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!