Wednesday, 31 October 2018

Advanced MS-The Missing Movie

In 2011 ProfG and Pharma dropped the baton (Stick in a relay race), but DrK picked it up and ran with it. Like Forest Gump he has been running ever since and Pharma has come back to help us finish the Race.

Tuesday, 30 October 2018

JCV in Brazilian MS

Arq Neuropsiquiatr. 2018 Sep;76(9):588-591. doi: 10.1590/0004-282X20180083.

Serological profile of John Cunningham virus (JCV) in patients with multiple sclerosis.

Branco LP, Adoni T, Apostolos-Pereira SL, Brooks JBB, Correa EC, Damasceno CA, Eboni ACB, Fezer L, Gama PDD, Goncalves MVM, Gomes S, Grzesiuk AK, Mendes MF, Morales RR, Muniz A, Parolin MFK, Pimentel MLV, Ribeiro MC, Santos GACD, Sato HK, Scherpenhuijzen SB, Scorcine C, Siquineli F, Sousa NAC, Varela DL, Winckler TCA, Fragoso YD.


Treatment options for multiple sclerosis (MS) have changed over the last few years, bringing about a new category of drugs with more efficient profiles. However, these drugs have come with a whole new profile of potential adverse events that neurologists have to learn well and quickly. One of the most feared complications of these MS treatments is progressive multifocal leukoencephalopathy caused by the reactivation of the John Cunningham virus (JCV).


To identify the serologic profile of JCV in patients with MS.


Data on serum antibodies for JCV were obtained using the enzyme-linked immunosorbent assay provided by the STRATIFY-JCV program.


A total of 1,501 blood tests were obtained from 1,102 patients with MS. There were 633 patients (57.1%) who were positive for antibodies for JCV and 469 patients who were negative (42.9%). Twenty-three patients became positive after initially having negative JCV antibody status. The rate of seroconversion was 18.5% over 22 months.


The JCV serologic profile and seroconversion in Brazilian patients were similar to those described in other countries.

In healthcare decision making it is not unusual to stumble across fear. The worry over whether you are making the correct decision assumes that you would be rewarded in some way for that decision, and the opposite if you were wrong. More over, there is a certain caveat emptor (the buyer beware) when in comes to these decision making processes; the buyer in this case you, has less information about the good or service that they are purchasing than the seller, in this case the healthcare professional, who has more information.

The only problem is that the universe has no fixed agenda, and once you make that decision it simply works around it, at times impervious to the outcome. So how do we overcome this uncertainty?

Infection with JCV is one such massive problem in multiple sclerosis. Not surprisingly then, most countries have reported on their local prevalence of the virus. The Brazilian JCV status, as published in this study involving 633 PwMS is in line with that reported by other countries.  The worldwide prevalence of JCV in MS taking into account data from 26 countries is 57.1% (so there is more than a 50:50% chance that if you have your blood tested today that you'd be positive) and the range of positive antibodies to JCV is also 40-69%. The rate of conversion from negative to positive JCV is roughly 11% per year from a further two large studies, although low conversion rates, such as 6% have been reported from a study in Portugal after 5years. In this Brazilian study, the rate of seroconversion was 19% over 22 months - again comparable.

As a majority of these worldwide epidemiological studies have now reported similar findings, it is important that we strategize on finding solutions to this problem, since we all know that immunosuppressants are here to stay in so far as MS treatments are concerned. The solution has to be simple to keep the probable outcomes manageable. In this case, restrict exposure to therapies linked to PML (JCV infection), work out the correct sequencing approach if you're more comfortable using escalation approaches, or stick to induction treatments and check JCV status at specified time points, in order to evaluate future risk.

Monday, 29 October 2018

Teriflunomide is not a high efficacy agent...predicted by B cells

We have been suggesting that the activity of drugs relate to their capacity to deplete memory B cells. 

Baker D, Marta M, Pryce G, Giovannoni G, Schmierer K.
Memory B Cells are Major Targets for Effective Immunotherapy in Relapsing Multiple Sclerosis. EBioMedicine. 2017;16:41-50.

A student looking at table 1, said what happened to teriflunomide?

Sunday, 28 October 2018

Saturday, 27 October 2018

Which is Best..I don't know, they are much of a muchness

You asked which is best based on brain volume.

The immune reconstitution agents (some people call this induction therapy..but it is a confusing terminology as it is used to describe the initial dosing schedule of oreclizumab) agents). These are alemtuzumab (Cohen et al. 2012, Coles et al. 2012) and cladribine (Giovannoni et al. 2010, Comi et al. 2013, de Stefano et al. 2018)) and possibly ocrelizumab (Baker et al. 2017) although it is used as a continuous immunosuppressive (Hauser et al. 2017).

Which is best?

ProfG says the influence on the changes of brain volume by an agent from Cambridge makes it looks good.

However, I have an issue

Friday, 26 October 2018

Too much vitamin D is not good for you

ProfG has been urging people to ensure that you are vitamin sufficient.

He recommends the dose advised by the Vitamin D Council

This will maintain bone health and maybe, just maybe it will impact on your MS.

However some people have gone overboard and have found that to much of a good thing is bad.

Thursday, 25 October 2018

The third course of Alemtuzumab

Yesterday some asked about the third cycle of alemtuzumab and if they had break through.

If you live in England you may want to view this document

It says 

Wednesday, 24 October 2018

Tuesday, 23 October 2018

Alemtuzumab 8y outcomes (ECTRIMS 2018)

  UK NHS England MS Treatment algorithm

If you don't know where you are going, all roads lead there; and in this case to alemtuzumab! 

But can alemtuzumab puts its money where it's mouth is? 

In ECTRIMS we saw the publication of one their original clinical trial (CARE-MS II) follow up results after an 8 year period (see poster below).
  • 56% (77% of the original participants were included in this analysis) required no further doses of alemtuzumab, i.e. only the first 2 cycles an year apart
  • 88% relapse-free
  • 78% with disease stability, i.e. stable or improved EDSS scores
  • 67% free of MRI activity
  • Brain volume loss from baseline though to yr8 was -1.83% (i.e. normal rate as those without MS)
  • Side effects were the same as previously described
I'll leave you to come to your own conclusions on these findings, but alemtuzumab is here to stay.

Monday, 22 October 2018

Cladribine has no significant effects in progressive MS...The data says differently

Based on the recent report that cladribine can eliminate the occurrence of oligoclonal bands in people with relapsing MS, there was a comment that cladribine has no effect on progressive MS.

So lets look back at the paper

A mechanism for dimethyl fumarate

This is one for the scientists reading the blog

Saturday, 20 October 2018

Cladribine is getting rid of oligoclonal bands

Off-label Cladribine use has been championed by DrK and this in part led to the re-emergence of the oral variant, which remerged after a 6 year holiday.

During this time we have generated a large cohort  (See Stephanias ECTRIMS work below) of people taking this drug and we have defined a new working mechanism for cladribine .

Whilst memory B cell targeting is not uniqure to Cladribine, it has one potential advantage over other highly effective MS drugs.

This is that it enters (about 25% the blood level) and can be active within the CNS (Fingolimod enters the brain but its main mechanism is in the lymph glands) . Therefore it can target elements of disease that are relevant to progressive MS.

However, the centre of off-label cladribine was not the East-End of London, it was the East-End of Europe. Indeed our friends in Poland have been using off-label cladribine for years and they have asked what happens to the oligoclonal bands.

Interested read on.

Friday, 19 October 2018

Whats Lost is Lost, Why CRAB can sometimes mean CRAP

This German studies shows real life data that dimethyl fumarate is better than the CRAB drugs plus teriflunomide......So why are we still using them?

Thursday, 18 October 2018

Why is Prof G dissatisfied?

I have been espousing the message that time is Brain in the treatment of MS, but the NHS makes it difficult to practice what you preach. MS services in the NHS are not configured at present to react quickly in terms of new referrals and as a result, MSers pay the price. In the last few months, two MSers have lost brain and spinal cord because of how long it has taken them to get into the Barts-MS system. This upsets me and leaves me feeling very dissatisfied with my NHS practice. 

Guest Post: DrMaria from Spain explains about relapses

Hello everybody

First of all, I would like to introduce myself. I am Maria Mateo, I am a Neurology registrar from Spain and I have the pleasure of spending three months at Barts-MS to learn about MS.
As a part of my stay here, I have been attending MS clinics. As we know, MS patients can experience a broad variety of symptoms during their disease that can be difficult to explain. Thus, I have noticed that some MS patients have difficulties interpreting whether their symptoms are due to a new relapse or not, or if their symptoms are related to something else. Therefore, I have thought that it would be useful to clarify some main concepts around MS relapses.

Wednesday, 17 October 2018

ECTRIMS2018 Time is Your Brain,

There is no doubt that some people do OK on CRAB (copaxone, rebif, avonex and betaferon) drugs, but many do not and there are a number of more effective agents out there. 

However there are consequences of not getting disease under control as shown at ECTRIMS 2018

Guest post: A different MS Chariot

I have been encouraged by ProfG to write a post about my “MS Chariot” experience. It's a good example of an activity that those with limited leg function can enjoy, but for which it is important to preserve upper body function.

Monday, 15 October 2018

triMS-online: helping female academics

Another development at ECTRIMS 2018, which I heard about via the ECTRIMS grapevine, is that female academics are mobilising and have formed a group to demand gender equality at the top table of MS academia. Good!

Sunday, 14 October 2018

Early reflections on ECTRIMS 2018

I am writing this post on the flight back to London from Berlin. Being trapped in a tin tube at over 10,000m above sea level is always a good time to think.

under&over - ProfG's #1 non-scientific highlight at #ECTRIMS2018

Guess what my #1_scientific_highlight was at #ECTRIMS2018?

Rixtuximab in the brain trial...Why?

As the MS community reels from the news of the MS-SMART trial, there have been some comments on the blog chastising the science community for their role in another failure a MS SMART seems not so SMART.

Saturday, 13 October 2018

Is it time to reunify MS as one disease?

I am just about to leave Berlin tired but content that the MS world is finally beginning to acknowledge that #MS_is_1_and_not_2_or_3_diseases. We have covered this topic extensively over the last 4-5 years and I did so again in my talk as part of the Roche satellite symposium.

I have also uploaded all my other ECTRIMS-related slides and posters to my new SlideShare site for download.

CoI: multiple

Friday, 12 October 2018

Late Breaking Bad News from ECTRIMS

We have the top-line results of the MS SMART trial.

This trial compared the effects of riluzole, amiloride and fluoxetine and placebo in secondary progressive MS in a phase II trial. 

This indicates that ....

Broadcasting from ECTRIMS 2018

Mouse Dr and Neuro Doc Gnanapavan will broadcast from the ECTRIMS meeting currently happening in Berlin. The will cover data and results presented in paper presentations, keynotes and posters from the past few days.

The broadcast is now over but you can view the video here. Viewers commented and tweeted questions to us while it was on live. 

Pre-broadcast revision

ECTRIMS2018. Relapses with B cells present

Disease activity with ocrelizumab in the absence of B cells
Should we start panicing about the B cell hypothesis?

Thursday, 11 October 2018

ECTRIMS2018.La La La La, Alemtuzumab neutralizing antibodies are not important

As Greg Winter from Cambridge got the Nobel Prize for his part in the making of antibodies, notably humanizing antibodies, we can celebrate his work on the production of the world's first humanised antibodies (CAMPATH-1H) that was designed to stop anti-antibody responses , which were common when rodent antibodies were used.

Although it achieved its aim somewhat....It is in fact probably one of the Worlds worse antibodies for inducing an anti-drug response.
Did these stop the drug working?

ECTRIMS 2018. A Trial too Far...Spasticity study outcome reported

You have been asking “When will I be making the millions?” as you have been following our 17 year adventure into pharma-land as we try to develop a new treatment for spasticity in MS.

Today, you have the answer as the trial results in MS are made public at ECTRIMS 2018.

Wednesday, 10 October 2018

ECTRIMS2018. Hot Topics

Is there a new MS subtype. Nerve loss without Demyelination

Myelocortical multiple sclerosis: cortical neuronal loss in the absence of cerebral white matter demyelination B. Trapp, Cleveland, US
Background: Demyelination of cerebral white matter is thought to drive neuronal degeneration and permanent neurological disability in individuals with multiple sclerosis (MS). Brain magnetic resonance imaging (MRI) studies, however, support the possibility that demyelination and neuronal degeneration can occur independently. The purpose of this study was to investigate whether post-mortem MS brains show pathological evidence of cortical neuronal loss that is independent of cerebral white-matter demyelination. 
Methods: Visual examination of centimeter-thick slices from 97 postmortem MS brains identified 12 without evidence of cerebral white-matter demyelination. Demyelination was quantified histologically in cerebral white matter, cerebral cortex, and spinal cord and compared with demyelination in 12 cases of MS with cerebral white-matter lesions. Atrophy, MRI metrics, cortical neuronal densities, and pathological correlates of MRI abnormalities were compared. 
Results: Cases without cerebral macroscopic lesions had demyelination in spinal cord and cortex, but a paucity of histologic cerebral white-matter demyelination. Despite the lack of cerebral white-matter demyelination, cortical neuronal loss, cortical thinning, and cerebral white-matter MRI abnormalities were significantly increased compared to brains from healthy controls and were similar to those in MS brains with cerebral white-matter demyelination. In the 12 brains without cerebral white-matter demyelination, swollen myelinated axons were the pathological correlate of white-matter regions with MRI abnormalities.
Conclusions: A subtype of MS, which we call myelocortical multiple sclerosis (MCMS), is characterized by demyelination of spinal cord and cerebral cortex, but not of cerebral white matter. Cortical neuronal loss is not accompanied by cerebral white-matter demyelination and is therefore an independent pathological event in MCMS.

It has been suggested that there is an MS subtype that displays nerve loss without significant demyelination in the outside of the brain, in people with demyelination in the spinal cord.

ClinicSpeak stand at ECTRIMS - What’s new this year?

For the past couple of years we’ve worked hard to put on a stand in the exhibition hall at ECTRIMS. The exhibition hall is where companies, other research projects and charities showcase their work to conference delegates. The main purpose of our stand is to share our #ClinicSpeak resources with others working in MS research and care.

Tuesday, 9 October 2018

ECTRIMS 2018: will MS become one again?

I arrived in Berlin yesterday and already I am seeing ECTRIMS 2018 turning into a battle between the lumpers and splitters, i.e. is MS one, two or three diseases. 

Making Berlin one again

Cannabis as good as copaxone in animals: Two wrongs don't make a right

Avidekel Cannabis extracts and cannabidiol are as efficient as Copaxone in suppressing EAE in SJL/J mice.Gallily R, Yekhtin Z.Inflammopharmacology. 2018 Oct 5. doi: 10.1007/s10787-018-0536-3. [Epub ahead of print]
Multiple sclerosis (MS) is an autoimmune disease leading to the destruction of myelin with consequent axonal degeneration and severe physical debilitation. The disease can be treated with immunosuppressive drugs that alleviate the symptoms and retard disease aggravation. One such drug in clinical use is glatiramer acetate (Copaxone). The non-psychotropic immunosuppressive cannabinoid compound cannabidiol (CBD) has recently been shown to have beneficial effects on experimental autoimmune encephalomyelitis (EAE). The aim of our study was to compare the efficacy of CBD and standardized extracts from a CBD-rich, ∆9-THClow Cannabis indica subspecies (Avidekel) with that of Copaxone. Our data show that CBD and purified Avidekel extracts are as efficient as Copaxone to alleviate the symptoms of proteolipid protein (PLP)-induced EAE in SJL/J mice. No synergistic effect was observed by combining CBD or Avidekel extracts with Copaxone. Our data support the use of Avidekel extracts in the treatment of MS symptoms.

This is not something I would be boasting about, because although Copaxone is number one treatent for MS, the animal data that supports this use is pretty pants . 

Therefore to suggest that cannabidiol is just as good..actually says that cannabidiol is pants too. 

Of course we can get copaxone to work  but not in the way it is used in humans. 

However, we know that cannaidiol is rubbish already and we had shown it does very, very little as an immunosuppressive to inhibit EAE. Shame that others maintain the opposite. 

Either we are rubbish in how we do experiments, or they are . There is not inbetween. We tried to get cannabidiol to do something for years. Therefore Time will tell and I predict the human trials will show that it is indeed rubbish.

Tetrahydrocannabinol can induce immuomodulation in animals, but only when they are so out-of-it that we think it is meaningless for human use. However you can believe this if you want

Does contrast need to be given for MRI scans?

AJNR Am J Neuroradiol. 2018 Oct 4. doi: 10.3174/ajnr.A5828. [Epub ahead of print]

Do All Patients with Multiple Sclerosis Benefit from the Use of Contrast on Serial Follow-Up MR Imaging? A Retrospective Analysis.

Mattay RR, Davtyan K, Bilello M, Mamourian AC.


Patients with multiple sclerosis routinely have MR imaging with contrast every 6-12 months to assess response to medication. Multiple recent studies provide evidence of tissue deposition of MR imaging contrast agents, questioning the long-term safety of these agents. The goal of this retrospective image-analysis study was to determine whether contrast could be reserved for only those patients who show new MS lesions on follow-up examinations.

Monday, 8 October 2018

ProfG's MS-related Twitter activity: week 1st-7th October 2018

Measuring progression a blast fromm the past

This study measures markers in the blood to monitor disease activity. Astrocyte proteins can be found

Sunday, 7 October 2018

Infection risk after alemtuzumab drops with time

Alemtuzumab is the a sledgehammer drug that depresses the immune system such that your T and B cells, monocytes and sometime neutrophils drop, leaving you open to infection. However, the cells rapidly recover  and the infection risk will drop.

The 6 year follow up of the alemtuzumab trials says

Saturday, 6 October 2018

PPMS v RRMS what's the difference?

PPMS v RRMS what's the difference?

Besides cost effectiveness of treatment and the fact of loads of treatments for RRMS and only 1 (maybe depending where you live) for PPMS

Friday, 5 October 2018

Q & A October

Dock Tarn Lake District photo by MD2

               If you have a question unrelated to the thread this is the place for you

Mouse and Man..when does it become unethical

Uyttenhove C, Gaignage M, Donckers D, Nasr Z, Cheou P, van Snick J, D'Auria L, van Pesch V. Prophylactic treatment against GM-CSF, but not IL-17, abolishes relapses in a chronic murine model of multiple sclerosis. Eur J Immunol. 2018. doi: 10.1002/eji.201847580. [Epub ahead of print]

The pathogenic role of IL-17 and GM-CSF has been unravelled in experimental autoimmune encephalomyelitis (EAE), a murine (mouse or rat) model of multiple sclerosis (MS). However, in most models (Meaning C57BL/6 mice, Lewis rat and marmoset) , EAE is characterised by a monophasic attack which is not representative of the relapsing nature nor the chronicity displayed in MS. Here, we used proteolipid protein peptide (PLP139-151 ) to trigger EAE-relapses (EAE-II) in SJL mice that had recovered from a primary-EAE episode (EAE-I). This procedure resulted in severe and irreversible disease that, unlike EAE-I, was not abolished by anti-IL-17-mAb (In virtually all papers published anti-IL17 ameliroates but does not abolish disease) . In contrast, prophylactic anti-GM-CSF-mAb treatment prevented EAE-I and -II. Strikingly, the expression of T-cell transcription factors and cytokines/chemokines in mice treated with anti-GM-CSF during both EAE episodes was silenced. Anti-GM-CSF-mAb treatment administered only during EAE-II did not completely prevent relapses (Therefore it will probably fail in MS) but mice ultimately reached full recovery. (I doubt it, we can always see residual deficits if you look) Anti-GM-CSF treatment also strongly impaired and ultimately resolved monophasic MOG35-55 -induced EAE in C57Bl/6 mice. In such protected mice, anti-GM-CSF treatment also prevented a further relapse induced by MOG-revaccination. These results underscore the critical role of GM-CSF on pro-inflammatory mediator production. Furthermore, we observed a strong preventive and curative effect of anti-GM-CSF neutralisation in two EAE models, relapsing and chronic. Altogether these findings are relevant for further MS research. (How?)

So where are we on this one?

Thursday, 4 October 2018

ProfG are you walking-your-talk or just huffing-and-puffing?

I was asked after my 'ProfG is fuming' blog post from a few weeks ago, if I was walking-my-talk and doing something about NICE's decision about ocrelizumab for PPMS? Or was I just huffing-and-puffing and doing nothing about it? 

My response was yes; I am walking-my-talk. The following is a summary of some of my activities.

ECTRIMS 2018 - Burning Debate

On Wednesday 10th October at ECTRIMS 2018, we will be running another Burning Debate. Like previous years, the aim of this session is to encourage MS clinicians and researchers to use social media (specifically Twitter) to discuss topical issues in MS research and treatment. 

The topic this year is: The new McDonald diagnostic criteria are controversial, making them difficult to use in clinical practice.

(Image: The 2016 debate got slightly inflated)

Wednesday, 3 October 2018

EAE: Dendritic cells starting the Immune response or are they

It sounds like it is time for me to eat some more humble pie as I said "I don't think that the CNS is the right environment to initiate immune responses"

Dendritic cells are reported to be present in the CNS and they are critical for autoimmunity according to a new report

or are they?

CCSVI..the last nail?

People with chronic diseases that are not adequately controlled, often turn to alternative medicines.

This is not a surprising response, but few of these alternative treatments have generated so much polarisation of opinion as the CCSVI phenomenon.

MS was caused by blocked veins...a bit of venoplasty to open the vessel and a wonder cure was born. 

Even better you didn't have to deal with neuros as you could get the treatment, at a price, by non-neurologists. Social media, unchallenged by neuros until it was too late, propelled this into the public eye.

Canda and Italy were CCSVI-central and the MS Socieites there felt compelled to use their research budgets on validating the presence of blocked veins and the value of venoplasty.

It all came to nothing

Is this the final nail?

Tuesday, 2 October 2018

Optic neuritis in MS

J Neuroimmunol. 2018 Sep 22;324:115-118. doi: 10.1016/j.jneuroim.2018.09.010. [Epub ahead of print]

Recurrent optic neuritis - Different patterns in multiple sclerosis, neuromyelitis optica spectrum disorders and MOG-antibody disease.

Lotan I, Hellmann MA, Benninger F, Stiebel-Kalish H, Steiner I.


Optic neuritis is a frequent finding in multiple sclerosis (MS) and in neuromyelitis optica spectrum disorder (NMOSD), as well as in Myelin-Oligodendrocyte Glycoprotein (MOG) -positive disease. While both NMOSD and MOG-antibody disease are known to be associated with a humoral, antibody-mediated attack against a specific antigen, much less is known about the etiology and pathogenesis of MS. The aim of this study was to determine if the localization of recurrent episodes of ON follows the same pattern in MS as in NMOSD and in MOG-positive recurrent ON.


We retrospectively reviewed our database to identify patients with recurrent ON. The eye affected in each episode of ON was recorded, and the findings were analyzed.


Forty-seven patients met the inclusion criteria. In the MS group, all episodes of ON recurred on the same side in 15 of the 29 patients (51.7%), accounting for 32 of the total 78 episodes (41%).In the NMSOD group, all episodes of ON recurred on the same side in 2 of the 12 patients (16.6%), accounting for 6 of the total 49 episodes (12.5%).In the MOG-positive group, all episodes of ON recurred on the same side in 1 out of 6 patients (16.6%), accounting for 2 of 21 episodes (9.5%).The between-group difference in the rate of recurrences affecting the ipsilateral side was statistically significant (p = .0007 and p = .0085 for the MS-NMOSD and MS-MOG groups, respectively).


The pattern of recurrent ON differs significantly between MS and NMOSD and MOG-positive recurrent ON. This finding suggests that in MS recurrences may be provoked by previous tissue damage, disruption of the blood-brain barrier, and other local factors while in NMOSD and MOG-antibody disease attacks are indeed due to localization of the auto antigen.

There once lived a disorder called optico-spinal MS, who's origin was Asian by distinction, but a decade on its existence in Western MS was sought, and went by the name of Devic's.

However, that's where the similarities end. Unlike MS, Devic's or NMO spectrum disorders (NMSOD) and MOG-MS disorders as they're now known have well- defined antibody targets; namely aquaporin 4 and MOG (myelin oligodendrocyte glycoprotein), respectively. They're also more severe in their relapses, with longitudinally extensive cord lesions and long optic nerve lesions. Unlike MS, however, a majority are OCB (oligoclonal band) negative.

Lotan et al's. aim was to investigate to what extent the localization of recurrent attacks of optic neuritis (ON) were similar between the disorders. Until this study, no one has paid any attention to this in MS. Whereas, in NMSOD the optic neuritis is predominantly posterior/or chiasm predominant, whilst in MOG ON they tended to involve the whole nerve/anterior predominant. As all the disorders essentially involve a pathogenic attack on antigens (although MS is believed to target more than one), there is no reason why the recurrent ON episodes should not occur at random in each eye, whether it be MS or NMSOD or MOG-MS.

The study involved MS  (n=29), NMSOD (n=12), MOG-MS (n=6) with two or more attacks of ON. They found that in the MS group that recurrent ON was on the same side in 51.7%, accounting for 41% of the events (see figure on the left for the breakdown). In the NMSOD group, 16.6% had ON affecting the same eye, accounting for 12.5% of the events. In MOG-MS group 16.6% had ON affecting the same eye, accounting for 9.5% of the attacks. The difference between the ipsilateral location of recurrent ON attacks in MS vs NMSOD and MS vs MOG-MS was statistically significant.

So why is MS-ON different from NMSOD and MOG-MS? Is it because the recurrent attacks become a response to previously damaged tissue? The latter may serve as inference for attacks elsewhere in the body. This work, fortunately/unfortunately, if replicated by others raises more questions about MS than we have answers for at the moment.

Monday, 1 October 2018

Guest Post: MS and Alcohol: Friend or Foe? Prof G responds… as do MSers

By now, we all know the lifestyle drill.
Exercise = good
Smoking = bad
Alcohol = possibly, maybe?

ProfG's MS-related Twitter Activity (24th-30th Sep)