Disability: the bald truth

A few weeks ago, I thought I saw a squirrel running along the top of my front garden hedge. Turned out it was a bloke on the other side of the hedge with a really bad toupee. Truth.

Bad toupee                       Squirrel

But it reminded me of  a case about three years ago, when a Scottish teacher tried (and failed) to establish that being bald meant he was disabled. He'd been the victim of terrible harrassment from his pupils: if his baldness was a disability, he would have the protection of the Disability Discrimination Act to support his claim of constructive and unfair dismissal.

The judge in that case said that just because the teacher's baldness was used by others to taunt and harrass him did not make it a disability:

It seems to me it would be to take the definition of impairment too far. If baldness was to be regarded as an impairment then perhaps a physical feature such as a big nose, big ears or being smaller than average height might of themselves be regarded as an impairment under the DDA. That, to me, cannot be right

So what is a disability? The judge seems from that quote to use the words impairment and disability interchangeably. But are they?

The medical model of disability sees impairment and disability as closely linked: disability arises directly from impairment, which is a physical dysfunction of the body. Disability is therefore clearly the individual's "fault", may reduce their quality of life, and causes clear disadvantage to them.

In the social model of disability, by contrast, society is the main factor in disabling people. Impairment is a necessary factor for disability, but it doesn't lead to disability unless society fails to take regard of and include people regardless of their individual differences.

The legal situation in the UK is governed by the Disability Discrimination Act 1995 (now consolidated into the Equality Act 2010). It uses predominantly a medical model: disabled people are defined as people with certain conditions (someone diagnosed with MS, for instance, is automatically covered under the Act), or with certain limitations on their abilities.

But when it's placing requirements on employers and service providers, it uses the social model, requiring them to make "reasonable adjustments" to their premises, policies and practices to make them accessible.

What make an adjustment "reasonable" is not defined, and most court cases focus on this point. It could, for instance, be entirely reasonable for a large department store to install an entrance ramp in view of the shop's size and number of shoppers; it might not be reasonable to expect an office with only a few staff, rarely visited by members of the public, to do the same. On the other hand, someone from the office could perhaps go to visit a customer who can't access the premises at home. It's about...well, what's reasonable.

Some people are very militant about the issue, insisting that only the social model should be used. But really, you could have the most accessible environment, the most enabling society in the world, and I still couldn't take a full part in it because of my fatigue and pain - the main symptoms of my MS, for me. These are called impairment effects: they're not recognised by everyone working in the field of Disability Studies, but for those of us experiencing invisible symptoms, they are a major factor in our experience of disability.

So, what is disability? To me, it's a mixture of the dysfunctions of my body caused by lesions in my brain, and society's response (or lack of response) to me as a result of those dysfunctions. Others may have different answers, depending on their own particular experiences and understandings.

Perhaps, in the end, disability is one of those things that means something different to every one of us. But a bad toupee? That'll always be a bad toupee!

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!

Walking back to happiness?

Walking. It's such a significant ability, isn't it? Being able to walk is one of the markers of development from babyhood to childhood.

And to many of the general population in our culture, it's whether someone can walk or not that determines whether or not they're disabled. Many of us with MS quite rightly complain that our invisible symptoms disable us just as much, if not more, than mobility problems. Even so, we often resist using mobility aids such as sticks, crutches or wheelchairs for as long as possible: visible symbols of our disabilities.

The worst symptoms of my MS are fatigue and pain. Even so, any improvement in my mobility would make my life far easier! I'm currently able to walk very short distances, and use a power wheelchair outside the house.

That's why I've been so excited watching the trials of the new drug Fampridine (Fampyra), which was finally released in the UK this week.

Fampridine is a tablet taken twice daily. It's not like Beta Interferon, Copaxone or Tysabri - it has no effect on disease progression. It's effective for roughly 33-40% of people with MS with walking problems: when it does work, it gives an average 25% improvement in walking speed.

Back when it was in trials, I discussed Fampridine with my neurologist. She said that she would want to put me on it as soon as it was approved.

So far, so excellent. But like every medication, Fampridine has potential side effects. Some of these are relatively minor, and pass as you get accustomed to the drug. But some are potentially very dangerous.

Among these is a slight risk of seizures (fits). Now in general, for most people, that very small chance would be a risk worth taking. But I already have epilepsy. So although it's well controlled, anything that increases my seizure risk is not really very good news.

It's all about swings and roundabouts: balancing risks and benefits. At the moment I don't know if my neurologist will consider me suitable for Fampridine, given the seizure risk. I'm seeing her in 6 weeks, and will be asking about it.

But if she leaves the decision up to me, will a possible improvement in my walking be worth risking losing control of my epilepsy? If I have a seizure, I'll lose my driving licence for a year, and I really don't want that to happen. But easier walking would make my life so much simpler.

At the moment, I really don't know what my decision would/will be. I suppose I'm going to have to do some hard thinking over the next few weeks. And who knows? Pretty soon, like Helen Shapiro, I might be Walking Back to Happiness!

Book review: or how The Good Table bruised my toe

I was lucky enough to be sent this recipe book - The Good Table, by Valentine Warner - by the publisher, as a competition prize. The only condition was that I might like to write a review of it, here or on Amazon.

And truly, that's been no hardship to do, because overall this is a beautiful book to handle, look through, and read. The photographs of the finished dishes are stunning. The only complication really was that it somehow ended up tucked away under the sofa, at the furthest corner. (I blame the cat.)

I'm physically disabled, and inevitably that affects my perception of everything I do and experence.. The Good Table is a big book (hardback, nearly 12 inches tall,over 7½ inches wide and over an inch thick.). I just dropped it on my toe while I was moving it to go for a drink and it hurt like hell. Seriously.

For those of us with weak arms and hands, that can cause significant problems. It's very difficult for me to lift The Good Table at all! The binding does mean though that the book lies open at the chosen page, even if that's at the start or end of the book. A rare thing, and very useful for a recipe book.

As you can imagine, there are a huge number of recipes spread throughout its 368 pages, ranging in complication level from 'Boiled new potatoes with Stinking Bishop & spring onion' and 'Baked potatoes with garlic & cream' up to...well, I looked through the book for a dish that would be particularly complicated, and couldn't find one.

Certainly there are some that wouldn't be for novice or nervous cooks, but part of the stated aim of the The Good Table is to help restore the cooking skills of the country.The book includes a number of  'how-to' guides: for instance, how to put together a steak & kidney pudding. If less experienced cooks follow these, and move from less to more demanding recipes, Warner hopes that some of our lost cooking skills can be reestablished.

I haven't yet cooked anything from Warner's book: but some of the recipes sound so tempting, that I know I will very soon. How could anyone resist 'Floating islands with espresso caramel sauce'? And it's wonderful to have a recipe for chai.

Looking at the recipes from a disability point of view, things are a little more difficult. Many of the recipes are well within my capabilities, and I look forward to making them. There are however very many that would just be far too tiring: taking too long, or involving too much stirring or lifting, for instance. Others could possibly be risky because of chopping, cooker flames, and so on.

So speaking as a disabled person, I'm delighted to have won The Good Table. Would I pay out £25 for this heavy hardback version, with more than half of the recipes being ones I can't make? Well, no. I don't think I would, to be honest. But if you're able-bodied and you like cooking, or want to learn more about it, go for it. It's brill.

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!

The right model for killing yourself

"Martin" is 46 and has locked in syndrome He's asking the courts to clarify the law so that doctors and other medical staff who might help him end his life would not  be prosecuted.

This is an extension of Debbie Purdy's case, from two years ago. Purdy successfully argued in court that it was a breach of her human rights not to know if her husband would be prosecuted for assisting her suicide if he accompanied her to a clinic in a country where assisted suicide is legal.

"Martin's" case extends this to doctors and other medical staff, rather than lay-people. His wife has accepted his decision, but does not feel able to assist him.

At least 10% of suicides in the UK are by people with a chronic or terminal illness, and coroners believe that people are increasingly killing themselves at a younger age rather than wait until they are in severe pain. Some coroners avoid probing into what they suspect might be a case of assisted suicide, to avoid causing problems for those left behind.

So why do all these people with long-term illnesses feel that the appropriate response to their circumstances is to kill themselves? (Either with or without help). Opinions, inevitably, differ.

Some argue that the decision is made because the condition - the illness, the disability, whatever - has become too much to bear. Others say that these feelings are often because the individual has not had the chance to live as independent a life as possible within society at large.

The individual's condition on one side and society on the other. That sounds very familiar. And yes, it's our old friends the medical and social models of disability again.

Which is more important in an someone's decision whether they want to live or die?  The way their physical disability affects them as an individual, or how easy it is for disabled people to be part of mainstream society?

Just to be upfront, I have no intention (in the foreseeable future) of seeking assisted suicide. But as I've told you in a couple of posts recently, I've been having major problems getting out because of physical problems. At the moment, the accessibility or otherwise of society is kind of irrelevant to me, and my physical impairments are totally primary. At other times, or for other people, the physical problems may be secondary to accessibility, housing problems or employment discrimination.

So overall, I think sometimes the medical model is the right one and sometimes the social model. Or, at least, there's a continuum. At one end is "pure" medical model thinking, at the other end is "pure" social model thinking. Most of us are somewhere in the middle, and we move back and forward along the continuum depending on circumstances. (It's made of nice slidey material. Makes it easy.)

The vast majority of us could never kill ourselves, in any circumstances. And if someone is considering it, whether that decision is rational or irrational is a whole other packet of Jaffa cakes. For those few who have decided to seek assisted suicide though, reasons differ. And that fact must be acknowledged by the disability community.

Not going out

For the last couple of months, I've been having real problems in getting out. Not because of agoraphobia: I'd love to get out. Because of physical difficulties, and complete and utter lack of spoons. I just haven't had the energy to go out.

I used to be - well, not exactly a party animal (though I've had my moments!), but I went out a fair bit. Part of it was day-to-day getting out, of the going-to-the-shops, paying-the-bills type. And of course work, back when I was still able. In these teched-up days, the internet offers alternatives to much of that kind of going out, for those who want them.

But part of it was the joyous, wonderful kind of going out: meeting your mates, going to the pub, going to gigs. Falling in love with the band who were supporting the one you'd actually gone to see. Your table in the pub laughing so loudly that the landlord has to ask you to quieten down. An evening at the fair, throwing balls at coconuts to win teddy bears.

It's that kind of going out I miss so much. I have wonderful friends I'm in contact with online, by text or by phone: but it's just not the same as when I meet up with them in real life.

And even the boring, everyday kind of going out means you're still part of the community at large. You're still "normal" (whatever the hell that means!) rather than stuck permanently indoors.

So I'm still hoping I'll beat these damn recurrent infections, and get enough energy back to do some going out again. Because this not going out is really getting me down.