Barts-MS rose-tinted-odometer: zero-★s (black Monday; playing roulette with your patients’ brains)
I recently saw a patient for a second opinion. He was about to start dimethyl fumarate (DMF), but his wife who had spent a lot of time reading about MS wanted him to be treated with something more effective. She had read the MS-Blog (formerly the Barts-MS Blog) and wanted him to have a higher efficacy DMT.
He is only 43 years of age and has had MS for at least 12 years. He had an episode of transverse myelitis when he was 31. At the time his MRI of the brain had no MS-like lesions, but in retrospect, there was subtle brain volume loss; his so-called Sylvian fissures were much too large for a 31-year-old and he had largish lateral ventricles (the fluid-filled spaces in the brain). The clue to the diagnosis of MS was in the spinal fluid analysis that showed the local synthesis of oligoclonal IgG bands; these can now be used in the diagnosis of MS to indicate dissemination in time. This patient was sent away and told to come back if he developed any new symptoms. He did come back with an episode of vertigo and unsteadiness of gait 12 years later. His MRI of the brain was full of MS lesions and he had gross brain volume loss. He was told by his neurologist that he now had relapsing-remitting MS and was eligible for treatment and been offered DMF.
When taking a neurological history this patient had had numerous symptoms that indicated he had had several attacks in the last 12 years. An episode of sharp shooting pains in legs, a period of urinary frequency and urgency, an episode when he had noticed difficulty running with a partial dropping of his right foot. All of these were clearly relapses, which he ignored. The onus of reporting these symptoms had been put on the patient. Maybe things would have turned out differently if he had been seen annually and had regular monitoring MRIs.
On our video consultation, he said he was fully functional, working full-time and had no problems with activities of daily living. This was in keeping with his neurologist’s clinic letter that didn’t mention any abnormal neurological signs and the letter actually played down the MRI findings, by not even mentioning the gross brain atrophy that had been reported by the neuroradiologist on the current MRI.
As I was doing this consultation via a video platform something told me I need to examine this patient. I arranged a face-2-face consultation and when I saw this patient a few weeks later his neurological examination was far from normal. He has jerky eye movement with square-wave jerks indicative of cerebellar involvement. He had bilateral optic disc pallor indicative of optic nerve involvement. He was unable to walk heel-to-toe due to an unsteady gait and he had a positive Romberg’s test, i.e. his body swayed from side to side when he closed his eyes and he would have fallen if I had not told him to open his eyes. He had mild triparesis; i.e. weakness in three out of four limbs. He also had clear cerebellar signs with incoordination in both upper limbs with a mild intention tremor. Finally, he had impaired joint position sensation in the joints of the big toe.
On taking his history again he now volunteered mild to moderate urinary frequency and sexual dysfunction. His wife who attended with him told me that he had had to stop running a few years ago because of exercise-induced left foot drop, which had been getting worse and now was visible after 2-3 km of walking. She also mentioned limb jerks in bed at night, nocturia and that he had become very forgetful and was having difficulty at work.
It is clear this gentleman has advanced MS with severe end-organ damage affecting all functional systems. Sadly he has been let down by the system. He should have been told upfront it is likely he had MS. Just maybe cognitive testing and a set evoked potential 12 years ago would have shown dissemination in space and he would have been diagnosed with MS and treated. Instead, his diagnosis of MS has been delayed by 12 years. Based on his history and examination this paint has secondary progressive MS (SPMS).
Should I label him as having active SPMS and offer him siponimod? Should I say he has highly active MS or rapidly evolving severe MS and try and manipulate the NHS England treatment guidelines to offer him a choice of several high efficacy DMTs? Should I just take the path of least resistance and offer him ocrelizumab or ofatumumab the two very high-efficacy DMTs that can be used first-line in the NHS? Should I not offer him a licensed DMT and refer him for possible enrollment into the high-dose simvastatin trial?
What this pandemic has taught me is that my real skill, which won’t be replaced soon by a robot, is doing a neurological examination and eliciting signs of end-organ damage and then integrating this information with the history, MRI and other investigations. I wonder if the many MS self-monitoring applications that are emerging would have detected and interpreted the clinical examination the way I have done with this patient?
Interestingly, when I examined this patient he told me that his neurologist, apart from getting him to walk and test his eye movements, had not done a detailed neurological examination. This is not unusual in clinical practice; in fact, one of our colleagues at the Royal London Hospital has even argued for us not doing the neurological examination at all as it doesn’t add much to either the diagnosis and/or management of his patients. Do you agree with him?
Christopher H Hawkes. I’ve stopped examining patients! Pract Neurol. 2009 Aug;9(4):192-4.
If you are interested in finding out about what changes to our MS services from the pandemic will stick I suggest you log into the webinar that I am doing later this week with Trishna Bharadia when we will be discussing the impact and changes the pandemic has had om MS services and what I think will change. What is clearly not going to go away is the need for face-2-face consultations and neurological examinations. But then this is referring to my take on things and I may not be correct.
General Disclaimer: Please note that the opinions expressed here are those of Professor Giovannoni and do not necessarily reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust.
A scary example of how not to be diagnosed and managed if you have MS. Does this patient have a legal case against this neurlogist?
No legal case. This case will be assessed in the context of how MS was being managed in 2009. With the MRI and CSF, this patient did not fulfil the diagnostic criteria of MS and hence would not have been eligible for DMTs. Asking the patient to come back to see you when they develop new symptoms is reasonable and is probably standard neurological practice in the NHS, particularly in 2009. Monitoring MRI was not routine in 2009 and is still not mandatory in 2021. The management of this patient is what MS and MS-like conditions such as transverse myelitis / CIS were managed in 2009 and in many other places in 2021.
Do you agree with Prof Hawkes?
No. This is the letter I published with Professor Vivian Fritz, my mentor, from South Africa.
Gavin Giovannoni & Vivian Fritz. A plea to neurologists, especially privileged British neurologists. Published on: 1 March 2010
Sometimes it is necessary to make a point with overemphasis and we believe that was done in the letter by Chris Hawkes. We agree that it is essential to talk to a patient and to watch them and observe how they speak, what they are saying and what they are doing with their body as they walk in and out of a room. However, to exclude the examination is a form of conceit. The only reason that a very senior neurologist can observe so much is from a long period of diligently examining all patients and slowly learning shortcuts by pattern recognition. But you can’t teach neurology that way. Students must first be taught the discipline of a routine in order to learn which part of the routine can be discarded in individual patients. When a TIA is caused by atrial fibrillation a finger on the pulse will lead you to the ECG as the first test. A stethoscope on the neck will suggest that a Doppler should happen immediately. When resources are limited (which occurs in much more than half the world) it is important to direct your tests sensibly rather than blindly ordering a battery. If a student can’t distinguish between an upper and lower motor lesion then the differential of a paralysed limb trebles and an EMG, as well as an MRI, needs to be done routinely. We are not against spending more time talking to a patient, even if it means less time examining, but don’t eliminate the examination. It’s like throwing the baby out with the bathwater. When in doubt the most cost-effective investigation is to retake the history and to examine the patient. We mustn’t forget that an essential part of any consultation is to gain the trust and respect of the patient; if a patient doesn’t trust the consultant they are unlikely to accept the diagnosis and treatment plan. We have all seen patients for second and third opinions when completing the examination they compliment you on how thorough you have been and inform you that their previous consultants hadn’t bothered to examine them. The “laying on of hands” is as essential to today’s consultation as it was in the past. In today’s litigious environment not examining a patient would be welcomed by the opposing legal team with glee. We doubt any expert witness would support the notion of not examining a patient as standard clinical practice. In the new era of revalidation admitting to your peers that you do not examine your patients would be inviting an early retirement or a change in career.
This neurologist needs to be named and shamed. What did you tell this patient to do about how they had been managed?
Not sure what naming-and-shaming will achieve. Isn’t it better to invite this neurologist an MS update and get them to buy into the ‘Time Matters in MS’ concept? I have no desire to shame this neurologist who I know quite well. He like most of us is overworked and doesn’t have much bandwidth. I have copied him into my letters so that he will be kept up-to-date with my thinking. I will also be referring this patient back to the local team for treatment and monitoring.
I fear this is a common scenario…..at the time of my own ‘CIS’ diagnosis, my brain scan identified several non-specific lesions and was considered to be in the borderlands of normal. There was a clear lesion at T5 but with a normal brain scan i was told to forget about it and go and enjoy life. Good news to someone with no previous health conditions and with the confidence that nothing bad would happen to me. Roll forward 5 years and a second event eventually led to a diagnosis but not before a third. My new neuro (the old one retired) looked again at my scans from 2015 and agreed the white spots in the brain were ‘non-specific’ and that lumbar punctures were not routinely requested until 2017. However, my trust has gone. I read posts like this and think that even without the benefit of hindsight, you may have been able to find enough to confirm a diagnosis or at least carry out further investigations. The mentality of some neurologists is the part of the problem for me. My old nuero couldnt wait to get me off his books. Treat early and effectively couldnt of been further from his mind and now i feel that i am living with the consequences. I blame myself to a degree….for not pushing harder…..at the time though, i paid privately for scans twice when the NHS referral was refused so it felt like i had forced the issue
“Should I label him as having active SPMS and offer him siponimod? Should I say he has highly active MS or rapidly evolving severe MS and try and manipulate the NHS England treatment guidelines to offer him a choice of several high efficacy DMTs? Should I just take the path of least resistance and offer him ocrelizumab or ofatumumab the two very high-efficacy DMTs that can be used first-line in the NHS? Should I not offer him a licensed DMT and refer him for possible enrollment into the high-dose simvastatin trial?”
Prof G,
Surely the question is the other way round. What does the patient want (I’m assuming to reduce end organ damage and to really slow down further progression) and then identify the treatment that is most likely to achieve this. The patient won’t have a clue as to what to select from the handful of possible choices listed above.
As a physician, do you not think “what would I do if I was in this position given all the knowledge I have about the effectiveness of current treatments and ongoing trials?”
If the real MS is smouldering MS I’d likely steer the patient to an Anti-CD20 therapy, but pushing for inclusion in the DoDo or Sizomus trials (although with trials brings the risk of the placebo arm). I’d don’t envy your position, but as a patient I’d be asking “what would you do in my position doc?”.
Sid, I assume you understand what playing ‘Devil’s advocate’ is?
I will let you know in due course the diagnostic label and the treatment approach this patient has chosen.
A real eye-opener for me.
The first part of this gentleman’s story is eerily similar to mine. An episode of INO in 2011 and then looking back an episode of numbness in my leg a few months prior, all led to a diagnosis of MS. However MRI completely normal at this stage and so I was also diagnosed by lumbar puncture.
Told it was mild and I may never have another problem. Advised to go and have my family (which I did….3 kids later!). Then after 8 years of nothing (and for me at least, genuinely nothing) I had a mild-ish relapse but luckily ended up on anti CD20 quickly this time as there were now lesions on MRI.
I am happy to have had a full neuro examination twice by my team and am fully functional with zero issues. My MRI is also ‘much improved’ after this treatment. However your story makes me wonder about brain volume loss and whether we could ever truly say my first MRI was normal?
Food for thought.
A normal neurological examination doesn’t necessarily mean your nervous system is normal, i.e. undamaged.
The problem actually is likely to go back further in the patient’s history.
If a person is generally fit and healthy and only minded to bother their GP in extreme circumstances, it is very unlikely they will be referred to a Neurologist before they have accumulated a fair number of symptoms. With GPs operating a phone triage system will this be even worse?
I have never seen why (unlike most diseases) the rate of new cases occurring decreases with age? If it was strongly genetic, then the pool of people would become smaller. Is it being under diagnosed in the older population because it is easily confused with symptoms that occur with age? Or is it because it is primarily associated with young women?
I know that some of the control brains dissected by the MS Society Tissue Bank have had pathology that suggested MS.
Dr Google does not automatically flag MS and almost any symptom can be attributed to MS.
As my MS was not described as rapidly evolving, I was only offered a limited set of options. This meant I didn’t need to consider the trade-off between more effective and increased risk of side effects. I do not think any of the DMTs would be taken lightly. Perhaps personalised prescribing will come, but I did not see any treatment that guaranteed no progression at no risk
If I had been better informed 4 years ago or under a different consultant would I/he have gamed the classification? My natural disposition is to do nothing or as little as possible, which explains why I seldom bothered my GP. This way of thinking is fine for a viral infection, but not for MS.
If this patient was categorised as RES MS would they not qualify for alemtuzumab? i thought i had read this in a recent post. Also, at the point he has reached….would alemtuzumab even be an effective treatment option? alongside HSCT it is considered to be the most effective DMT at normalising BVL and stopping the smoulder but as it does not penetrate the CNS, how does this even work for a patient with well established disease?
When I was going thorough the diagnostic treadmill the one experience that really struck me as defining was the neurological examination. I had eye signs, balance problems, lost reflexes and parasthesia of which I was unaware. This left me far more informed and led to a much better understanding of where I was. Losing the physical examination would remove the list of real phenomena which MRI’s can’t reveal as well as the intangible benefits of the hands on experience.
Theres no point in the bloke in the phone exchange telling me everything is fine if the bloody phone doesn’t work!
This patients story sounds awfully similar to my own. I was diagnosed in 2009 following a period of numbness in my torso, MRI found a number spinal and brain lesions at that time. I wasn’t offered any DMT and was told to go away and live my life while I could so I basically ignored every symptom from there on. I took myself to a different neurologist in 2019 when I couldn’t ignore the symptoms any longer and have since joined the simvastatin trial but I can’t help wondering what would be different if I had of been seen by a doctor during this time. Would I be deteriorating at this speed? Would my long term prospects be any better? I am considering HSCT as a last chance solution but it’s possibly too little too late.
“Would I be deteriorating at this speed?”
“considering HSCT as a last chance solution but it’s possibly too little too late.”
It does a good job of stopping progression in spms from all anecdotes…so it may be worth it.
Only way to know is to try it though.
Simvastatin at best will be moderately neuroprotective. It probably won’t do anything significant at all if it isn’t layered on top of an effective anti-inflammatory.
I think it’s insane that you weren’t put on a DMT in 2009, by the way. That really sucks.
I can write a real sad story about my second opinion, but I choose not to do that. This neuro prof set his kitchen alarm clock and kicked me and my mom out as soon as the clock did triiiing!
You know who you are!
Professor G,
I know I sound like a “broken record” that plays over and over again. Since I am in the USA and have access to all MS DMT’s, I know your hands are tied by the NHS MS Guidelines. As in my previous response to your recent 2nd opinion post, are you able to use injectable generic Cladribine, assuming you do not have access to Mavenclad as I do?
This patient has PIRA, as most patients have, beyond the 10-12 years of the “big peripheral burn”, after obvious MS presentation(not the often overlooked and retrospective subtle smoldering MS before MS dx). The large monoclonals do not adequately penetrate the 3 compartments of the CNS and trials were negative for SPMS expect the modest effect of Sipinomod in “active SPMS “. In my opinion, B cell depletors do not take out enough dim CD20+ T cells to halt progression. I think the terminology “active SPMS”, based on relapses and Gad+ MRI, is infrequent, as “active SPMS” in my experience is smoldering PIRA and also independent of Gad+ MRI lesions.
Cladribine has the proper MOA, small size, CNS ( end organ )penetrant, relative safety ( selective immune reconstitution therapy), rebooting into a self tolerant immune regulatory environment over the short, intermediate and long term. It has a durable long lasting MOA to stop progression, with about a 25% chance of slight motor and cognitive improvement, based on my 50-60 SPMS patients having been through monoclonals, fumarates, S1P’s and injectables I transitioned to Mavenclad. . I also think Fingolomod is the more effective S1P because of S1P( 1,3,4,5 ) compared to S1P (1,5 )agents, which is another discussion, based on the numerous S1P receptors on neurons, glia and the BBB.
Clifford Reed MD — Reading, Pennsylvania
“but as it does not penetrate the CNS, how does this even work for a patient with well established disease?”
No..alemtuz does not work in sp…cause b cell follicles are already in brain…and being large
molecule alemtuz does not get into the brain.
hsct gets into brain and is only hope to rid brain of follicles… to normalize brain loss and stop progression/smolder.
“Since I am in the USA and have access to all MS DMT’s, I know your hands are tied by the NHS”
You seem only u.s. neuro ever posting here..or anywhere in the world neuros…for that matter.
“based on my 50-60 SPMS patients having been through monoclonals, fumarates, S1P’s and injectables I transitioned to Mavenclad. ”
Does Mavenclad stop their progression..? what percentage..?
Its a bit late to protect, but not late to salvage & protect. emphasis on regaining function and protecting it. Not sure what the optimal process whether is be the high eff DMTs, simvastatin or siponomid.
This tale is very familiar to my own experience. Despite eventually getting an MRI confirmed MS diagnosis, the subsequent extremely poor management of my condition, meant vital potential treatment years were lost. It wasn’t until a second opinion and very skilful neurological examination I got some sensible answers. By that time I found myself with SPMS, lost upper and lower limb function. I’m very concerned by the move to routine telephone appointments, forced by Covid, but I suspect perpetuated by economics and the increasing burden on neurologists from Long Covid patients. Yet again are MSers going to find themselves at the bottom of the heap.
Out of interest what is the reason he is considered SPMS? Especially as ‘he said he was fully functional, working full-time and had no problems with activities of daily living’ (however it sounds like he was downplaying that anyway)
Progressive weakness in the lower limb with exercise-induced foot drop; a few years ago it came on when he was running in now comes on after walking. In addition, he has developed weakness and spasticity in his legs, bladder and sexual dysfunction, cerebellar and balance problems all of which don’t appear to be relapse related. Although this is on history it hard to draw any other conclusions. However, the strict clinical definition requires confirmation at 6 or 12 months, which allows you a window to still label this as relapsing MS and not be called a liar.
That makes sense. Thanks for explaining!
In answer to the question of my 50-60 Cladribine ( Mavenclad ) patients who had progressed ( smoldering SPMS ) on all classes of prior MS DMT’s, 100% of my transitioned Cladribine (Mavenclad) patients stopped progressing after primarily the first round of Mavenclad (year 1 ) and about 25% ( year 1 ) had slight motor and cognitive improvement, based on patient reported cognition, and motor improvement, based on my sequential motor exams. I am sensing that these parameters of progression will be even better after the final round 2 ( year 2 ) of Cladribine( Mavenclad ). Professor G is the world’s expert on Cladribine, along with his colleagues, and I fully expect the scientific Chariot Trial( Cladribine in SPMS ) with Dr. Schmierer, et. al. will show the results I have found outside of a clinical trial in my 50-60 Cladribine( Mavenclad ) at the bedside that I have shared with you.
Clifford Reed MD–USA
If Cladribine is so effective regarding progression, why don’t we see that in the original trial?
“During the 96-week study, there was a relative reduction in the risk of 3-month sustained progression of disability in both cladribine groups, as compared with placebo, with a 33% reduction in the cladribine 3.5-mg group (hazard ratio, 0.67; 95% CI, 0.48 to 0.93; P=0.02) and a 31% reduction in the cladribine 5.25-mg group (hazard ratio, 0.69; 95% CI, 0.49 to 0.96; P=0.03) (Table 2 and Figure 1D). There were corresponding increases in the odds for remaining free of 3-month sustained disability progression in both cladribine groups, as compared with placebo (P=0.02 for the 3.5-mg group and P=0.03 for the 5.25-mg group) (Table 2).”
It’s something but nowhere as spectacular as your claim (and IIRC not quite competitive with ocrelizumab) . Is it something about SPMS? Especially considering SPMS has been a far tougher nut to crack than RRMS… I know you did not do it in the context of a trial, but it would definitely justify a serious posthoc study.
In the high-activity group at the licensed dose, it reduced disability progression by 82% compared to placebo. This is why it is considered a high-efficacy DMT.
Giovannoni et al. Efficacy of Cladribine Tablets in high disease activity subgroups of patients with relapsing multiple sclerosis: A post hoc analysis of the CLARITY study. Mult Scler. 2019 May;25(6):819-827.
Background: In the CLARITY (CLAdRIbine Tablets treating multiple sclerosis orallY) study, Cladribine Tablets significantly improved clinical and magnetic resonance imaging (MRI) outcomes (vs placebo) in patients with relapsing-remitting multiple sclerosis.
Objective: Describe two clinically relevant definitions for patients with high disease activity (HDA) at baseline of the CLARITY study (utility verified in patients receiving placebo) and assess the treatment effects of Cladribine Tablets 3.5 mg/kg compared with the overall study population.
Methods: Outcomes of patients randomised to Cladribine Tablets 3.5 mg/kg or placebo were analysed for subgroups using HDA definitions based on high relapse activity (HRA; patients with ⩾2 relapses during the year prior to study entry, whether on DMD treatment or not) or HRA plus disease activity on treatment (HRA + DAT; patients with ⩾2 relapses during the year prior to study entry, whether on DMD treatment or not, PLUS patients with ⩾1 relapse during the year prior to study entry while on therapy with other DMDs and ⩾1 T1 Gd+ or ⩾9 T2 lesions).
Results: In the overall population, Cladribine Tablets 3.5 mg/kg reduced the risk of 6-month-confirmed Expanded Disability Status Scale (EDSS) worsening by 47% vs placebo. A risk reduction of 82% vs placebo was seen in both the HRA and HRA + DAT subgroups (vs 19% for non-HRA and 18% for non-HRA + DAT), indicating greater responsiveness to Cladribine Tablets 3.5 mg/kg in patients with HDA. There were consistent results for other efficacy endpoints. The safety profile in HDA patients was consistent with the overall CLARITY population.
Conclusion: Patients with HDA showed clinical and MRI responses to Cladribine Tablets 3.5 mg/kg that were generally better than, or at least comparable with, the outcomes seen in the overall CLARITY population.
Thanks, much appreciate the pointer.
Will look into the study over the weekend.
More data on Dr Reed’s patients would be most interesting, in any case.
“the lower limb with exercise-induced foot drop; a few years ago it came on when he was running in now comes on after walking. ”
Foot has to be floppy/weak for foot drop….This is typically spasticity
caused by tight ..gastrocnemius, soleus, and posterior tibialis in back of the leg. The muscles are in extensor spasticity which point the foot down and turn the foot in or invert the foot. Makes it impossible to lift the leg and dorsiflex
the ankle/foot to walk. Exercises that statically keep the joints from extending is how you treat it. This spasticityis what leads to hyperextended knees also.
It’s ok we’re all still learning here.
https://orlandoneurotherapy.com/stroke/leg-spasticity/
Are these exams standardized?
When my GP sent me to the hospital, I got a very extensive one by a young doctor/student(?) in the ER. Another doctor in the hospital gave me another, shorter exam a few days later.
The first neurologist I saw gave me yet another exam that was pretty close to the one in the hospital. Since I didn’t like him (he was hell-bent on getting me off Tysabri and onto Tecfidera), I switched to a different neuro. She does a brief exam every time I visit that’s close to the second one I got at the hospital.
That’s 4 doctors, 3-4 different sets of tests. I don’t have an issue with that, but I wonder why they have these vastly different approaches.
Hi Prof G, such a sad story but all too familiar and in particular with my own diagnosis too! When you’ve gone through the mill with all the tests, probabilities what is could be and having contacted Dr Google – you found yourself completely overwhelmed & very frightened that some of the symptoms (problems) that you have overlooked and just got on with life, becomes so important and relevant. If you are trying to hold on to your job full-time and have a young family (especially) that you have to try and come to terms with what is going on in your body. You are so grateful to get across the line, just to visit a Neuro and for those who do not have the contacts or the well health to pursue a 2nd opinion – you have to allow the process to go ahead. If you start reframing, re-organising and give more time to spend it with your patient to do a thorough examination and to allow a support network to takeover once that patient has been seen by you – would help keep the communication, support, care and patient/doctor relationship more invested in and hopefully, achieve a better way forward for the future care of your patient. My own Neuro – sent me away for 1 year with CIS but I also had a whole year prior waiting to be seen by someone. So you can imagine my response when I finally got an appointment! I guess, I don’t know – if there are lucky (not sure if that is the right word) but only have CIS or possibly a lesser destructive type of neurological disease. I look back in my life and can say after quite a few strange neurological symptoms, that I just shrugged off, as I though it was just me or my age – that could have been the first episodes or the disease and it was festering away, way before I was diagnosed – which has left me in my mid 50s, with daily horrible pain, difficulties with mobility, urology problems, probable but no link given, heart problems, spasticity, weakness, confusion, lack of ability to multi-task (I used to be able to juggle and have a great conversation 🙂 – the list goes on. Along with menopause, dmt side effects and huge weight problems – that I can’t seem to shed! My head feels like its been possessed – and paresthesia all over my face, head and fingers and feet! If neurological appointments aren’t stand practise to do all the tests (obviously if this person shows various neuro problems). TIME is not on our sides – if for a change this type of diagnosis and given the length it takes for a patient to visit GP/HCP – then to be referred, it would give this person a greater chance if they are started (in agreement) on a DMT. Even it is one the would help to delay any further attacks. Then start to discuss/educate the patient as to the best options (DMT) diet, exercise and so on. Appointment – Support – Care (interdepartmental communication) Physio (mandatory if in agreement) & ongoing conversation about urology, bowel, diet & optical and so on. All talking together, communication from a central hub and access when you need – not taking over weeks to see someone who then makes a telephone consultation. Of course, sometimes a telecon will be fine if its a general update and meds check but not when it comes to seeing a patient with a full on MS/Parkinson/MND etc – they/I don’t have TIME. Co-ordination, understanding & trying to establish a relationship that will help all sides make the most of TIME.
Take care and good to hear from you and please get all Neuros/HCPs to re-boot their MS knowledge and communications with their patients.
I was diagnosed in 2018 under private healthcare and transferred to NHS in 2019. I have seen my neurologist once in 2019 and based on the initial MRI it was decided no treatment was necessary.
I was invited for an MRI in 2020 and told in a telephone appointment that two new lesions meant I should think about starting treatment. I was only offered Plegridy.
I asked to start on Ocrevus but was told this wasn’t possible due to Covid. I asked if I could start it after being vaccinated and was told I could, but having been vaccinated am being told Plegridy is still the only option.
I don’t have many outward systems of MS currently, ON twice. But, I do feel there are things going on in the background.
I don’t know what to do. It feels like the relationship with the neurology team is poor and I’m worried about not being on any treatment. I don’t want to start Plegridy as my concern is disability progression and I feel like once started it would be even harder to get on a more effective treatment.
Can anyone offer any suggestions?
Thanks
In the NHS in England if you have active early MS and are naive to DMTs you are eligible for interferon-beta, glatiramer acetate, teriflunomide, dimethyl fumarate and anti-CD20 therapies (ocrelizumab and ofatumumab). These are NICE approved and greenlighted by NHS England, which has a legal obligation to allow access to these treatments.
Thanks for your comment. It’s not clear why Plegridy is the only option but it seems to be a combination of Covid and the cost. My concern is that it doesn’t seem to be based on my specific condition, I’ve only seen the neurologist for a short consultation once two years ago. Looks like I’ll need to try and switch neurologists
“It feels like the relationship with the neurology team is poor and I’m worried about not being on any treatment. I don’t want to start Plegridy as my concern is disability progression and I feel like once started it would be even harder to get on a more effective treatment.”
Yes..you are correct in your concerns and your neurology team seems like they care
nothing about you and your health. Get out of there and get new people.
Alemtuz and hsct are only dmt that get you to normal brain loss.
Ocrevus does not…As long as you have abnormal ms yearly brain loss you will progress.
There are pay clinics all over the world that do hsct.
One just opened in Bulgaria by Israel trained doctor…So if you can’t get hsct in u.k. in 2021
it’s not good.
Thanks for your comments. It’s not clear why Plegridy is the only option but it seems to be a combination of Covid and the cost. My concern is that it doesn’t seem to be based on my specific condition, I’ve only seen the neurologist for a short consultation once two years ago. Looks like I’ll need to try and switch neurologists
“My concern is that it doesn’t seem to be based on my specific condition,”
You have ms like everyone else you need the best treatment from day one.
That is for now alemtuz/hsct…although cladribine too might fit the bill.
At a minimum you should get cladribine…Plegridy should be outlawed
so people like your neuro can’t harm people with it.
at 5:00 he is speaking to newly diagnosed
Vlog: Take MS Shots OFF the Market!
Therapeutic Inertia is Worsening Your MS
[youtube=https://www.youtube.com/watch?v=GccRVJZTuKI&w=720&h=405]
I guess the neurologist can tell a lot in a face to face appointment without examining the patient. Including watching the patient entering/walking into the consultation room, watching for jerks, twitches, weakness, gait, foot drop, shaking of head and limbs. Looking at the patients face. If the neurologist is familiar with the patient already and has met them face to face before, then I guess bypassing an examination could be ok but not great. If an appointment time is very limited due to a full clinic, then a discussion between neuro and patient might be more valuable than an examination on some occasions.
I’ve thought a lot about this patient over the last couple of day. Having now read all the comments I’ll add my voice to the ‘this was me’ shout. My heart goes out to him.
Re diagnosis and dmt: I’m minded to go with active SPMS; siponimod and STAT2 trial (yes, trial permits siponimod).
Or, as you say, take advantage of the diagnostic window and go for RRMS and ocrelizumab.
I reckon you should be honest and explain these options to this gentleman and let him decide. If you prefer one over the other then say so but leave choice to him and his wife.
As an aside:
Being on a trial can bring many other benefits apart from the 1 in 2 chance of taking the active medication eg 6 monthly monitoring, meeting other trial members, and sense of worth.
Would this gentleman be happy for you tell us the outcome? (Assuming he is real and not one of your litersry licence stories?)
Re: “he is real and not one of your literary licence stories?”
He is real, but the details of the case are changed to anonymise it. I can think of many other real-life patients with similar histories; this scenario is quite common.
Yes, reading comments here sadly shows how common.
He has been diagnosed as relapsing-MS and is mulling over a choice between DMF (dimethyl fumarate) and ocrelizumab (anti-CD20) with the recommendation of the latter. In an ideal world, I would like to have given him a few more options.
Did he consider hsct..?
I guess only you as neurologist can call the diagnosis… patient can’t pick which one he’d prefer! As you say you don’t have evidence of recent progression… all the things from the past may or may not have been incomplete recovery from relapses? Besides, SPMS and siponimod are a one way street…
In my (biased from experience) opinion the risk of long term lymphopaenia with dmf is not worth the moderate gains. Seems crazy to preclude possible future treatment with something way better.
Good recommendation for ocrelizumab and all the very best to the anonymous pwMS 🙂