What is the current state of play regarding Sativex? Is it still being prescribed or has NICE effectively killed it off in the UK by deeming it "not cost-effective" and advising against prescribing it?
Also, what do MS clinicians and researchers think about the UK Government's rejection of the recommendations of the All-Party Parliamentary Group for Drug Policy Reform’s 2016 report ‘Accessing Medicinal Cannabis: Meeting Patients’ Needs’ ?
(For those who may have missed it, the Government's response to this comprehensive report was:
"Cannabis is controlled as a Class B drug under the Misuse of Drugs Act 1971 and, in its raw form, currently has no recognised medicinal benefits in the UK. It is therefore listed as a Schedule 1 drug under the Misuse of Drugs Regulations 2001." )
I'd be interested to know if any clinician or researcher who has read the report actually supports the UK Government's stance?
It is not cost-effective based on NICE assessments, but I think NHS wales may have supported its use.
I don't know the report however it is irrelevant what we think and we are conflicted as we are developing alternatives to cannabis.
"Cannabis has no recognised medical benefit" is clearly not supported by the view of the EMA otherwise it would not have been licenced as a treatment for spasticity. Sativex is an alcoholic extract of cannabis.
There are over 20 states that support medical use of cannabis.
If you remember that David Nutt the Government drug tsar (goverment science advisor) was sacked because he did not support the reschuding from class C to class B by Gordon Brown.
In the late 1990s I attended a meeting at Westminster sponsored by the Association for Cannabis Therapies, asking for decriminalisation for therapeutic use in MS. We were told this could not happen as there was evidence of neither safety nor efficacy; but such evidence could not be obtained as the drug is illegal. The softener was advice that an approach to the Home Office to undertake a trial would be favourably received. Of the doctors at the meeting, two of us got on with our jobs, one died, and the fourth set up a company to address this problem, and that led to the development of Sativex. The problems with Sativex, I think, are firstly its high cost, and secondly the lack of convincing benefit in clinical trials. The paradox is that to undertake convincing clinical trials would be expensive and therefore make a price cut unlikely. Some MSers tell me that cannabis, in its various forms, helps their symptoms and I believe them. I suspect that only a minority achieve this benefit and that is why the trials have been disappointing. N.B. this is use for symptom relief, not disease modification. There is also a problem with delivery of this non-water soluble drug: hence the Sativex spray; if a reliably absorbed oral formulation could be achieved, this should reduce cost. Of course the medical establishment could not condone a smoked drug!
I have already posted this question, but saw no reply so again….. it has come to my attention that Blueteq exists and will actually restrict neurologists from prescribing expensive drugs for MS in some instances where a neurologist previously would have. For example, wheelchair users will be exempt from most treatments regardless of how their MS actually presents and even if the reason they are in the wheelchair is predominantly not MS related. This can also mean that a drug will be stopped despite the patient already receiving it. Is there a team of people arguing this change? Reply
I have no real knowledge about blueteq http://www.blueteq.com/ but it is easy to read between the lines. This is a means to cut people of (expensive) treatments… you put in criteria and when met it will say stop. These guidelines already exist with NICE but if you us an IT solution there is not going to be grey and compassion just black and white
You would need to ask the Department of Health etc.and the UK MS Society for comment and when enlighted you can come back an tell us.
I am not a medic but working in IT am very aware that looking at problems from a different perspective can sometimes enable you to draw new conclusions.
All MS research centres on the evidence that the disease is an attack on the Myelin sheath from the outside of the nerve – a belief that dictates all research into possible treatments and draws the majority of research funding every year. What if the attack first comes from inside (as it does in some other diseases) resulting in demyelination and axonal damage starting in the axon?
Surely this would create the potential for a low cost and simple cure – the ingestion of the pure antigen (non-myelin) in order to de-sensitise the patient to the auto-immune response? I believe the principles behind this have been tried by the MS researchers in Harvard without success, but their approach was based on the belief that the attack is from the outside and involves the ingestion of myelin.
Has the ingestion of non-myelin approach been investigated, and if so could you point me at the results?
If it has not been investigated, could you explain in simple terms why the "inside out" approach has never been considered?
The ingestion of myelin didn't really work in sensitised animals so i think the approach is no good.
If you view autoimmunity as the problem even if it starts inside the effect is outside in because now you have a glymphatic pathway. The inside out started because of looking at pathology
We have fed total spinal cord to animals and it does not stop established disease hence being a sceptic
I understand your skepticism and your answer raises 3 points that I would like to explore:
MS causes thinning of the retina – measurement of inflammatory cells and thinning in the retina being used to determine the progress of the disease. However, the retina does not contain Myelin. MS is considered to be an autoimmune response to a myelin antigen. Because of the retinal pathology, could a non-myelin antigen be present which affects the axon? https://www.facebook.com/notes/ccsvi-in-multiple-sclerosis/retinal-thinning-and-ms-why/10151303448922211/
I presume the glymphatic pathway operates at pressure to remove dying cells from the axon? If the axon is damaged there will be more dying cells and would it not operate at a higher pressure to ensure removal? If the glymphatic pathway is pressurised and flows away from the axon, would T cells be hard pressed to reach the source (in the axon) and attack the next best thing – the myelin sheath.
Ingestion as a means of de-sensitising animals does work, as the Harvard Study proved. It also works for allergy de-sensitivity so my face does not explode when I eat a peanut. However I could see why feeding total spinal cord (myelin, non-myelin and other cells) would not work as the non-myelin would be too dilute to have any effect.
The thinning of the retinia is due to die back of demyelinated/myelinated nerves in the optic nerve so the fact that nerves in the retina are demyelinated is irrelevant.
I think the glymphatics are a mechanism to clear the effects of a day's brain activity. I.e remove the rubbish. It is like a toilet flush to clear the crap of memories during the day. So pressure of the system is not relevant.
Ingestion as show by Harvard actually did not work in humans and the animal data was not great either. Feeding spinal cord would have have the relevant targets as we could have great effects with intravenous delivery. Simple fact was the oral route was pants and the idea was dropped a decade ago.
I am afraid as an engineer I do not understand why you believe the absence of myelin in the retina is irrelevant?
https://academic.oup.com/brain/article/134/2/518/401472/Primary-retinal-pathology-in-multiple-sclerosis-as shows there is no myelin in the retina, which is principally composed of unmyelinated axons. How can MS be an autoimmune attack on myelin, when the retina is affected and contains no myelin? MS could in fact be triggered in the Axon / non-myelin, a premise which logic and science (not to mention curiosity) demands investigation. Can you explain why there there has been no research into this?
The optic nerve is heavily myelinated and is where you see inflammatory demyelinating lesions. This can cause nerve atrophy which moves back in a retrograde manner towards the retina causing thinning of the retina.
Your answer appears wedded to the view that MS starts with an attack on Myelin and then affects everything else.
Could you point me to the evidence MS always starts with an autoimmune attack on the Myelin sheath, never attacking the axon in the CNS, in 100% of cases (which is the only evidence that supports your view)? In the absence of such evidence your position is illogical, bordering on dogmatic. It is also directly contradicted by the authors in Brain 2001; 134: 518 who “identified an unique subset of patients with multiple sclerosis…. which may be occurring as a primary process independent of optic nerve pathology”
2011 BTW. Not wedded to any view really. John Prineas, a while back suggested oligodendrocyte death was a primary event in MS, before the development of inflammation. It might be possible that the retinal thinning is linked to brain atrophy in response to inflammatory events, which may be sub-clinical and perhaps this particular group are particularly susceptible to this. In the main though, optic neuritis, often a primary indicator in the development of MS is seen before retinal thinning. You also find myelin in grey matter too (at lower levels), which was dismissed in the past.
I kept reading last year that there is a shortage of MS nurses in some areas in the UK. Is this still the case? I know there are some pwMS who feel they do not need to see an MS nurse.
Afternoon all!! I know Prof G likes cladribine but what if your not suitable for it? What alternative is there? It seems like lots of progress is being made in the field of MS but PPMS still does not see it filtering down to patient level. I love my OH and wish there was some good news for him. Any chance that the EBV Pender stuff might mean a clinical trial here in the UK? Can Barts be involved?
They had planned it on June 10 at church house but when we told them it was the Queens birthday and trooping of the colour it was delayed until the autumn. I do not know of any dates.
It is interesting, what is it would specifically cause women to have their B cells changed, or would T-bet transcription factor be modified in women? Could it be hormones, or a hormonal change, or some genetic difference between genders?
What is happening during sleep when the CNS creates sensations such as vibration in the spine or loud bangs and the feeling that neurons are firing off in all directions in the head? Or realistic sounds outside the body, like a door knocker, that aren't actually happening?
In sleep the brain is partly or largely disconnected from the body: the extent of this disconnection depend on the sleep stage. Sometimes, there is unusual reconnection and this causes the phenomena you are describing which are known as parasomnias. A simple analogy would be to observe the engine of a car revving when the clutch is depressed. Common parasomnias include sudden jerks on the brink of sleep, or sleepwalking. The brain needs some disconnection time to repair and regenerate. I see many people who get together in middle age and come to clinic saying "you wouldn't believe what (s)he does in sleep".
Perhaps some similarity to sleep paralysis? I "awoke" once convinced there was a hairy person in the bed next to me who was not my partner. I spent a few moments terrified, unable to move, trying to work out how they had got into my flat/bed unnoticed.
Am aware of people describing micro dosing LSD as improving their performance. Has anyone researched micro dosing to see it has an effect on MS fatigue?
Some of trains in my area do not have toilets (not tube trains). The train journey I take can be 25 mins long and the only option is to get off the train at the next station, if I need the toilet. Then not all train stations have toilets. This is the kind of thing I have to plan when I go out for the day.
To our resident troll. Save your effort, none of your silly little comments will get past moderation. I'm sure you have better things to do with your time.
But it seems that the patient had previously treated with Natalizumab, which may represent a problem if you wish to transition from Natalizumab to Ocrelizumab. We could have a real treatment against PML, it would facilitate and much the treatments themselves.
Is treatment with alemtuzumab associated with hair loss? Started to lose my head hairs right after first dosage of alemz three years ago. And this only intensifies with time
And any thoughts of safety of minoxidil in ms? it is said it has some systemic bioavailability and activate potassium channels which is not so good I believe
Yes. In the INN for alemtuzumab alopecia is listed as a common side effect. As alopecia is an autoimmune problem it must be one of the B cell autoimmunities caused, although one would think it would take abit of time to materialise.
Just because on potassium channel blocker has some benefit it does not mean all will be good or bad. There are lots and lots of different potassium channels …over one hundred so activation may be good and may be influenced whether potassium moves in or out of a cell.
last May, my GP discovered that I was well and truly perimenopausal. I have had two courses of Lemtrada which I know can have accelerated my menopause. Leading up to this discovery my fatigue was a lot worse, I had constant problems with my bladder and all my MS symptoms, particularly my mobility were a lot worse. It had not even occurred to my neurologist that the menopause could be a factor in my worsening of symptoms. I have been on and off various HRT but have just started a new version which is a gel application rather than tablets. What I want to know is, apart from a small comment on the MS Society website about how HRT seemed to help some women going through the menopause, why there is not a lot more information and research on an unavoidable part of a woman's life which can affect even the most healthy woman quite badly.Considering that MS affects more women than men surely something which will make MS worse is worth serious investigation. Is there anywhere you could direct me for more information or is there a neurologist with a particular interest in the menopause and MS. My gynaecologist acknowledges that my menopause will affect and is affecting my MS but my neurologist seems to be less interested in what it could be doing and puts everything down to a worsening of my MS, which is potentially quite detrimental for me.My constant hot sweats inability to sleep and ability to cry quite unexpectedly is affecting my MS.
Sorry I don't know but am not a clinician, maybe the neuros may respond but they will only be general and are unlikely to respond about a specific question as they cannot do personal consultations.
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What is the current state of play regarding Sativex? Is it still being prescribed or has NICE effectively killed it off in the UK by deeming it "not cost-effective" and advising against prescribing it?
Also, what do MS clinicians and researchers think about the UK Government's rejection of the recommendations of the All-Party Parliamentary Group for Drug Policy Reform’s 2016 report ‘Accessing Medicinal Cannabis: Meeting Patients’ Needs’ ?
(For those who may have missed it, the Government's response to this comprehensive report was:
"Cannabis is controlled as a Class B drug under the Misuse of Drugs Act 1971 and, in its raw form, currently has no recognised medicinal benefits in the UK. It is therefore listed as a Schedule 1 drug under the Misuse of Drugs Regulations 2001." )
I'd be interested to know if any clinician or researcher who has read the report actually supports the UK Government's stance?
It is not cost-effective based on NICE assessments, but I think NHS wales may have supported its use.
I don't know the report however it is irrelevant what we think and we are conflicted as we are developing alternatives to cannabis.
"Cannabis has no recognised medical benefit" is clearly not supported by the view of the EMA otherwise it would not have been licenced as a treatment for spasticity. Sativex is an alcoholic extract of cannabis.
There are over 20 states that support medical use of cannabis.
If you remember that David Nutt the Government drug tsar (goverment science advisor) was sacked because he did not support the reschuding from class C to class B by Gordon Brown.
In the late 1990s I attended a meeting at Westminster sponsored by the Association for Cannabis Therapies, asking for decriminalisation for therapeutic use in MS. We were told this could not happen as there was evidence of neither safety nor efficacy; but such evidence could not be obtained as the drug is illegal. The softener was advice that an approach to the Home Office to undertake a trial would be favourably received. Of the doctors at the meeting, two of us got on with our jobs, one died, and the fourth set up a company to address this problem, and that led to the development of Sativex. The problems with Sativex, I think, are firstly its high cost, and secondly the lack of convincing benefit in clinical trials. The paradox is that to undertake convincing clinical trials would be expensive and therefore make a price cut unlikely. Some MSers tell me that cannabis, in its various forms, helps their symptoms and I believe them. I suspect that only a minority achieve this benefit and that is why the trials have been disappointing. N.B. this is use for symptom relief, not disease modification. There is also a problem with delivery of this non-water soluble drug: hence the Sativex spray; if a reliably absorbed oral formulation could be achieved, this should reduce cost. Of course the medical establishment could not condone a smoked drug!
I have already posted this question, but saw no reply so again…..
it has come to my attention that Blueteq exists and will actually restrict neurologists from prescribing expensive drugs for MS in some instances where a neurologist previously would have. For example, wheelchair users will be exempt from most treatments regardless of how their MS actually presents and even if the reason they are in the wheelchair is predominantly not MS related. This can also mean that a drug will be stopped despite the patient already receiving it. Is there a team of people arguing this change?
Reply
I have no real knowledge about blueteq http://www.blueteq.com/ but it is easy to read between the lines. This is a means to cut people of (expensive) treatments… you put in criteria and when met it will say stop. These guidelines already exist with NICE but if you us an IT solution there is not going to be grey and compassion just black and white
You would need to ask the Department of Health etc.and the UK MS Society for comment and when enlighted you can come back an tell us.
have neurologists not tried to question this or do they think it is a good idea?
I'm shocked that there has not been more made of this.
They are not politicians and suspect they find out after things are rubber stamped.
So after the AAN post from Dr.G , isn't it a no brainer to chose Lemtrada over Ocrelizumab ?
I am not a medic but working in IT am very aware that looking at problems from a different perspective can sometimes enable you to draw new conclusions.
All MS research centres on the evidence that the disease is an attack on the Myelin sheath from the outside of the nerve – a belief that dictates all research into possible treatments and draws the majority of research funding every year. What if the attack first comes from inside (as it does in some other diseases) resulting in demyelination and axonal damage starting in the axon?
Surely this would create the potential for a low cost and simple cure – the ingestion of the pure antigen (non-myelin) in order to de-sensitise the patient to the auto-immune response? I believe the principles behind this have been tried by the MS researchers in Harvard without success, but their approach was based on the belief that the attack is from the outside and involves the ingestion of myelin.
Has the ingestion of non-myelin approach been investigated, and if so could you point me at the results?
If it has not been investigated, could you explain in simple terms why the "inside out" approach has never been considered?
The ingestion of myelin didn't really work in sensitised animals so i think the approach is no good.
If you view autoimmunity as the problem even if it starts inside the effect is outside in because now you have a glymphatic pathway. The inside out started because of looking at pathology
We have fed total spinal cord to animals and it does not stop established disease hence being a sceptic
I understand your skepticism and your answer raises 3 points that I would like to explore:
MS causes thinning of the retina – measurement of inflammatory cells and thinning in the retina being used to determine the progress of the disease. However, the retina does not contain Myelin. MS is considered to be an autoimmune response to a myelin antigen. Because of the retinal pathology, could a non-myelin antigen be present which affects the axon?
https://www.facebook.com/notes/ccsvi-in-multiple-sclerosis/retinal-thinning-and-ms-why/10151303448922211/
I presume the glymphatic pathway operates at pressure to remove dying cells from the axon? If the axon is damaged there will be more dying cells and would it not operate at a higher pressure to ensure removal? If the glymphatic pathway is pressurised and flows away from the axon, would T cells be hard pressed to reach the source (in the axon) and attack the next best thing – the myelin sheath.
Ingestion as a means of de-sensitising animals does work, as the Harvard Study proved. It also works for allergy de-sensitivity so my face does not explode when I eat a peanut. However I could see why feeding total spinal cord (myelin, non-myelin and other cells) would not work as the non-myelin would be too dilute to have any effect.
The thinning of the retinia is due to die back of demyelinated/myelinated nerves in the optic nerve so the fact that nerves in the retina are demyelinated is irrelevant.
I think the glymphatics are a mechanism to clear the effects of a day's brain activity. I.e remove the rubbish. It is like a toilet flush to clear the crap of memories during the day. So pressure of the system is not relevant.
Ingestion as show by Harvard actually did not work in humans and the animal data was not great either. Feeding spinal cord would have have the relevant targets as we could have great effects with intravenous delivery. Simple fact was the oral route was pants and the idea was dropped a decade ago.
I am afraid as an engineer I do not understand why you believe the absence of myelin in the retina is irrelevant?
https://academic.oup.com/brain/article/134/2/518/401472/Primary-retinal-pathology-in-multiple-sclerosis-as
shows there is no myelin in the retina, which is principally composed of unmyelinated axons. How can MS be an autoimmune attack on myelin, when the retina is affected and contains no myelin? MS could in fact be triggered in the Axon / non-myelin, a premise which logic and science (not to mention curiosity) demands investigation. Can you explain why there there has been no research into this?
The optic nerve is heavily myelinated and is where you see inflammatory demyelinating lesions. This can cause nerve atrophy which moves back in a retrograde manner towards the retina causing thinning of the retina.
Your answer appears wedded to the view that MS starts with an attack on Myelin and then affects everything else.
Could you point me to the evidence MS always starts with an autoimmune attack on the Myelin sheath, never attacking the axon in the CNS, in 100% of cases (which is the only evidence that supports your view)? In the absence of such evidence your position is illogical, bordering on dogmatic. It is also directly contradicted by the authors in Brain 2001; 134: 518 who “identified an unique subset of patients with multiple sclerosis…. which may be occurring as a primary process independent of optic nerve pathology”
2011 BTW. Not wedded to any view really. John Prineas, a while back suggested oligodendrocyte death was a primary event in MS, before the development of inflammation. It might be possible that the retinal thinning is linked to brain atrophy in response to inflammatory events, which may be sub-clinical and perhaps this particular group are particularly susceptible to this. In the main though, optic neuritis, often a primary indicator in the development of MS is seen before retinal thinning. You also find myelin in grey matter too (at lower levels), which was dismissed in the past.
How can MS be an autoimmune attack on myelin, when the retina is affected and contains no myelin?
It is called nerve death. The head of the nerve travelling via the optic nerve to the brain. Kill the body of the nerve the head dies.
Why are you asking for evidence about where MS starts?. We don't know. I suspect it is in the uterus before you are born when the die is cast.
But thanks its the first time I've be called dogmatic
What have lymphocyte subset levels been for pwMS who have had breakthough activity after Alemtuzumab?
based on the cambridge data from their phase II people there was no relationship for CD4. CD8, CD19. The phase III data is not published
In my initial scan where I was diagnosed with CIS, i had an MRI of both brain and spinal cord. Since then only my brain has been scanned. Why is this?
Cost?
But I have lesions in my cord. Surely these should be monitored too?
I agree, but is this affecting your treatment
I kept reading last year that there is a shortage of MS nurses in some areas in the UK. Is this still the case?
I know there are some pwMS who feel they do not need to see an MS nurse.
Maybe someone from the MS trust can comment
There has been a rise in avoidable hospital admissions for pwMS. This was posted as news on the MS Society website on the May 2nd. Is this something this blog might discuss?
https://www.mssociety.org.uk/ms-news/2017/05/rise-avoidable-hospital-admissions-people-ms
Maybe profG will oblige
Any comments on this?
Surprising Role Omega-3 Fatty Acids Play in Keeping Blood-Brain Barrier Closed. 05/05/17.
http://neurosciencenews.com/bbb-omega-3-6601/
Thanks I'll do a post on the paper as to omega 3 and closing I'll have a think, but I doubt it.
Afternoon all!!
I know Prof G likes cladribine but what if your not suitable for it? What alternative is there? It seems like lots of progress is being made in the field of MS but PPMS still does not see it filtering down to patient level. I love my OH and wish there was some good news for him.
Any chance that the EBV Pender stuff might mean a clinical trial here in the UK? Can Barts be involved?
The question may be why it is not suitable it is quite versitille as a generic ocrelizumab has been approved for PPMS the European decision is soon.
Pender style trial I don't know.I imagine the need for special facilities restricts where it can be done.
Can't spell and not helped. By using phone
Dear Vasy
Sorry I can't comment on this one it is not something we can condome
Does anyone know when/where/how to register for the next UCLP research day please? I can't seem to find any information…..
They had planned it on June 10 at church house but when we told them it was the Queens birthday and trooping of the colour it was delayed until the autumn. I do not know of any dates.
Thanks Mouse! 🙂 (I recall something similar happening last year with the date………..!?)
Yes that why I checked the Queens birthday may she is not important enough that her diary was checked before picking the date. I would be away.
Are there any obvious reasons why the Reasearch day cannot be moved to a May or late June date on a permanent basis or is that too easy?
You are familiar with the phrase "easier to herd cats", Patrick? 😉
Are their reasons…..Yes that would be too easy.
At least in mice, Cytomegalovirus infection makes MS worse…
http://www.nature.com/articles/s41598-017-00645-3
Viruses make EAE worse…..Tell me about it, trust me I know:-(
Sheesh, ain't that the truth!!!!!!!!
https://medicalxpress.com/news/2017-05-trigger-autoimmune-disease.html
It is interesting, what is it would specifically cause women to have their B cells changed, or would T-bet transcription factor be modified in women?
Could it be hormones, or a hormonal change, or some genetic difference between genders?
Many questions still unanswered…
Contrast agent used for MRI scans…. there's news that the agent can stay in the body for some time.
Any thoughts please?
http://www.ema.europa.eu/docs/en_GB/document_library/Press_release/2017/03/WC500223209.pdf
What is happening during sleep when the CNS creates sensations such as vibration in the spine or loud bangs and the feeling that neurons are firing off in all directions in the head? Or realistic sounds outside the body, like a door knocker, that aren't actually happening?
In sleep the brain is partly or largely disconnected from the body: the extent of this disconnection depend on the sleep stage. Sometimes, there is unusual reconnection and this causes the phenomena you are describing which are known as parasomnias. A simple analogy would be to observe the engine of a car revving when the clutch is depressed. Common parasomnias include sudden jerks on the brink of sleep, or sleepwalking. The brain needs some disconnection time to repair and regenerate. I see many people who get together in middle age and come to clinic saying "you wouldn't believe what (s)he does in sleep".
I appreciate the explanation, thank you.
Perhaps some similarity to sleep paralysis? I "awoke" once convinced there was a hairy person in the bed next to me who was not my partner. I spent a few moments terrified, unable to move, trying to work out how they had got into my flat/bed unnoticed.
My eternal doubt about oral contraceptives and MS…
http://journals.sagepub.com/doi/abs/10.1177/1352458517692420?journalCode=msja&
Am aware of people describing micro dosing LSD as improving their performance. Has anyone researched micro dosing to see it has an effect on MS fatigue?
I saw this story in the Guardian about a pwMS forced to wet himself on a train due to a broken toilet and was wondering how many others have been faced with a similar situation. Perhaos time for one of Prof G's famous polls?
https://www.theguardian.com/society/2017/may/21/disabled-man-forced-wet-himself-virgin-trains-toilet-out-of-order
Some of trains in my area do not have toilets (not tube trains). The train journey I take can be 25 mins long and the only option is to get off the train at the next station, if I need the toilet. Then not all train stations have toilets. This is the kind of thing I have to plan when I go out for the day.
This is the sort of reason why I wear Tena lady – or budget versions thereof – on trips out. I don't imagine it's so easy for men, I don't know.
To our resident troll.
Save your effort, none of your silly little comments will get past moderation. I'm sure you have better things to do with your time.
Yeah please stop…we know who you are.
First case of PML in treatment with Ocrelizumab.
But it seems that the patient had previously treated with Natalizumab, which may represent a problem if you wish to transition from Natalizumab to Ocrelizumab.
We could have a real treatment against PML, it would facilitate and much the treatments themselves.
https://www.medpagetoday.com/neurology/multiplesclerosis/65537
Is treatment with alemtuzumab associated with hair loss? Started to lose my head hairs right after first dosage of alemz three years ago. And this only intensifies with time
And any thoughts of safety of minoxidil in ms? it is said it has some systemic bioavailability and activate potassium channels which is not so good I believe
Yes. In the INN for alemtuzumab alopecia is listed as a common side effect. As alopecia is an autoimmune problem it must be one of the B cell autoimmunities caused, although one would think it would take abit of time to materialise.
Just because on potassium channel blocker has some benefit it does not mean all will be good or bad. There are lots and lots of different potassium channels …over one hundred so activation may be good and may be influenced whether potassium moves in or out of a cell.
Merci, Professeur Mulot.
If there was pain (including 'touch pain')and numbness in head, neck, ear and face, right side, where would the lesion likely be?
last May, my GP discovered that I was well and truly perimenopausal. I have had two courses of Lemtrada which I know can have accelerated my menopause. Leading up to this discovery my fatigue was a lot worse, I had constant problems with my bladder and all my MS symptoms, particularly my mobility were a lot worse. It had not even occurred to my neurologist that the menopause could be a factor in my worsening of symptoms. I have been on and off various HRT but have just started a new version which is a gel application rather than tablets. What I want to know is, apart from a small comment on the MS Society website about how HRT seemed to help some women going through the menopause, why there is not a lot more information and research on an unavoidable part of a woman's life which can affect even the most healthy woman quite badly.Considering that MS affects more women than men surely something which will make MS worse is worth serious investigation. Is there anywhere you could direct me for more information or is there a neurologist with a particular interest in the menopause and MS. My gynaecologist acknowledges that my menopause will affect and is affecting my MS but my neurologist seems to be less interested in what it could be doing and puts everything down to a worsening of my MS, which is potentially quite detrimental for me.My constant hot sweats inability to sleep and ability to cry quite unexpectedly is affecting my MS.
hi could someone please respond to my e-mail above? many thanks
Sorry I don't know but am not a clinician, maybe the neuros may respond but they will only be general and are unlikely to respond about a specific question as they cannot do personal consultations.
hi okay it really was just a very general response I was after as it is not something I see discussed very often, which surprises me