Sunday, 20 May 2018

Saturday, 19 May 2018

Have your say on the big NHS England MS debate?

You may be aware that NHS England has just closed the public consultation period for the new NHS England Treatment MS DMT Algorithm. The aim of the algorithm is part of a troika, along with Blueteq and MDTs (multidisciplinary team meetings) to reduce the variation in prescribing of DMTs across England. The question is will this algorithm achieve its aim?

The following is the debate we had on this topic last week at the ABN in Birmingham. Please have your say; watch the debate and vote.


2018 List of Best MS Blogs

We have made the Healthline 2018 list of "Best MS Blogs". We have changed the blog in the last 6 months; fewer posts, more guests and less science. Do you think this has improved the blog? We would welcome suggestions going forward. For example, we are thinking of migrating the blog from Blogger onto a better and more responsive platform. 

Friday, 18 May 2018

Your brain stiffens

Rheology is the study of the flow of matter

An interesting brain fact if you are interested

Thursday, 17 May 2018

Depression to reduce MS

Sacramento PM, Monteiro C, Dias ASO, Kasahara TM, Ferreira TB, Hygino J, Wing AC, Andrade RM, Rueda F, Sales MC, Vasconcelos CC, Bento CAM. Serotonin decreases the production of Th1/Th17 cytokines and elevates the frequency of regulatory CD4+ T cell subsets in multiple sclerosis patients. Eur J Immunol. 2018 May 2. doi: 10.1002/eji.201847525. [Epub ahead of print

Excessive levels of pro-inflammatory cytokines in the central nervous system (CNS) are associated with reduced serotonin (5-HT) synthesis, a neurotransmitter with diverse immune effects. In this study, we evaluated the ability of exogenous 5-HT to modulate the T-cell behaviour of patients with multiple sclerosis (MS), a demyelinating autoimmune disease mediated by Th1 and Th17 cytokines. Here, 5-HT attenuated, in vitro, T-cell proliferation and Th1 and Th17 cytokines production in cell cultures from MS patients. Additionally, 5-HT reduced IFN-γ and IL-17 release by CD8+ T-cells. By contrast, 5-HT increased IL-10 production by CD4+ T-cells from MS patients. A more accurate analysis of these IL-10-secreting CD4+ T-cells revealed that 5-HT favours the expansion of FoxP3+ CD39+ regulatory T cells (Tregs) and type 1 regulatory T cells. Notably, this neurotransmitter also elevated the frequency of Treg17 cells, a novel regulatory T-cell subset. The effect of 5-HT in up-regulating CD39+ Treg and Treg17 cells was inversely correlated with the number of active brain lesions. Finally, in addition to directly reducing cytokine production by purified Th1 and Th17 cells, 5-HT enhanced in vitro Treg function. In summary, our data suggest that serotonin may play a protective role in the pathogenesis of MS.


In this study they found that serotonin (5-HT), which is the "happy" neurotransmitter that stimulates brain areas, may help animals with EAE. If this is true they we should have the answer quite soon as MS SMART has been using fluoxitine, which is also known as a prozac and is an SSRI (selective serotonin reuptake inhibitor) meaning that it induces more serotonin in the system....leading to less depression, but does it mean less Th1/Th17 and less MS.

"The objective of the Fluoxetine for Progressive MS study in Belgium and the Netherlands was to see if fluoxetine could slow the progression of MS. The trial (ECTRIM2016) covered both people with primary progressive MS and secondary progressive MS. Participants were divided into two groups. The 69 people in the first group received a 40 mg-per-day dose of fluoxetine (Prozac) for 108 weeks. The 68 people in the second group received a placebo.
Researchers found no significant difference in disease progression between the two groups".

So is the idea a bad one or was it that the trial design meant that a sensible answer could not be found.

Wednesday, 16 May 2018

The Cost of MS is more than just your Health

Last week, we said that Neuros could supplement their income from pharma-related activities.

Next there was a flurry of emails, asking for disclosure of how much, if anything, I get from MS pharma and elsewhere.

Having skirted round the issue, as I am not discussing my personal life, the question is what happens to your income?

Whilst on an individual level, I think it is none of my business, but as I am sure you know, MS does not just cost you your health...but also your wealth.

Even more reason to make sure you deal with MS as best you can as early as you can.

Tuesday, 15 May 2018

The importance of weight in MS

Acta Neurol Scand. 2018 May 11. doi: 10.1111/ane.12959. [Epub ahead of print]


Body mass index and cardiorespiratory fitness in persons with multiple sclerosis.

Monday, 14 May 2018

Guest Post- Animal Studies Enough Already

In response to Yesterday's Post


My photo
Enough with the mouse studies, already! In the 15 years since my diagnosis, I've read countless research reports involving EAE and other mouse models of multiple sclerosis. Only an infinitesimal amount of these reports have ever proven to have any real relevance to the human MS population.

The simple fact is this: mice don't get ms. You can inject them with myelin or other toxins and achieve something that kind of sort of looks like MS, but it's not ms. Then, it seems as if staring intently at the mice long enough or breathing on them shows some kind of benefit. Honestly, it's almost come to that level of ridiculousness.

We must come up with better models of the disease to work on. The amount of time and money wasted on mouse studies is – given the the enormity of the impact of MS on those humans it attacks – obscene.

Really, it's time to rethink our entire approach to MS research. Thus far the best we've come up with are treatments that profoundly suppress parts of the intricate human immune system, the long-term effects of which are a complete unknown. And these treatments do absolutely nothing towards effecting a cure.

Given modern laboratory techniques, the rapid advances in computational power, the emergence of AI, and the vast body of knowledge accumulated by ms researchers and clinicians, one would think a coordinated, concerted effort to finally identify the cause or causes of the disease might finally bear fruit. Time spent fixated on mice with induced conditions that sort of resemble MS is, at this point, time wasted. And those of us forced to watch ourselves disappear by inches don't have that time to waste.

Patients should be rising up against the status quo, but unfortunately most are too busy just trying to get through the day with some modicum of functionality and dignity left intact. MS has gone from medical backwater to one of the most profitable areas of medical practice in the last two decades. It's high time to cure the damn thing and send it back from whence it came. We now have the technology and basic understandings of the mechanisms to get this done, given the will. Coming up with an effective anti-EBV treatment would be a great first step…"
This was a comment made yesterday and is an opinion I am sure many people hold. Likewise, many neuros think the same.  However, basic science is the basis of where treatments come from. 
I was at a recent meeting about finding treatments, which may involve a bit of screening in animals and a very eminent scientist said (Paraphrased) I'm not going to do that as I'm not interested. All I am interested in doing is looking at mechanisms of biology. 

However they are very happy to take money from disease-related charities.


What you do think?


The science publishing system has created a "mechanism is all mentaility" and disease can simply be a vehicle to get research support. 

However times are changing and it is increasingly difficult to get funding for animal studies. However, without knowledge, we will continue to shoot in the dark.

Sunday, 13 May 2018

Care Home vs. Independence

A commentator brought this BBC interview to our attention as an example of what is happening to people with MS living in England. I would be interested to know if there are any other examples of this happening across the country. We need to do something about it. Can anyone help? 


ProfG    

Imaging the Rim




A chronic Active Lesion has a demyelinated centre and rim of myelin damage/removal by macrophages. These can be seen on a 7T magnetic resonance imaging scanner, but this study shows they can also be seen on a lower power 3T machine. If you can see it then you can monitor it.

Absinta M, Sati P, Fechner A, Schindler MK, Nair G, Reich DS. 
Identification of Chronic Active Multiple Sclerosis Lesions on 3T MRI. AJNR Am J Neuroradiol. 2018. doi: 10.3174/ajnr.A5660. [Epub ahead of print]

BACKGROUND AND PURPOSE: MR imaging-pathologic studies have reported that paramagnetic rims on 7T susceptibility-based MR imaging identify, in vivo, the subset of MS lesions with compartmentalized inflammation at the lesion edge and associated remyelination failure. Here, we assessed the reliability of detecting these rims on high-resolution 3T phase images.
MATERIALS AND METHODS: High-resolution T2* and phase MR imaging was collected in 20 patients with MS at 3T (3D segmented EPI, 0.65 mm3) and 7T (2D gradient-echo, 0.2 × 0.2 × 1 mm) MR imaging. In each case, 5 discrete chronic (non-enhancing) MS lesions were selected on T2 FLAIR images for rim evaluation. Five raters experienced in MS imaging contributed to the rim assessment, of whom 3 worked independently on 3T data, and 2, on 7T data. Consensus agreement was reached for both 3T and 7T rim evaluations. Discrepancies between 3T and 7T were discussed, and consensus was reached.
RESULTS: Phase rims were seen in 34 lesions at 7T and in 36 lesions at 3T by consensus. Inter- and intrarater reliability were "substantial/good" both at 3T and 7T analysis (Cohen κ, >0.71). Based on consensus agreement, the reliability of rim visualization at 3T versus 7T was 0.78 (κ) with a pair-wise agreement of 90%. More lesions were judged to be false-positive or false-negative at 3T than at 7T.
CONCLUSIONS: Nearly all 7T paramagnetic rims can also be seen at 3T. Imaging at 3T opens the possibility of implementing paramagnetic rims as an outcome measure in multicenter, MR imaging-based clinical trials aimed at treating perilesional persistent inflammation and its potential effects on remyelination.


http://www.ajnr.org/content/ajnr/early/2018/05/03/ajnr.A5660/F2.large.jpg?width=800&height=600&carousel=1