chariot-MS trial in which we will be testing whether or not oral cladribine will slow down the worsening of upper limb function.
There is mounting evidence that exercise encourages plasticity, i.e. axonal plasticity and sprouting and synaptogenesis and recovery or maintenance of function. Sadly due to lockdown this patient had not been having physiotherapy and was unable to attend her regular aqua aerobics. Could she be losing function because of this? I suspect this could explain some of her deterioration.
3. SB (slow burn): Some MS lesions never recover and become slowly expanding lesions or SELs. SELs have a rim of hot microglia at their edges and continue to swallow up the myelin and axons of the surrounding ‘normal-appearing’ tissue. These lesions don’t have much acute inflammation left in them, i.e. there are very little T and B cells in these lesions. SELs continue to expand over years to decades and are responsible for the slow accumulation of damage over many years. SELs can be seen on MRI; they typically cause black holes on so-called T1-weighted MR images and have a dark rim of iron around them when viewed with special MR sequences (susceptibility imaging). The iron rim is a marker of these so-called ‘hot microglia’.
I would not be surprised if this patient had a SEL in a critical position in her cervical spinal cord. At present we have no idea what causes some MS lesions to regress and recover and for others to expand and become SELs. What we do know is that our standard anti-inflammatory DMTs have very little or no effect on SELs once they have developed. It is important to realise that SELs are found throughout the course of MS and are even seen in people with a radiologically isolated syndrome (RIS) or asymptomatic MS. In other words, the so-called ‘progressive MS pathology’ is found very early in the MS disease course. We do know that the number and size of the SELs increase with disease duration, i.e. the more MS lesions that develop the more SELs will be formed. Another important observation that has recently emerged is that a single strategically located SEL can cause an extraordinary amount of damage; for example, a single SEL in the so-called pyramidal tract or motor pathway can cause progressive weakness down one side of the body. I have a few patients like this and it is very disheartening when their weakness fails to respond to standard anti-inflammatory therapies.
An interesting debate is whether or not the ‘hot microglial’ response is abnormal, i.e. pathological, or is occurring in response to something in the surrounding tissue. I support the latter view and hypothesise that there is something in the surrounding tissue that is activating the microglia and they are just doing their job and trying to clear-up the inciting agent. Others have suggested these microglia are responding to the back-end, or Fc-end, of antibodies and activated complement components as a result of these antibodies reacting with their target or in a non-specific manner. Other hypotheses include viruses, e.g. EBV and HERVs, are driving the expansion of these lesions. The way to test these two competing hypotheses is to use drugs that switch off or suppress microglia. If the ‘hot microglia’ are the problem these drugs will work and stop SELs getting bigger. If the microglia are just doing their ‘job’ these agents are unlikely to work. It is also important to remind you that myelin debris inhibits remyelination so these microglia may be needed to help with the repair. The problem is that without being able to switch off the abnormal processes that are causing SELs to enlarge trying to stimulate repair mechanisms may be futile.
Another factor that can’t be ignored is recurrent infections, which sometimes affects a lot of people with advanced MS. Recurrent urinary tract infections (UTIs) are the biggest problem. This is why we take UTIs so seriously. Every time you get an infection it causes your immune system to produce cytokines, or inflammatory messengers, that travel to the brain and boosts the activity of the microglia. The hot microglia then exacerbate the damage that MS is doing to your brain and spinal cord. This is why many of you tolerate infections so poorly and often don’t recover back to baseline after a severe infection. There is a lot we can do to reduce recurrent bladder infections. For example, the judicious use of intermittent self-catheterisation, drinking lots of liquids to flush the bladder, using urinary antiseptics to suppress the growth of bacteria in the bladder and screening for asymptomatic UTIs using self-monitoring home dipsticking and prompt treatment.
This patient has had several UTIs in the last 12 months. To manage this I recommended she starts taking daily urinary antiseptics and she starts self-monitoring her urine twice weekly with dipstix and to start antibiotics ASAP as she picks up an early UTI. I hope the GP will do what I recommend; not all GPs are prepared to allow their patients to self-monitor and manage their bladders in this way.
The upshot of ‘slow burn’ is that we need additional therapies to add on top of DMTs that stop new lesions, and in particular chronic expanding or SELs, from forming. These treatments may be drugs to purge the CNS of antibody-producing B cells and plasma cells, drugs that inhibit complement activation and/or the activation of Fc receptors on microglia, anti-virals that target EBV and HERVs, and/or drugs that inhibit activated microglia. In other words, there are many therapeutic targets that still need to be explored as add-on therapies in MS.
4. PA (premature ageing): Most of you are aware of the effects of ageing on the nervous system. The brain and spinal cord were never designed by evolution to last longer than about 35 years. It is only relatively recently that as a species we have extended our lifespans. Once you go beyond approximately 35 years of age there is a gradual loss of nerve cells and axons. This explains why as you get older you notice the effects of ageing; reduced vision, loss of hearing, poor balance and sadly age-related cognitive impairment. In short, life is an age-dependent neurodegenerative disease. If we all live long enough we will all develop cognitive impairment. What protects us from age-related changes is so-called brain reserve capacity, i.e. the size of the brain and spinal cord, and cognitive reserve, which relates to education level and environmental enrichment (social capital, adult learning, cognitive exercises, etc.). We know that MS reduces both brain and cognitive reserve and as a result people with MS experience the impact of ageing much earlier. I refer to this as premature ageing. Can we do anything about this? Yes, we can. We know from studies in the general population there are many things that you can do to maximise your brain and cognitive reserve. This is called Brain Health and involves lifestyle factors such as exercise, diet, sleep and avoiding smoking and excessive alcohol consumption. It is also important to be screened for comorbidities or other diseases and have them treated; these include smoking, hypertension, diabetes, obesity and abnormal lipids. As for diet, there have not been any that have been studied specifically in MS. However, data from animal and other studies indicate that calorie restricted, intermittent fasting and ketogenic diets have the most promise with regard to brain health. However, we need more evidence of their beneficial effects before promoting these to pwMS.
Yes, this patient is in late 50’s and ageing mechanisms are clearly contributing her loss of function.
Ageing is also a biological process and as we decode the molecular programmes that cause ageing we may be able to develop treatments that reverse ageing. An example of this is metformin, a drug for treating diabetes that has recently been shown to reprogramme oligodendrocyte precursors in older animals to behave as if they were young cells and become more efficient at remyelinating axons. I envisage in the future using anti-ageing drugs as add-on therapies to treat MS.
At the moment we don’t have enough evidence to recommend an add-on treatment for this patient. However, trials are happening so maybe in the next decade of so we will have add-on treatments to slow down or reverse these premature ageing mechanisms.
Finally, we know from other diseases that mood and other social determinants affect outcomes in other diseases and likely play a role in MS. This patient was clearly socially-isolated and depressed. The social-isolation was self-inflicted due to her anxiety about getting COVID-19. Now that she has been vaccinated and with national cases numbers falling she start to get-out and meeting her family and friend again. I suspect she will improve, maybe not back to her pre-COVID-19 baseline, once she starts exercising and reconnencting with the world.
Does this patient’s story sound familiar to you? Have you managed to cope with the lockdown? What have you done to keep going?
CoI: multiple
Twitter: @gavinGiovannoni Medium: @gavin_24211
My MS has been steady for five years and the last four months have shown a relapse and more general symptoms coming up that I haven’t experienced in years. I live with my family but lost my job in October and winters in the UK are depressingly dark. I haven’t been able to go away because of lockdown so daily walks are all that happens for me. It’s definitely taken its toll.
Post of exceptional quality and clarity. Thank you Prof G. I think that before you go to ‘preventive neurology’ you really should write an “MS Wikipedia” or even a book describing all you know about MS. Blog posts are great but they don’t stay.
I really sympathise with the lady mentioned. I really hope that the lady in question gets offered aHSCT. MS is a lifelong quest for knowledge and these are a few things I have pondered and experimented with during lockdown.
1 ) Ketogenic diet with Intermittent Fasting. I fast for 16 hours a day and eat during an 8 hour “window” every day.
2) I have detected that a sugar-free, gluten free, dairy free diet does reduce some MS symptoms.
3) I agree with Prof G that when possible regular exercise (whether outdoor or indoor) really helps. Bizarrely I find this positively affects me the following day.
4) A sense of purpose
5) Social interaction
I have read about the benefits of e-stim in the USA but have no idea what this is. Also I keep reading about the huge benefits of gardening but one would have to have a huge garden with wheelchair access and raised beds surely?
Definitely agree with the gluten-free, dairy-free. I am low sugar as anytime I overdo it with sugar or white rice, the muscle spasms are outrageous. As for the gardening – there are beneficial bacteria in soil that have a positive effect for those who garden bare-handed. A raised bed with some real soil vs. a sterilized bag of potting soil would probably have the same effect as toiling in the ground soil. I would add playing a musical instrument- helps with dexterity, mental alertness, emotional state, memory.
Jane, thank you for sharing your list of tips. These are excellent ways to stay well, with the addition of good sleep habits and meditation if you find it relaxing. Can you recommend a keto cookbook or blog that helps you plan meals? I got a TRX suspension trainer several months ago to exercise at home and cleared it with phiso. And At the recommendation of a friend, I found a yoga instructor video series online that goes at my pace, with good verbal instruction for body placement, and, honestly, doesn’t annoy me to listen to everyday. “Kassandra” . E-stim, or Electric Muscle Stimulation (ems) is in the States for MS, but in very few places. I haven’t been able to access. I think it’s because US insurers want to see measurable gains and permanent results after a short course of treatment. This measurement is not consistent with managing Ms. If you are interested in learning more about EMS, Dr. Whals is a good place to start. She is a strong proponent and credits it in part to her MS recovery. By the way, I found a lot of info on the internet about diy hydroponic gardening, which looks fun to try. Best wishes.
SueBee
I use “The Wahls Protocol Cooking for Life” book for meal planning 😎
Please note the Whals diet is not evidence-based.
Thanks Prof G. I have been trying to get clarity on this from my Consultant for 6 months. That is very helpful.
Thank you Prof G for reminder to verify diet recommendations And your time spent with this blog! And thank you Jane for the cookbook recommendation : I actually have this cookbook published in 2017, but I wasn’t sure if Dr. whals had modified her earlier “whals diet” to respond to critics in this book. She offers 3 tiers: whals diet; whals paleo; whals paleo plus. I’ve cherry picked ideas from it such as Striving to eat 9 total cups of fruits and veggies a day, and how to meal plan. She also gives basic templates for salads and smoothies, with many variations that are easy to follow. Is there a resource or book you recommend Prof. G for Keto? (I apologize if you’ve posted answer to this before, I could not locate. ) And btw, my top notch neuro reflexively rolls his eyes into his forehead at my mere mention of Dr. Whals. Jane, Maybe why your consult is non responsive?!? Dr. Whals is controversial, but really all bad???
For keto, I would recommend the Banting diet, named after William Banting a portly victorian who pioneered the low-carb high-fat weight loss diet. I have been recommended the Real Meal Revolution, which is the bible for the Banting community. In summary, it is a ketogenic diet.
https://realmealrevolution.com/
Prof G,
Thanks for this post.
It confirms what most of us now know – MS is a relentless progressive disease of the brain / CNS. I suspect it ranks alongside Parkinson’s – it’s a slow death sentence (although both diseases progresses at different rates depending on the patient).
Your analysis, I suspect, flatters to deceive. It appears that the different elements driving progression have been identified. I suspect more mechanisms will be uncovered in the years to come. It the really sad bit (apart from the woman’s dreadful situation) is that these various elements driving progression can’t be treated. The sad bits of the post are:
“sadly, we don’t have any add-on treatments we can offer her at present.”
“What we do know is that our standard anti-inflammatory DMTs have very little or no effect on SELs once they have developed.”
“there are many therapeutic targets that still need to be explored as add-on therapies in MS.”
“trials are happening so maybe in the next decade of so we will have add-on treatments to slow down or reverse these premature ageing mechanisms.”
You have to wonder what has been happening in MS research for the last 15-20 years – many of the elements driving progression eg SELs have been known about for some time. This isn’t a dig at Barts, but the xxx MS research teams around the world and the xx,000 MS researchers who turn up at the various international conferences each year. Surely a risk taking team could pull together a trial looking at using HAART and metformin? The lack of ambition to address progression is staggering.
I couldn’t do your job and fully understand why you feel drained after clinic. The case you describe is horrendous in this day and age and the patient’s life is petering out (let’s be honest – would you enjoy such an existence). As you move into MS Prevention, I hope there is a Prof H, I or J who can take on the baton of bringing anti progression treatments to the clinic. If not, I fear that many readers of this blog face a similar future to the patient in the post – a depressing thought,
Sid, part of tackling MS prevention is exploring the viral hypothesis in established MS. So I will be trying to get funding for these studies.
We will miss posts like this when you go Prof and i for one will miss Sid’s replies as well. I would love to see a friendly respectful debate between the two of you. The leading nuerologist questioned by a very informed patient. I would be hugely informative. Can we arrange it before you leave, maybe add a few more of the key contributors. It could be your swansong
Good Morning Dr. G. It Has been a rough year, for us all.
I’d like you to think beyond exercise in this woman’s situation.
I think of Routine. Her Routine have been turned upside down.
Routine is how I get up every day, take my meds, do all my activities of daily living.
This C*vid has thrown our Routines out the window.
Grocery, Doctor office, school, social time, even Seeing people’s full Face to gauge their mood.
I did start a PT program which has helped. Using Apollo neuroscience device to gradually raise my HRV,
Adjusting skin care routine. Virtual visit good for me. Others might need in person exam.
Doctors going through what we all are. Do some self care, too, Dr. We need you.
Could cellulitis (treated with 2 antibiotics) trigger a relapse? If so for how long after the treatment does the risk of relapse remain? How would you know if the cellulitis has completely gone?
The viral hypothesis in established MS is what gives me, with my slow PPMS, hope. Not various add-on drugs.
I’m very intrigued by your idea of using antiviral therapies to treat MS. Do you believe valacyklovir could play a part in MS treatment, considering its impact on EBV?
No it is not potent enough against EBV you need something stronger such as an antiretroviral medication and that is easily capable of crossing the blood brain barrier which do exist today. We do have these medications today but are not being fully tested in multiple sclerosis yet. Here is a link to a case study of a medical student using combivir ( basically it is 2 antiretroviral combined together called zidovudine and lamivudine ) that not only stopped her multiple sclerosis but significantly improved her symptoms. This result is probably due to zidovudine and not lamivudine since zidovudine is a potent against EBV (epstein barr virus ) Here is the study :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6100748/
We present the case of an HIV-negative patient clinically diagnosed with relapsing-remitting MS who achieved significant disease improvement on Combivir (zidovudine/lamivudine). Within months of treatment, the patient reported complete resolution of previously unremitting fatigue and paresthesiae, with simultaneous improvements in lesion burden detected by MRI. All improvements have been sustained for more than three years. This response may be related to the action of zidovudine as a known inhibitor of EBV lytic DNA replication, suggesting future directions for clinical investigation.
People take HAART as PreP to screw around (pun intended) so side effects can’t be too bad. Can I please try it for MS (on my own dime if need be)? What do I have to lose, realistically?
Nice post
What will you do if you were in the patient shoes
Luis,
This is my issue with the type of case presented in Prof G’s post. The woman is watching herself lose function, independence….. yet the MSologist response is “nothing we can do for you”.
I think a different approach is needed – in a decade’s time, this woman could be in a care home or six feet under.
Alpha Lipoic Acid is being trialled (it showed positive results in early trials in reducing brain volume loss) – I would advise her to start taking ALA.
Simvastatin is a drug in trial which showed similar results) – I would advise her to start taking simvastatin.
Metformin is in trial as a potential therapy to encourage remyelination – I would advise her to start taking Metformin.
There is a planned mega trial of drugs to potentially tackle progression:
https://www.mssociety.org.uk/research/latest-research/research-blog/full-steam-ahead-our-mega-trial-progressive-ms
(I hope we don’t have a repeat of the MS Smart trial.
Why not (when the therapies are known) get the patient started one / some of these drugs.
The doctors oath is to do no harm, but doing nothing in the case above is doing harm. Doctors are watching patients go from cane, to wheelchair, to bed, to coffin and using “safety” as the excuse for doing nothing. There must be ways to circumvent the barriers faced by doctors in order to give patients a fighting chance – or at least push back accumulating disability. We must move on from the “wait to the trials are finished” scenario. If a patient wants to take a risk with metformin, simvastatin and Alpha Lipoic Acid the doctors should be supporting them (patients happy to sign a disclaimer so that there is no comeback on the doctors trying to help patients in desperate need without any other options.
While I largely agree, one quetsion:aAs for no harm, do you take ALA? No burning throath/esophagus? Was unbearable for me, maybe I was using it wrong…
I relate to your frustrations Sid.
Yes, we have to advocate for our own satisfactory care, we have to take risks to get meaningful rewards, and we have to think creatively to incite change….. however, I am not sure loading up on various random drugs is the answer. Might end up doing more harm than good. There has to be some basis of safety and efficacy when experimenting.
Unfortunately, none of these agents is likely going to resolve any problems. They may help to slow down deterioration by an unnoticeable amount. We really have no solutions as not even Prof G has a clue what is driving the disease.
I have my suspicions. EBV or HERVs may be two agents driving the disease, which is why we need to explore antiviral therapies in MS.
Excellent post, albeit born out of frustration, explaining what is happening. I feel that my decline is definitely impacted byrestriction related to Covid. However now that the weather is getting better and we have more daylight I feel very hopeful. I was finally able to see one of my doctors in person and it was so nice to have real world feedback.
Yes, I agree with you Christine, I feel Covid restrictions impacted my personal MS decline but the springtime better weather has made me also more hopeful for better times ahead. But I didn’t notice anyone in this post referencing the emotional impact caused by the lack of care shown by “Non maskers” toward the immune compromised. “Looking good” can make my MS invisible to some, causing me frustration on occasion over lack of understanding about my limitations. But I would explain it all away as a lack of understanding. During the pandemic, however, whenever I go in public I am forced to deal with the brazen selfish lack of care by nonmaskers. My immune compromised state is irrelevant to nonmaskers, who do not care if I have MS, and do not respect my personal space while they voice their liberties and callous disregard for the life of others. This has caused me reluctance to go out, great disappointment, and made me feel I have been too generous dismissing those who judge that I “don’t look sick” . The impact of isolation, lack of activity and routine have all taken a toll on my health for sure, as well as disillusionment. Thankfully, there are some caring souls like Prof. G and staff, with plenty of compassion to go around and ability to expose MS for what it is. Very grateful.
A question – is there a trade off between using it and losing it / potentially wearing it out. For instance, I would love to resume my 5 a side football but if the downside was that my exposed nerves were having to work too hard and that was going to make my life miserable in terms of symptoms and then in the future, worn out pathways, I’d settle for a standing spectator role
At the same time the ‘MS lesion’ remains inflamed and some of the chemicals produced as part of the inflammation poison the mitochondria, which are energy factories of the axons. A further reduction in energy production puts further stress on the system.
Enhancing mitochondrial activity in neurons protects against neurodegeneration in a mouse model of multiple sclerosis
https://elifesciences.org/articles/61798?utm_source=content_alert&utm_medium=email&utm_content=fulltext&utm_campaign=29-March-21-elife-alert
Fantastic tour de force article: thank you so much. Power to your own full recovery, Prof G!
Hello ProfG,
The last year has not been easy because of the restrictions placed upon us all by covid. We have all had to adapt in one way or another.
I think everyone’s routine has changed. I have worked really hard to maintain a daily routine such as getting up at the same time going to bed at the same time. It’s only too easy to pick up bad habits.
Exercise, I’m sure this has been really difficult especially for people who are used to getting their exercise from team games. I have advanced MS so I’m challenged in many ways. Since January I have tried to get out for a daily walk and I have challenged myself to do it at least 25 times a month. It’s only a few hundred metres and now a routine, this has made the process of getting out a lot easier.
This pandemic has made social interaction very very difficult. Thank goodness for social media, I am not a great fan of it but it is there so I have taken advantage of it. It is even provided me with new opportunities.
I am lucky, my MS has not declined significantly over the last 12 months. Yup, use it or lose it. Add to that you are never too old to learn new tricks and you have two avenues to survival.
Deconditioning in MS is very interesting. That the lack of using muscles in itself can cause weakness and other secondary impairments. Are MS patients fully aware of this? I’m not sure they are.
It would be interesting to discuss how quick deconditioning can happen.
Yes, MSers are painfully aware! Unfortunately “de conditioning” is a loaded term, suggesting mere lack of activity due to personal choice. Semantically, it is unfortunate that the medical community uses this term since deconditioning in an MSer is caused by a different process than deconditioning in a couch potato. MSers have a very deep understanding of why it hard to be active with this disease, and I think for that reason we use different vocabulary to describe the same phenomenon (unfortunately it is also non precise): lack of endurance, muscle weakness, fatigue, and “bad” day. These are all obstacles to a continuous exercise and a rehab plan. Never mind lockdowns and other pandemic restrictions. The origin of the MSer’s weakness of course is that the smooth flow of nerve impulses needed to do an activity is interrupted by damage done to the CNS by MS. So why would it be I surprising to us that We expend more energy to do an activity and even need to expend more energy to just maintain muscle strength! Thus, When an MSer uses their limited energy reserves to exercise it is in exchange for not doing another activity. If the other activities are employment, grocery shopping, family responsibilities, or even a shower, what needs to give? If this sounds the same as an issue a healthy person encounters when seeking proper life work balance, it is not. Once an MSer’s energy reserves are spent, it’s over, it’s not possible to continue. I’ve skipped showers and folding clothes in order to use that energy for other activities. How do we address “deconditioning” in an MSer, you may ask? First Acknowledge its cause: a damaged CNS makes inefficient muscle recruitment, which drains limited energy stores resulting in MSers becoming less physically active, which further weakens the muscles. A stinking vicious downward spiral. Second, and I feel most importantly, address the cause better. Yes, better. If Physical therapy interventions, as it is set up now, work so well, why do so many MS patients have such a hard time fighting “deconditioning”? what about dynamic maintenance and strengthening of muscles exercise plans using evidence based proven techniques for people with other CNS injuries.? For ex, Perhaps EMS could augment exercise, essentially augmenting from outside the damaged CNS with an artificial nerve stimulus to improve muscle conditioning, as is done with stroke and accident victims. If I’ve got too long winded on this subject, I apologize, well sort of. So called deconditioning is the personal demon I have been battling. I feel many, even medical practitioners sometimes, don’t appreciate MS related muscle fatigue and poor endurance and attribute deconditioning solely to lack of compliance with exercise plans or, ugh laziness. I have had too much time to reflect, done too many professionally taylored exercise plans, and my own self directed exercises that has not improved my strength. I don’t think the word “deconditioned” fully or adequately describes my current physical condition. Do you?
https://multiplesclerosis.net/living-with-ms/bucket-of-disability-ms-or-deconditioning
I came across this discussion, “The big question comes down to are the physical limitations we experience due to our multiple sclerosis or is it from deconditioning? And how do we sort out the difference………..”
” Most of us can use the help of a professional physical therapist to determine what might be in our own bucket of disability and whether it is MS or deconditioning.”
Thanks for this.
However, I hope you will re-consider use of a belittling phrase like ‘wheelchair bound’.
I know this is not the main point but it’s very incidental and casual insertion reinforces and perpetuates misconceptions and disparaging attitudes.
https://www.freewheelintravel.org/please-stop-saying-wheelchair-bound/
A dispiriting but wonderfully-informative primer on what is going on for us and why. Thank you very much for this, Prof G.
I’ve spent the last year exercising (daily walks using my stick got further). This is the first year on tysabri, in 9 years, that I haven’t had a flare. My drop foot doesn’t like it, but I keep pushing. It gives me physical exercise and I see people from outside my household to be social with. It’s been a win for me.
This rings a bell for me. Between diagnosis in 2013 and 2020, I didn’t notice progression and didn’t think about MS. I went to the gym three times a week, socialised and travelled. In August 2020, I had the first new lesions since diagnosis and now notice weakness in my left leg. I think there has to be a link with the stress of not being able to travel home for a year and reduced exercise.