Writing semi-autobiographical fiction about disability #BADD14

This is my post for Blogging Against Disablism Day 2014.

Well. I've finally taken the leap of faith, and started writing the novel that's been tunneling out of my subconscious for the last couple of years. And they do say write about what you know. So I'm writing in the first person about a woman who develops MS.

But is writing semi-autobiographical fiction really worthwhile? And can a novel about disability be interesting to a general audience?

If my story was purely autobiographical, it would be a thinly disguised version of my own life story, with names and locations disguised. Firstly, this would certainly be excruciatingly boring for the reader. Secondly, parts of it would probably be actionable!

So what I'm doing instead is using my personal knowledge of my condition - multiple sclerosis - and how it affects me, and inventing a background, relationships, and story for my protagonist. I have access to the emotions I felt when I developed and was diagnosed with MS, and anecdotes from friends with MS of how their family, friends, and work colleagues reacted.

A novel is not just about the one central plotline, or it would be very short indeed. I can use my experience, both of disability and everyday life, as inspiration for plot points and to help me understand my characters' emotions. So, for instance, a real-life neighbour who takes her ferret for a walk every day in an animal carrier will be making an appearance, along with her pet.

Real life isn't connected. Random things happen at random times. Wild coincidences take us by surprise, that we wouldn't believe for a second in fiction. In a novel, however much it draws on your own life, you have to order and arrange your material to make some sort of coherent narrative .

In the end, as Tom Clancy said:

The difference between fiction and reality is that fiction has to make sense.

Do novels about disability have to be serious? Not in the least. You can see humour in any situation. My heroine is a strong, funny woman. Yes, being diagnosed with MS is a major, serious life event. But looking back on it, the process is full of humorous moments. If I can see that, so can she. Real life isn't always funny at the time. But a book can be.

And who knows? Perhaps if I can make it funny and accessible (and anyone wants to read it anyway!) it'll get over a bit of information about disability in general and MS in particular along the way. Which would be no bad thing, right? The more people know, the less stigma and disablism we'll hopefully all encounter.

So. If there's anything you think from your own experience I should try to include, please let me know in the comments. Otherwise, I'll keep you updated as much as I can. And rest assured, once it's finished I'll pimp it to death!

Multiple sclerosis and depression

We all feel down sometimes. That's natural, and part of life's rich tapestry.

But sometimes, for some of us, that short-term feeling turns into something much longer-lasting and more profound. Clinical depression can involve feelings of sadness and hopelessness, irritability, losing interest in activities, loss of ability to concentrate of make decisions, tearfulness, tiredness, sleep disturbances, and physical aches and pains. It is often linked with anxiety.

 

Each year, around 6% of the UK population have an episode of depression, and more than 15% will have an episode during their lifestime.Having a long-term physical illness increases your risk of depression up to about one in three, and NICE have recently issued guidelines for this situation.


Multiple sclerosis, being a long-term condition, follows this pattern. Up to 50% of people with MS experience depression at some point in their lives, and around 20% within each year. People with MS are at 7.5 times the risk of suicide of the general population.. There are several reasons for this:

• To have MS is to be in a state of uncertainty. Your life has changed completely. You have a long-term condition with a variable course, which could potentially progress to severe disability. Your self-image changes: you fear losing independence, you may lose your job or friendships.
• Depression can also be caused by MS's physical changes to the brain. If it damages the parts of the brain that control mood and emotional expression, behavioural changes can result, including depression.
• MS can also affect the immune and neuroendocrine systems. For instance, studies have found changes in immune markers in people with MS who are depressed.
• Depression can be a side-effect of certain drugs, such as the corticosteroids often prescribed for MS relapses.

There is some evidence that depression is (not surprisingly) more common around the time of a relapse, but people with more severe physical disability are not more likely to be depressed. Nor is it related to how long you've had MS.

There is no shame in having depression. It's a disabling condition just as much as a broken leg, heart disease - or, indeed, MS. It's important that we learn to recognise its onset in ourselves, and seek help. It doesn't mean weakness or need to be hidden. I see my depression as a long-term condition to be managed, like my MS.

Treatments for depression can be very effective. If you think you may be depressed, please visit your doctor and explain how you feel. If you are suicidal, contact the Samaritans.

So, if you have MS, it's entirely possible that you also have depression. Clearly not an ideal situation, but entirely treatable and manageable. As I said: all part of life's rich tapestry!

Multiple Sclerosis Awareness Week #MSAwarenessWeek

MS Awareness Week starts today, 29th April 2013.

This is the one week a year when we - people with MS, our families and friends, and the organisations that support and inform us -  try to spread the word about what multiple sclerosis is and the many ways, often invisible but nonetheless potentially devastating, it can affect us.

This year's awareness week comes with the disturbing news that only 40% of those eligible to receive one of the seven licensed MS drugs are actually getting them. This may be down to a lack of information and problems accessing specialists. The UK ranks 25th out of 27 in Europe on prescription rates, which given our relative wealth is really not good enough.

Decisions should be taken nationally about this kind of treatment and specialist care plans drawn up for each patient, with regular reviews allowing for treatment options to be assessed on a regular basis.

People with MS tend to do a lot of falling, both physically and mentally. That's OK. The thing is getting up again. Those of you who don't have MS, please understand that this can sometimes take us a little while.

It's MS Awareness Week. But we have to be aware of MS every day of the year.

For more information on MS, please visit:
MS-UK
MS Society
MS Trust

Placebos, sham surgeries and CCSVI

Recently GPs took part in a survey which showed that 97% of them had used placebos at some point in their careers. The truth is inevitably more nuanced than that headline figure: 97% had used what the researchers called "impure" placebos such as antibiotics for viruses, and the figure for "pure" placebos, treatments containing no active ingredients at all, was in fact 10%.

"Pure", inactive placebos such as sugar pills may seem the more dangerous, but "impure" placebos may be actively dangerous to health. For instance, antibiotics can have side-effects and may promote antibiotic resistance.

Most of the doctors questioned thought that any risk of damaging the trust between doctor and patient was unacceptable, but that it was possible to prescribe a placebo to a patient without actively lying to them. For instance, half of the doctors told the patient that the intervention had helped others.

Is this ethical, particularly if it's possible that the patient would have got better anyway? If something is at the extreme ends of a range of measurements, the likelihood is that it will move towards the average. This is the statistical phenomenon called regression to the mean. The medical application of this is that if someone is ill, on the whole they're likely to get better whether there's any intervention or not.

There may be a psychological effect from receiving a placebo, even if the patient knows that's what it is. One study found that even when the patient was fully aware that their treatment had no active ingredients, the placebo effect was still seen. However there were methodological flaws in that study. More research is needed, to see if the results can be replicated.

Placebos are commonly used in trials to assess whether a new medication is better than no treatment at all. How can a surgical intervention be tested? Sometimes sham surgery is used. Sham surgery forms an important control, as anaesthesia, the incision, post-operative care, and the patient's perception of having had an operation are the same.

However again there are ethical issues, as all surgery has the potential to harm the patient. As a result, sham surgical procedures are rare in human subjects.

In a classic study in 2002, patients with osteoarthritis in the knee either had standard surgery, had their knee joint washed out, or had an incision made in the skin and sewn up again. All the patients in the trial therefore experienced "surgery" of some sort, but didn't know which type. All three groups reported similar levels of pain reduction and improvement in mobility, suggesting that the standard surgery produced no advantage over placebo.

A sham surgery trial has recently reported relating to the controversial CCSVI theory of the causation of MS, which hypothesises that MS is caused by compromised drainage of blood from the central nervous system. The proposed treatment is balloon venoplasty, whereby a small balloon is threaded into the vein and then inflated to clear the blockage. Since 2009, around 30,000 MS patients worldwide have had this treatment, almost always privately rather than as part of a trial.

In this small trial, 30 patients received either the balloon venoplasty treatment or a sham surgery. The treatment did not provide sustained improvement in patients. In fact in some cases, there was a deterioration.

Clearly this was a small study, and more research is needed. But in the meantime, the researchers, who studied under Paolo Zamboni, the developer of the CCSVI theory, have urged patients to enroll for trials rather than pay for the treatment privately.

Overall I believe placebos certainly have a valuable place in research, assuming of course that patients know they may receive the placebo rather than the active treatment. In the GP surgery, I'm not so sure. We should be using evidence-based medicine: that means the best available treatment for the condition, not sugar pills or inappropriate antibiotics. I suspect placebos will always be with us though, one way or the other.

MS research roundup July 2012

Another research roundup, and so soon! But there's just been so much interesting research to tell you about.

We already know that someone's risk of getting MS is linked to where they were brought up: very roughly, the further away from the equator, the higher the risk. Another known risk factor is having antibodies to Epstein-Barr virus (EBV): people with MS are far more likely to have EBV antibodies in their blood than people without.

British researchers investigated the distribution of EBV infection, and found it was the same as for MS: infection was more common further away from the equator. We still have a lot to learn about what causes MS, but this could be a piece in the puzzle.

I've often written before about Vitamin D. Its importance is showing up over and over again in any number of different conditions, including MS. Now an Australian study is under way, to see whether taking Vitamin D can prevent MS. The trial will test 3 dosage levels of Vitamin D against placebo in people who've had a first attack of MS-like symptoms, and will run till 2016. It'll be interesting to see the results.

All of us with MS are different: each of us has different symptoms and a different disease course. We can look at averages, though. American researchers studied over 1000 people with MS. They found that RRMS does not inevitably develop into SPMS, and the onset of progression is more dependent on age than on how long the person has had MS.

As neurons are damaged by MS, cell metabolism is disrupted and there is a buildup of sodium. British and French researchers found that sodium buildup measured by MRI could indicate the degree of MS progression. In those with more advanced disease, sodium buildup in the motor cortex is correlated with greater levels of disability.

This is early-stage research, but could become really useful in monitoring disease progression. With advanced disease, sodium was raised even in apparently normal white matter. 

A group of researchers in Germany have discovered an antibody found in the blood of about half of people with MS that is not found in people without the condition. The antibody's implications aren't fully understood as yet, but in rodents it binds to and damages brain cells known to be important for neurological function.

In time this may lead to a blood test for MS and/or a treatment preventing the antibody from binding to brain cells.

Researchers in America have used monoclonal antibodies to stimulate myelin repair in mice with a condition similar to MS. Similar work had been done before, but using far larger molecules than in this research.

They found the molecules were effective, and quick and cheap to synthesise. They were also stable and unlikely to cause an immune response. Much more work needs to be done, but this could in time be a suitable candidate for human trials.

The nerve damage in MS is caused by T-cells, part of the immune system. American researchers are about to start clinical trials using an extract of sea anemone venom, which they've found is a highly selective suppressant of T-cell activity. They hope it should prevent further damage to the nerves.

It's already known that fingolimod (Gilenya / Novartis) reduces relapse rates and disease progression. Swiss researchers have now shown that it's also associated with a reduction in the number of lesions, and slowing of the rate of brain volume loss. Not everyone is able to have fingolimod, but for those who can, this is just another benefit of another hugely useful treatment.

Modafinil (Provigil) is approved to treat excessive daytime sleepiness in narcolepsy and some similar conditions. It is also used for fatigue and sleepiness in MS. In a small trial, people taking modafinil had no significant change in disability level over 3 years, while those not on modafinil did have significant changes.

A much larger study is needed, and particularly comparisons made between taking modafinil with different disease modifiers. This is a really interesting result though,with a lot of potential.

Taiwanese researchers carried out a meta-analysis of studies on the effect of cranberry juice on UTIs. The results confirmed that cranberries do protect against UTIs. The effect was particularly strong in women with recurrent UTIs. There were,however, concerns about the amount of sugar in cranberry juice.

Finally, some excellent news: Canadian researchers have found that people with MS are less likely to get cancer than the general population, particularly bowel cancer. The risk level varied for different types of cancer.

Further studies are needed to find out why people with MS have these different levels of cancer: it may be because both MS and cancer involve the immune system. Still, good news is good news!

MS Research Roundup June 2012 Part 2

This is the second part of the current research roundup. Part 1 is here. In this part, I'll be looking at MS treatments.

The symptoms of MS are caused by damage to the fatty myelin sheath round nerve cells. American researchers found that the immune systems of people with MS were targeting 4 particular lipids (fats). In autopsy, these lipids were depleted in areas of MS damage.

Working with mice with an MS-like illness, they then injected the lipids over several weeks. Disease severity was limited and even reversed. Some tests now show that the mice can take the lipids orally and still improve.

This research is at very early stages, but it holds huge promise for a treatment that can actually repair our damaged myelin.

Omega-3 fatty acids are thought to be helpful for many conditions, but not much work has been done on how they work. American scientists fed three types of fatty acid to mouse macrophages, which they stored as phospholipids. The scientists then stimulated the cells to produce inflammatory responses.They found that Omega-3 inhibited an enzyme called cyclooxygenase (COX), which produces the prostaglandin hormones that spark inflammation.

Inflammation is part of the process of damage to nerve cells that leads to MS symptoms. This research is a big clue as to what could be happening inside the cells, and how Omega-3 oils could possibly help.

Now an exciting stem cell study. An American research group isolated hepatocyte growth factor from mouse mesenchymal stem cells. When they injected this into animals with an MS-like condition, inflammation reduced, neural cells grew, and the myelin sheath regrew over lesions caused by the disease.

Previous work by these researchers has led to a clinical trial where MS patients are being injected with their own stem cells. Now it looks like they may have found the important element for recovery.Watch this space!

Canadian researchers gave injections of either the MS drug interferon beta-1a or a placebo to people who had had signs of possible MS. After 3 years, those who had been on interferon beta-1a were less likely to have progressed to clinically definite MS. This confirms the importance of starting treatment as early as possible.

An oral drug, ONO-4641, is being trialled in the USA.  The investigators have found that after 6 months, those on the drug had a reduced number of brain lesions. The medication does have possible side effects, including short-term heart problems, raised liver enzymes, and lowered levels of lymphocytes, an immune system component. The drug does sound promising though, for those unaffected.

Most clinical trials for MS drugs are with people who have relapsing-remitting MS: perhaps natural, since that's the largest group of people with MS. What follows, though, is that in due course the treatments are only approved for use in RRMS, because that's the only group where there's evidence.

So it's good to see a (small) study, of a drug called MIS416, in secondary progressive MS. Although a far bigger study is needed, most of the patients in this trial saw some relief of their symptoms after only 12 weeks. I look forward to seeing further results on this drug.

Finally, some good news for those of us with MS: it seems we may be less likely than average to have heart disease. An American researcher analysed the reasons people with MS had been in hospital, and compared them with people without MS discharged from hospital. The people with MS were less likely to have had heart attacks.

To be honest, I'm not entirely convinced by this. The people with MS were (on average) younger than the others in the analysis, so would be less likely to have cardiovascular problems. And it doesn't seem to take account of the additional risk for people with MS of being hospitalised for infections.

But hey, I'll take all the good news I can!

That's it for this research roundup. See you next time?

MS Research Roundup June 2012 Part 1

Lots of interesting research to report again this time. It would be a very (very) long post if I did everything together, so I'm going to split it into two. This post will be about risk factors for MS and possible causes, and the second post (to follow shortly) will focus on treatments.

We know that more women than men have MS, and the proportion is increasing. Greek researchers compared the proportions in people living in urban and rural areas in Crete. They found that in rural areas there was less risk of MS generally, and the women:men proportion hadn't risen as it had in the towns.

This is an interesting finding. The researchers found that the urban women were more likely to smoke, drink pasteurised milk, use contraceptives, and various other factors. But so many things could possibly be involved - environmental pollution is one that springs to mind. More research needed!

Research is showing that Vitamin D is linked with a huge number of conditions, including MS. Now it seems it could also be associated with some cases where MS runs in families. British and Canadian researchers have identified a rare gene variant in these families, called CYP27B. People who inherit two copies of this gene develop a genetic form of rickets, a condition caused by vitamin D deficiency. One copy leads to lower than normal levels of vitamin D.

Out of over 3000 unaffected parents of people with MS, 35 carried the gene. In all 35 cases, the person with MS had inherited the gene. The odds against this happening by chance were enormous.

Not only does this finding go some way to explaining how MS can run in families, it also adds to the growing weight of evidence that vitamin D levels and MS are very closely linked.

We also know already that there are links between previous exposure to the Epstein-Barr virus (EBV), which causes glandular fever (mononucleosis), and the risk of developing MS. Spanish researchers discovered that naturally  lower levels of vitamin D in winter were linked with lower levels of an immune system component called TLR7. This controls the immune system response to viruses.

The researchers drew no conclusions about the impact of all this on other conditions: but could this be one piece in the puzzle of how the different MS risk factors are linked?

Several projects relating to the CCSVI theory have reported recently. First, two proof of concept studies from the USA, which examined people with MS, people with other conditions, and healthy controls using the Zamboni protocol, using ultrasound and MRV. They found that only a small proportion of people with MS had the venous constrictions said to be characteristic of CCSVI: the proportion for both people with other conditions and healthy people was similar. These studies showed no evidence that narrowed veins are linked with MS.


The European Society of neurosonology and cerebral hemodynamics examined the five criteria for diagnosing CCSVI in the Zamboni ultrasound protocol, along with the studies from which they were derived and the main studies looking at cerebrospinal drainage. Their view is that the criteria are questionable: one is based on data collected in other contexts, two have never been validated, one is technically incorrect, and two are subject to so many external influnces that it's difficult to state whether any "differences" are part of a disease or just normal variation.

As a result of these concerns, the Society strongly discourages venoplasty and/or stenting for CCSVI.

A small study in Canada followed 30 people before and after venoplasty for CCSVI. The researchers found no difference between the patients who had been treated and 10 who had not. Any initial benefits reported tailed off, particularly after about 3 months. By a year, several people's veins had reblocked, but their function was no different from those whose veins had not reblocked.

And a group of Italian reseachers carried out a meta-analysis. They critically analysed the proposed biological basis for CCSVI and reviewed all published studies on CCSVI and its ultrasound methodology. They found no supportive scientific evidence for any part of the theory that CCSVI is linked with MS. They feel that CCSVI may be a stand-alone condition, which should be investigated in its own right - but it's not linked to MS.

People have called me anti-CCSVI. That's not accurate - or wasn't. When I first heard about the idea I was interested. Who wouldn't be? I'd love a cure for my MS. But I knew really rigorous research was needed, to see if Zamboni's results could be repeated. As time has gone on, it's become increasingly apparent that the theory just doesn't hold water. If people want to have their veins Dyno-Rodded, well I suppose that's up to them. But I don't want scarce NHS funds paying for it.

On that (rather controversial) note I'll end Part 1 of this roundup. I'll try to do Part 2, dealing with treatments, tomorrow.

The MS Trust hits the airwaves!

The excellent MS Trust has been selected to give a Radio 4 appeal this Sunday. As well as bringing in much-needed donations, the appeal will raise awareness of the charity, letting people with MS, their friends and family know about the support available to them. Money raised will be going to help fund the Information Service, which is available free to anyone with a question about MS.

The appeal will be broadcast on Sunday at 07.55 and 21.26, and again the following Thursday at 15.27. Full details are here.

Please share this information, so that the appeal gets a really good audience! Please also listen, and consider donating if you're able to.

And if that doesn't grab your imagination, have a virtual stroll round the Secret Art Show: small pieces of art, some by international artists, all sold anonymously at the same price. You only  discover who yout piece is by when you receive it.

It's all as exciting as Mr Exciting, the Mayor of Exciting Town!

Taking the piss

So what would make you want to have a tube shoved up your bahookie and have someone give injections to your bladder from the inside? There's some people would pay good money for that I know, but it's not really to my taste.

Well, it was the latest treatment for my bladder problems.For a long time now, I've had frequency (needing to go all the time) and urgency (once I need to go, I need to go NOW.) I've also had regular UTIs. Last year this reached ridiculous levels. When I stopped antibiotics for one infection, I would have about one blissful bacterium-free week, before succumbing again.

All this was down to my detrusor muscle, the muscle that contracts when you're weeing to squeeze the wee out. I have overactive bladder as a symptom of MS, where the muscle reacts on a hair-trigger: it sends the "I'm full" signal to the brain well before that's actually the case; it responds to external stimuli like running water or opening the front door; and its contractions cause stress and urge incontinence.

So what could be done? Well, obviously, antibiotics for the infections: I worked my way through a wide range, collecting allergies and interesting side-effects along the way (mostly hallucinations - the gazelle giving me a jar of hand cream was my favourite).

I took part in a drug trial, self-injecting twice a week. I knew when I was on the drug rather than the placebo because I got skin reactions. It really, really helped. But then the trial ended, and I was back to the standard medication.

The standard medication is anticholinergic drugs, which help to stop the detrusor muscle from over-reacting. They help, a little, but not much. I still have a lot of problems.

So it was proposed that I should have botox. No, not up there. Down there. The idea is to partially paralyse the detrusor muscle so that it's not so twitchy. And the way they access it is through what's normally the exit.

In due course, therefore, I found myself on an operating table with my legs up in stirrups, with a charming consultant in there at the business end shoving a tube with a camera attached up where only one man has been before (the urologist who did my previous cystoscopy). The equipment that let him see what was going on also had a small screen that I could see (if I wanted, which being me of course I did), and he was good enough to give me a guided tour of my own bladder - this is the top, this is where the left kidney opens into the bladder etc etc.

The actual injections...weren't nice. But hey, I've got MS, I've experienced a lot worse. If you can imagine someone pinching a bit of your insides, FROM the inside, really hard, that's kind of what each one is like.

But it was soon over, and there was no pain afterwards. And the very next morning, I woke up, needing the loo, yes, but not desperate - I'd forgotten what that felt like! Generally the effects have been wonderful. I can hold on for absolute hours, as opposed to my previous average of about 40 seconds!

Predictably enough, with my history, I got an infection, but that was soon sorted out with antibiotics. I'm still on a low dose, to protect me against any more. The ongoing side-effect is that I've kind of gone the opposite way to where I was before. I now can't wee when I want to! Well, I can, but it's hard work, y'know? Seems the injections have worked a little too well. Hopefully that'll settle down in time. In the meantime it's still preferable to my previous problems.

So all in all a positive experience, and I'd definitely recommend botox if you have overactive bladder and the standard meds aren't helping you. I'll have to have it repeated every 6-9 months, but that's small price to pay for the benefits.

And, of course, for having the smoother, more youthful bladder I've always dreamed of...

MS Research Roundup April 2012

Some more really interesting MS research projects have reported recently. It's an exciting time!

All of us with MS have probably had MRIs, for diagnosis or to check on progression. But there has always been a paradox: the number of lesions in the brain doesn't correlate with the effects of the disease.

Researchers looked at the number of lesions in different parts of the brain, and found that they could be correlated with specific symptoms. For instance, lesions in the precuneus and precentral gyrus were most predictive of mobility problems.

MRIs have poor resolution, and contrast media such as gadolinium do not necessarily measure what they aim to: they often show fluid rather than inflammation. This research could help MRIs to be used with a new precision, as a truly useful clinical tool.

We already know that many women find their MS symptoms improve during pregnancy. Now Australian researchers have found that even one pregnancy halves a woman's risk of developing MS in the future.For women who have had two or more pregnancies, the risk is a quarter. The researchers suspect this may be the reason the rate of MS in women has inched up over the last few decades, as more and more women have decided to have babies later or not at all.

An interesting study from a group of Belgian researchers. They got nearly 1400 people with relapsing remitting MS about their diet, drinking habits, and whether they smoked. They found that people who consumed alcohol, wine, fish and coffee on a regular basis took 4-7 more years to reach the point where they needed a walking aid than those who never consumed them. They didn't find the same pattern in people with progressive MS. Those who smoked cigarettes needed walking aids earlier than those who didn't.

I'll just have to hope that my intravenous coffee drip offsets my cigarettes then...

Research is continuing on various aspects of the CCSVI theory. The theory states that malformed and blocked veins in the neck lead to the deposition of iron in the brain, which in turn leads to autoimmunity and demyelination of nerve cells.

A group of American researchers tested this theory by tying mice's jugular veins shut. The mice were then observed for 6 months. There were no signs of inflammation or demyelination on CT or MRI, and no clinical change. This result strongly suggests that CCSVI is not responsible for demyelination, and therefore not responsible for MS.

We've recently seen the approval of the first oral drug for MS, Gilenya. The next to come into clinical use is likely to be BG-12, which has had extremely good results in trials. When taken three times a day, it halved the relapse rate compared to a placebo tablet.

Now the manufacturers, Biogen Idec, have applied to the FDA for approval for BG-12. They're hoping for priority processing which will shave some time off the process: if they don't get it, BG-12 should be released in the USA by the end of 2012 or early in 2013. Hopefully it'll be introduced in Europe soon afterwards, and so on around the globe.

The next study is of particular interest to me, as I've recently had this treatment myself. (Watch this space - I'm planning to post about it.)

BOTOX^® is already approved in several countries including the UK and USA for the treatment of overactive bladder resulting from neurological problems such as MS and spinal cord injury. It works by relaxing the bladder muscles that were previously going into spasm, causing urgency, frequency, and possible incontinence.

Now two Phase 3 studies have shown positive results for BOTOX^® for idiopathic (cause not known) overactive bladder. These results are just further confirmation of the usefulness of BOTOX® in treating overactive bladder.

Many people with MS fall: falls can result in injury, and the fear of falling can result in severely restricted mobility. American researchers asked 575 people with MS about their level of disability, how often they fell, and how afraid they were of falling. Nearly two thirds were concerned about falling, and over two thirds restricted their activities because of fear of falling. People with moderate mobility problems had the highest number of falls, and those with the worst mobility (ie non-walkers) had the fewest.

What can we do with this information? I suppose it's a question of awareness.If you know you're in the group most at risk of falls - the group with moderate mobility problems - you need to take particular care not to lean too far over, not to turn your body without moving your feet, and so on.

Researchers in Germany asked several hundred people who felt severely affected by their MS whether they wanted their doctors to talk to them about their disease progression, and about end-of-life issues.Three-quarters wanted to discuss their disease progression, but less than half were interested in talking about end-of-life issues like whether they would want to go on a life support machine or whether they would want to be resuscitated should the need arise.

These are important but very sensitive topics. Doctors must show great sensitivity when raising them.

So that's it for this research roundup.See you next time!

Doctor Doctor, can't you feel I'm burning burning? #braveheart

Doctors do, in the main, appreciate that the symptoms of MS can include dreadful pain. It can be burning, stabbing, shooting, like an electric shock, pins and needles, or - my personal favourite - like your limb is being sawed through. Lovely.

When this pain is bad, it really stops you in your tracks: but the DWP don't seem to see it as relevant to whether you can work or not.

If you're claiming Employment and Support Allowance, you're likely to be called to a Work Capability Assessment, carried out by the private company Atos. Incidentally, Atos is getting these assessments spectacularly wrong - and that's if you can get into their offce, if it's not one of the ones that's inaccessible to people in wheelchairs.

The assessments are done by "healthcare professionals" - doctors, nurses, physiotherapists or occupational therapists - who may have no knowledge at all of your condition. They complete a computer questionnaire based on your answers.

The questions are all about your ability to perform physical tasks. There is no recognition of pain, fatigue, or the fact that you might be able to perform a task once, but not repeatedly.

Never mind us not being fit for work. The Atos tests aren't fit for purpose.

So it's great that Scotland's GPs have called for an end to Work Capability Assessments.We, sick and disabled people, have known about the problems with them for a long time, but it's great to have recognition  from the medical world. Dr Steven Carty, an Edinburgh GP, said:

This sends a ray of hope to some of the weakest and most vulnerable in society.

It also sends a clear message to other representative bodies including the General Medical Council (GMC) of the significant concerns shared by many GPs across the country.

In my opinion the current contractual arrangements between the DWP and General Practice are unsustainable. The WCA as performed by ATOS is not an effective or safe method of determining "fitness to work" and this must be addressed.

All doctors are duty bound by the GMC to report any system or process that may be harmful to patients. The WCA is a harmful process. Scottish GPs have spoken: the GMC cannot remain silent on this matter any longer.

Let's hope the BMA and GMC respond to this call and also condemn the WCA (so many acronyms!)

We certainly can't go on with this flawed system, which doesn't recognise symptoms which are such a major part of sickness and disability for so many people.

 

Life's a trial

When I'm doing research roundups, I quite often talk about clinical trials being "Phase 2" or "Phase 3". But what do these terms mean? The development of a new drug or other intervention is a long-term process. commonly taking 12 or more years before being available to patients. The regulatory process adds another hefty chunk of time.What's happening for it all to take so long?

Research begins in the laboratory, where potential treatments are tested on animals: for instance, there is a strain of mice which have a condition very like MS. Testing drugs on them gives a reasonable idea of whether they're likely to help people with MS. Around 1000 potential drugs are tested for each one that makes it to clinical trials.

The use of animals in drug trials is a whole other question, one I might discuss in a future blog post. If the drug is helpful for the animals (and how that's worked out is again a subject for a future blog post), the researchers will look for more funding to test it out on people, in clinical trials. The clinical trial process has four phases.

Phase 0 Very low doses of the drug are given to 10-15 people to see whether the drug does what was expected in humans. Tests are carried out to check what the drug does to the body, and what the body does to the drug.

Phase I The drug is tested on usually 20-100 healthy volunteers, to check that it is safe. These volunteers are normally paid, as they won't get any health benefit from participating, and are taking the risk of being given an untested drug. Some of you may remember news coverage of a Phase 1 trial in 2006 where 6 healthy volunteers became violently ill after taking a new drug.

Phase II Designed to assess how well the drug works, and what is the best dosage. Between 100 and 300 volunteer patients take either the drug or something else - the existing treatment if there is one, or a placebo.

Phase III The drug is tested on a large number of patients over a number of sites. This phase aims to be the definitive assessment of how effective the drug is, compared with any current treatments. Sometimes a manufacturer wants to prove that their drug works for other patients or other conditions than those originally established. In that case the Phase 2 or 3 trial would be the first stage.

Phase IV This is the period of surveillance once the drug is on the market. Safety continues to be checked, and technical support is available.

Clinical trials can take a long time to run. It can be difficult to recruit the number of people needed, particularly in Phase III. For many long-term conditions, it can take several months to see any effect from the drug. I recently participated in a Phase II trial for a full year.

Most Phase III trials (and some Phase II) are randomised, double-blind and controlled.

• Randomised means that participants are randomly assigned to the treatment or placebo groups
• Double-blind means that neither the participant nor the researchers know whether they're receiving the treatment or the placebo. It's important that the researchers don't know, as they might subconsciously behave differently to people in the two groups.
• Controlled means that one group receives a placebo (or the existing treatment, if there is one).This means that the effect of the new drug can be isolated. Is it better than the existing treatment? If so, how much better?
• Some trials are designed to cross-over, This means that halfway through the trial period, the participants swap over to receiving the other treatment. Those who were gettng the active drug will change onto the placebo, and vice versa.

After the trial process, the manufacturer will apply for the drug to be licensed, which has to be done separately in different parts of the globe.Here in the UK, once it's been licensed, the action then moves to an agency called NICE, who decide whether the NHS should fund treatments.

Their decisions are based on cost-effectiveness, potentially leading to some controversial outcomes. Recently they've refused funding to the new MS drug Gilenya, and there have been several decisions where funding has been refused for expensive cancer drugs which were likely to give only a few more months of life.

In some cases, local Primary Care Trusts still have to agree to fund the treatment. There have been problems recently with Sativex, which is licensed for use in MS spasticity if other treatments don't help. Many PCTs are refusing to fund it. The MS Society is campaigning on this: if you have funding for Sativex refused, they provide advice on what steps to take.

You're most likely to find out about trials through your consultant. If you'd be interested in participating in a research project (without commiting yourself to anything!) let them know.

It can't be denied that there are some risks involved, as there are with any treatment. But I found trial participation interesting, and if the drug concerned goes on to be approved I'll feel quite proud: I was part of that!

MS research roundup February 2012

With apologies for the long gap since the last one - here, finally, is my latest research roundup. And there's some real goodies this time!

MS is conventionally seen as an auto-immune condition. For some reason, not yet fully understood, the body's immune system begins to attack the myelin sheath surrounding the nerves. This has recently been challenged by the CCSVI theory, which states that MS is caused by blockages in the veins of the neck leading to back-up of blood and consequent deposition of iron in the brain.

Now an American researcher has developed a new theory. She believes that MS is a metabolic disease, caused by the body having problems dealing with fats in the diet. The rise in the number of cases over the last few decades is due to us, as a population, moving to a diet high in carbohydrates and saturated fats. Oxidised LDL cholesterol accumulates on nerve cells and triggers an immune response, leading to scarring of the cells. Men and women metabolise fats differently, which could account for the higher prevalence of MS in women.

It's an interesting theory, but obviously needs much research done to see if it holds water. Watch this space..

I've talked about vitamin D several times before: there's a lot of research going on in the field, and there seem to be many links between vitamin D and MS. Vitamin D is created in the body following exposure to sunlight, so people tend to be more at risk of deficiencies the further they are from the equator.

An international group of researchers are now suggesting that vitamin D should be added to foods like milk and fruit juice in Scotland, which has some of the highest levels of MS in the world. The Scottish Parliament is unconvinced. Food supplementation already exists: iodine is added to table salt to protect against goitre. Should vitamin D be added to the list?

As many of us know all too well, MS can be difficult and time-consuming to diagnose. This can cause distressing uncertainty, as well as delays in commencing treatments. Israeli researchers have developed an electronic "nose" which can diagnose MS, as well as some cancers, from a person's breath. They identified organic compounds in the breath that are a sign of MS, then produced sensors to detect them. They hope that their device will allow MS to be diagnosed at an early stage and without using invasive techniques like lumbar punctures. Still early stages for this research, but a very exciting development!

On to treatments. At least 80% of people using interferon-b eventually develop antibodies to it, meaning treatment has to be stopped. Instead, German researchers tried injecting mice with an MS-like disease with a type of RNA which stimulates the body to produce its own interferon-b. The results were excellent. This could prove to be an excellent way round the antibody problem.

As people with MS age, the rate of remyelination of nerve fibres slows, resulting in the loss of more nerves. A research group in the UK have managed to reverse this decline in mice by exposing them to stem cells from young mice. Stem cells show great promise in remyelination, and this is a great discovery.

Finally, research on treatments for MS symptoms.

The MS International Federation have released the results of a survey on fatigue. 86% of those who responded said that fatigue was one of their main symptoms, and 46% that fatigue has a high impact on their lives. For those of us with MS fatigue, this will come as little surprise. Interesting data, showing how important it is for healthcare providers to recognise the problem of fatigue. Important to remember, though, that those who responded had chosen to participate in a survey on fatigue, and might therefore be those for whom it's an important consideration. People unaffected by fatigue might not have been interested in participating.

An Israeli research group did a trial involving three groups of patients. One group received electrical stimulation of the left prefrontal cortex, one of the motor cortex, and the final, control, group received a sham stimulation. After 18 treatments, the group receiving stimulation in the motor cortex had less fatigue and less depression. There was a tendency towards less fatigue in the prefrontal cortex group. The control group had no signnificant improvement. Further research is planned to investigate the effect of the stimulation on metabolic and neural activity.

Many of us with MS also experience cognitive problems - short term memory loss, lack of concentration, and so on. Italian researchers used computer-based rehabilitation programmes to help with attention and information processing. One programme, for instance, is a train driving simulation: you have to observe the control panel of the train and the surrounding countryside while encountering increasingly difficult distractions. After a 12-week programme of treatment, patients had improved attention and information processing skills, although no changes were seen on MRI. It seems training can help, but it's no cure.

I hope you agree that there were some really promising bits of research this time. Let's see what happens next!

Getting DLA #spartacusstories #spartacusreport

In 2003, I took really poorly with what turned out to be MS.My condition progressed from there. It took two years for me to get a diagnosis.

After a while, when I was really becoming restricted badly, I decided to apply for Disability Living Allowance. I could only walk very short distances - less than 40 metres or so - and my fatigue and balance issues restricted me badly in what I could do. I was using a wheelchair for longer distances.

I filled in the hugely long and complicated form myself: a mistake, as I later discovered. There are certain ways of wording things that are "understood" by the decision makers at the DWP.

It's depressing filling in a form like that. When you're trying to stay positive and focused on living your life, suddenly having to list all the things you can't do, write about your problems with washing, dressing, going to the toilet, doesn't really help.

A doctor came to my house to give me a medical. He asked me lots of questions, and confused me. When I finally saw his report, some time later, I didn't recognise it as relating to what I'd said. Apparently I could walk for about quarter of a mile without needing to stop, and had few problems with self care.

The DWP sent me their decision. They'd awarded me low rate care, and nothing for mobility. I didn't think that was right, so I appealed against the decision. At the appeal hearing, I was called a liar to my face and had the low rate care removed as well. Now I was getting no DLA at all.

I decided to take it further. I appealed the tribunal's decision to the Commissioner for Social Security. He decided I hadn't had a fair hearing, and that I should have another one.

At the new hearing, I was awarded high rate mobility and middle rate care. The award is indefinite, because my MS is progressive. Sadly, it's not going to get better!

The media is full of stories about scroungers who get DLA. I genuinely don't know how these people do it. Considering all I went through to get DLA, with a genuine condition...

Anyway. Please. Support Responsible Reform, the #spartacusreport. Yes, some reform is needed in the benefits system, but not the manic rolling-eyed machete-wielding currently on display from the Coalition.

Research roundup December 2011: Blogger ate (most of) my post

This was going to be a lovely long, informative research roundup, full of interesting and groundbreaking stuff to take you through to the New Year.

Sadly, Blogger (the software on this site) decided to eat all my carefully saved links. And what with my terrible MS memory, I can only remember two of them!

Not to be daunted, I'm going to tell you about those two. I'm really sorry though. Hopefully I'll remember some of the others, and can add them to other roundups in the future.

I've often spoken before about vitamin D and MS. It's a very important area of research at the moment. Now a group of British and Canadian researchers have discovered a rare gene that seems to be linked to MS. The gene is called CYP27B1: a mutation in it affects a key enzyme, leading people with the variant to have lower levels of vitamin D.

They identified the mutation in CYP27B1 as being of interest, from looking at 43 people who came from families with 4 or more individuals affected by MS. Then they looked at over 3,000 unaffected parents of someone with MS. 35 of them carried one copy of the mutated version of CYP27B1 along with a copy of the normal version. In all 35 of these cases, the person with MS inherited the mutated version.

The likelihood of the gene's transmission being unconnected with MS are billions to one, the researchers claim. The very strong implication is that in these particular MS cases, low levels of vitamin D are directly connected to the disease.

It's always been thought that MS begins by attacking myelin in the inner layers of the brain, the white matter. Now American researchers have found that in fact the disease seems to move from the outer, cortical layers of the brain.

The next step for their research is to study these cortical lesions to identify new molecular targets for treatment, and to develop imaging techniques so that these lesions can be shown clearly.

And, well, that's it for December's roundup. Apologies again for the lack of content!

MS Research Roundup October 2011

There's been some very interesting research announced this month. Some of it is pretty technical, but once I've worked out what it means myself, I'll do my best to translate it!

American and Canadian researchers have developed an imaging technique using lasers that allows them to see the amount of damage the myelin sheaths around nerves have sustained. Previously, such measurements could only be obtained by removing the nerve and slicing it into layers - which was only possible once the patient was dead! So far, this research has only been carried out on animals, but it could in the future be used as a diagnostic tool for conditions like MS.

The body has developed what is generally a very effective barrier between the blood and the brain, to keep anything potentially harmful from moving between the two. While this is generally very useful, it can pose a problem with getting drugs into the brain to treat conditions like MS, Alzheimer's disease, and cancers of the central nervous system.

Now a group of American researchers have found that a molecule called adenosine can help large molecules enter the brain. An existing drug called Lexiscan, which is based on adenosine and is used in heart imaging for very ill patients, briefly opens the blood-brain barrier. In MS, confusingly, research is also focusing on how to tighten the barrier, to stop destructive immune cells getting in to the brain and causing damage.

There's been a lot of research, and talk in the MS community, about the possible beneficial effects of taking fish oils for people with MS. Researchers from America looked at the effects of taking omega-3 fatty acid. They found that it had a significant impact on a molecule called matrix metalloproteinase-9 (MMP-9), which is associated with disruption of the blood-brain barrier, and immune system T cells getting into the brain. Their results suggest that taking Omega-3 supplements may benefit people with MS: they don't suggest amounts. That (as ever) will be for further research.

Another group of American researchers looked at how the body metabolises fatty acids. The speed of metabolism is controlled by an enzyme called carnitine palmitoyltransferase 1 (CPT-1). The researchers controlled the amount of CPT-1 in the animals they were working with, and found a reduction in disease severity as well as less inflammation and demyelination.This research is a long way from any clinical use, but it sounds a potentially useful therapeutic target for MS.

Certain steroids in the brain (neurosteroids) have a protective function. Canadian and Iranian researchers discovered that brain tissue from people with MS had much lower levels of neurosteroids than tissue from people without, particularly a neurosteroid called allopregnanolone.This was due to the action of a specific molecule called micro-RNA (miRNA).

They then treated mice with a disease similar to MS with injections of allopregnanolone and found that they maintained a better protective myelin coating on their spinal cords than mice receiving the placebo.They also had significantly reduced disease severity compared both with the mice receiving the placebo and their own symptoms before treatment.

Next, two treatment stories relevant to particular countries. The first North American stem cell trial for MS has been approved: as a Phase 1 trial it will assess the feasibility and safety of using the body's own stem cells to treat MS.

The procedure will consist of harvesting the patient's mesenchymal stem cells, culturing them in a laboratory, and then injecting them intravenously back into the patient. Mesenchymal stem cells have a wide range of effects, varying from lessening immune activity to encouraging tissue repair. Study participants will be closely monitored for six months after the procedure. If it's shown to be safe and feasible, an application may be made for a larger, controlled trial, including the use of a placebo procedure.

Fampridine (Fampyra) has just been launched in the UK. I did a separate post about this drug, which aids walking in some people with MS.

Finally for this month, an Italian research group have been researching treatments for fatigue in MS. They used neurocognitive rehabilitation techniques. The information I have about the research doesn't say what specific techniques they used, but neurocognitive rehabilitation can include things like occupational therapy and hand/eye coordination exercises.

The researchers found that both immediately after 5 weeks treatment and 6 months later less fatigue was reported. There was no difference in physical disability. They suggest that neurocognitive rehabilitation could be a useful strategy for treating people with MS.

That's the roundup rounded up for this month. What will the next month bring? Only time will tell!

MS Research Roundup September 2011

Again, a short research review this month. My apologies.

First, an extremely interesting and important genetic study, that has received a lot of media attention. Researchers looked at more than 10,000 people with MS from 15 countries, as well as more than 17,000 healthy controls. We already knew about more than 20 gene differerences that may contribute to people getting MS. The large numbers involved in this study allowed them to find another 29 genetic variants that could contribute.

About half of all the gene variants known to be involved affect the immune system, and one-third have been implicated in other auto-immune diseases, such as Crohn's disease, coeliac disease, rheumatoid arthritis, lupus, and type 1 diabetes.Knowing which genes are involved in MS could potentially help new treatments be developed, including the possibility that treatments already in use for one auto-immune condition could be used for another.

I've mentioned the common herpes virus HHV-6 before. It causes the childhood infection roseola, marked by a chest rash and high fever. However very little is known about it, including how it manages to reach the brain to be implicated in causing conditions like MS, encephalitis and a form of epilepsy.

These American researchers found high levels of HHV-6 in the olfactory bulb (a part of the brain associated with smelling) and in nasal mucus, in over half of their samples. They also discovered that specialised cells connecting the nose to the brain are susceptible to infection by the virus. As ever, more research needed. It could be that infection entering the brain via the nose causes a different disease result from infection entering by another source. This is a really interesting study though.

It's well-known that MS, as well as other auto-immune diseases like lupus and rheumatoid arthritis, are considerably more likely to attack women than men, but it's never been clear why. Now American researchers have discovered a new type of immune system B cell: these make antibodies, which go on to bind to and attack the body's own tissues.

The researchers found higher levels of these cells in elderly female mice, young and old mice prone to auto-immune disease, and humans with auto-immune diseases. They are now seeking a way to treat these diseases by blocking production of the cells.

A very big MS-related story at the moment is vitamin D exposure. A group of American researchers compared vitamin D exposure between childhood (whether the individual had been given cod liver oil) and disease onset (sun exposure in the previous winter) with how rapidly they were progressing.

They found a close link between a low level of vitamin D exposure before disease onset and slower disease progression. They were working only with people with progressive MS, and with quite a small group, so research is needed with a larger group and with people with the relapsing remitting form as well to see if the same results are seen. A really worthwhile and interesting study though.

Daclizumab (Zenapax) is a monoclonal antibody, currently going through trials. In this recent global trial, where daclizumab was injected every four weeks, it reduced relapse rates by around half compared to taking a placebo. There was however an increased risk of infections. Daclizumab is now in phase 3 trials, where it's being compared with beta interferon 1a.

Finally, news on two treatments for MS symptoms. First, the Irish Medicines Board has given approval to the use of Botox for urinary incontinence for MS following the biggest ever clinical trial of Botox for neurogenic overactivity of the detrusor muscle. The study demonstrated that treatment was effective within a couple of weeks and lasted for 8-10 months.

Botox is already in use in the UK, and this large study just confirms its utility. It's an important step towards gaining licences in those countries where it's not yet used.

Many of us with MS, diabetes or shingles know the terrible, ongoing problem caused by nerve pain. Current drugs may not help at all. Now British researchers have discovered that a gene called HCN2 is involved in causing the excessive "firing" of pain-sensitive nerves.

In experiments with mice genetically modified to have the gene removed, disabling the gene was found to relieve chronic and inflammatory pain, but without reducing reactions to acute pain, the type caused by a sudden injury. This is crucial: responses to injuries can be vital to our survival. The researchers hope that they'll be able to develop a drug to block the protein produced by HCN2, so the same effect can be seen in humans.

That concludes this month's research review. Again, apologies for the limited number of items covered, but I hope you'll agree there are some really interesting studies in there.

See you next month!

"I'm better"

For the last month or so, I've really not been well. A succession of UTIs, along with the increase in MS symptoms they bring with them. Antibiotics would stop the symptoms of the infection during the course: but then, soon after, it would return.

Then, at the stage when my wee looked like creosote and smelt like something had died in it, I could barely stand, and was really just hoping I would die quickly...I discovered (/my doctor prescribed) nitrofurantoin. This seems to be the latest thing for persistent UTIs, as a friend has just been given it for the same thing. And you know the best thing? It works. Well, so far at least.

So, it seems I no longer have a UTI. I'm better.

Better.

What does that word mean to someone with a long-term illness? I'm never going to be really "better". I have a progressive condition. I'll always have dreadful fatigue. I'll always have cognitive impairment, and all my other symptoms. I can take tablets or injections to help with some things, or work around them, but they're always going to be there.

It seems to me we redefine what "better" means, for us, in our personal circumstances. I'm better because my UTI has gone away: in terms of my symptoms, I'm less worse.

Similarly, we redefine the words describing how we are. I can say "Yeah I'm good", even though I'm in pain and exhausted, because for me, in my terms of reference, that's good.

So...yeah, I'm better. Which is great!

MS research roundup July 2011

First this month, a very exciting discovery (for researchers and science geeks like me, anyway). Until now, MS researchers working in the very early stages of a project, when animals must be used, had only been able to use non-human primates when the illness had been artificially induced. Now a naturally occurring disease in Japanese macaques has been found by researchers in America.

This can give many more clues about the causes and development of the disease. It has already been discovered that the condition is associated with a herpes virus - linking in with previous research suggesting that MS in humans may be linked to previous infection with the herpes strain Epstein-Barr virus, which causes glandular fever (mononucleosis).

More herpes news. A Taiwanese research group have found that there may be an increased risk of MS in the year following an attack of shingles, caused by the herpes zoster virus, which also causes chickenpox. The study followed very large groups of people with and without shingles, and found that those with were almost 4 times as likely to develop MS as those without. This is a very interesting study, well designed and with a very large sample group: however it was limited almost entirely to Chinese patients, and Asian populations have considerably lower rates of MS than Western. This work needs to be repeated on other ethnic groups.

Now a piece of research that may not be news to many of us (including me!). American researchers have discovered that fatigue is the first symptom of MS in nearly 30% of cases, often months or even years before any demyelination can be observed. I can certainly remember multiple visits to my GP complaining of fatigue, when I was either told "But everyone gets tired." ("No this isn't NORMAL tired!") or offered anti-depressants. Not particularly helpful.

The group is planning studies to see if unexplained fatigue can be used as a predictor of MS, and another to see if people whose first MS symptom is fatigue differ in any other way from those who have multiple MS-related symptoms.

It's been known for some time that women with MS who become pregnant have a higher than normal likelihood of experiencing a remission during pregnancy, and then experiencing a relapse after the birth. Now Canadian researchers have looked at the effect of MS on the actual pregnancy. They found overall that pregnancy was safe for women with MS, with no significant difference in gestational age, birth weight or type of birth (vaginal or caesarian).

Women with a greater level of disability were more likely to have adverse birth outcomes, but these did not reach statistically significant levels. The researchers also found that women with MS were more likely to be overweight, which is associated with greater risk during pregnancy and birth.

Now, on to treatments, and first some news about existing drugs. I've spoken before about the highly promising treatment Tysabri.  Getting Tysabri carries the risk of developing the rare but severe condition progressive multifocal leukoencephalopathy (PML). PML is more likely if you have previous been exposed to (and therefore have antibodies to) anti-JC virus (JCV).

From now on, all patients in the EU will be tested for JCV antibody status before starting on Tysabri, and JCV antibody status will be included as a risk factor in Tysabri labelling. The risk of PML is still there, but it should be greatly reduced if people with antibodies to JCV do not take the drug.

Another existing treatment, of longer standing, is Copaxone(glatimer acetate). A group of Canadian researchers found that after a year patients receiving a new oral drug, teriflunomide, along with Copaxone, had only about 1/3 the number of lesions of a control group who took Copaxone plus a placebo tablet.

Teriflunomide has previously been tested with interferon: that trial also showed impressive results. It operates by stopping certain immune cells from dividing. This sounds like a very promising adjunct treatment. I hope it's trialled in larger groups, and against other therapies, as soon as possible.

American researchers have developed a very promising new approach to identifying the "self" proteins our bodies attack in auto-immune diseases like MS, rheumatoid arthritis and diabetes. Their new technique, called phage immunoprecipitation sequencing, allows the identification of any interaction between an autoantibody in the cerebrospinal fluid and the self-protein that drives the autoimmune response. This work is at very early stages, but could eventually be developed into diagnostic tests and even treatments.

Meanwhile, British researchers have discovered a synthetic chemical compound which both reduces the inflammatory response in the body and stimulates the body to produce interferon-beta, an anti-inflammatory molecule commonly given to people with MS. Together, these effects cause significant reduction of inflammation in an animal model of MS. The researchers also found that immune system cells from people with MS were more sensitive to the drug than immune system cells from people without the condition.

Excitingly, a joint research group from Britain and the USA have discovered a new molecule that they believe may lead to a drug able to repair myelin by stimulating stem cells. Again, this is very early stage research. Hopefully it will move to clinical trials and ultimately to some form of treatment, probably within 10-15 years. That would repay all the work that's being going on in myelin repair research.

So, that's what happened in June. Some really exciting news this time! See you, same place next month?