Tony Nicklinson, informed consent, and the community

Seven years ago, Tony Nicklinson was an active, busy, family man. His hobbies were rugby and skydiving. Then he had a massive stroke, and was left paralysed from the neck down and unable to speak. Intellectually, he's unaffected. His condition is called locked-in syndrome.

Tony describes his life as "increasingly miserable". With his family's backing, he's gone to the High Court to ask permission for a doctor to be able to kill him. It's important to note that this wouldn't be assisted suicide, but something quite different.

• Assisted suicide: others may help (eg provide drugs, help with transport) but the individual must perform the action themselves. Illegal. Seen by some as a disability rights issue: it's not illegal for an able-bodied person to kill themselves, but if someone's too disabled to do the deed themself and therefore needs help, the person who helps them commits a crrime.
• Voluntary euthanasia: The individual is not able to kill themself, even with assistance. The only way they can die at will is if another person will actively kill them.

When you listen to Tony's pleas, dictated laboriously by eye movements, it's difficult not to be moved. But emotion isn't a good basis for making law.

And many people are as disabled as him, and lead happy lives. If the courts decide that Tony's life is so miserable that it's OK for him to be killed, what does that say about the value of a disabled life? It's already common to hear able-bodied people saying things like "If I had to use a wheelchair, I'd kill myself." How would a decision that it's OK for a severely disabled person to be killed affect these attitudes?


While making a decision about anything involving healthcare, we must be in a position to give informed consent. That means we must be aware of all the pros and cons of the situation. I don't know enough about the facts of Tony's case to comment on that: but I've heard of previous cases where people requesting death had had no opportunity to live in the community (obviously with appropriate support). Could these people really be giving informed consent?

If assisted suicide and voluntary euthanasia are ever legalised, there will need to be very firm safeguards to make sure people are not being pressurised into requesting them. But research in the places where legalisation has already taken place suggests that this is not impossible.

The key factors for me are community living and social attitudes. We must be free to live as part of the community, and society must accommodate our needs and accept us as equal members of that society. Only then can we make truly informed decisions about whether or not to end our lives.

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.

Spoon overdrafts and the #WCA

It's difficult. I'd love to blog more. I'd love to do so many other things more too! Go out with friends, go shopping, go on holiday, keep on with my voluntary work, hold down a job...

But I'm a spoonie. I'm dreadfully, cripplingly fatigued because of long-term illness - in my case multiple sclerosis. And not only am I short on energy in the first place, but it takes me ages to recover after doing anything.

This weekend is an example. My beautiful, much loved cat Bing died on Friday. It was very, very stressful. Then on Sunday I drove to Oxford for lunch. Before I took ill, I wouldn't have thought twice about driving 60 miles each way for lunch. Now, it's an expedition of Amazonian proportions.

Today is Tuesday. I've not been out of my PJs since Sunday night. I really need to go into town to the bank, but my body's having none of it. It is, in fact, my spoon overdraft that's stopping me dealing with my financial one until I've got that blasted spoon level back up again.

And that's just one of the many problems with the Work Capability Assessment, which decides whether - and at what rate - people should get Employment and Support Allowance (ESA). It asks nothing at all about fatigue. It asks whether you can do a task once, but not whether you can do it repeatedly. It doesn't ask how your ability to work is affected by stress. ("Sorry, Mr. Employer, I can't come in this week. I'm tired cos my cat died.")

It's no wonder that so many people and organisations, including GPs, have denounced the WCA as inadequate. Staff members of ATOS, the company which carries out the assessments, have expressed concerns that not enough time is allowed for each appointment, for what are often complex cases with multiple comorbidities.

Karen Sherlock had multiple comorbidities - basically a lot of bad shit going on - but in her WCA she was put into the "work-related activity" group. That means they thought she'd be able to do some work, eventually.

Well, she couldn't. After a year's frantic, terrified gathering of evidence, Karen's appeal was successful, and she was placed in the support group.

And this week, two weeks after that decision, she died.

Wouldn't it be a wonderful memorial to Karen if this bluntest of blunt instruments were to be consigned to the history books forever? Let's continue to do åll we can, for Karen and its other victims.