LATIN WORD OF THE DAY

There's nothing I love more than a really good laugh, and being a generally happy person, I laugh quite often. The only problem is that I suffer from narcolepsy with cataplexy, and so "falling about laughing" is absolutely literal in my case. My favourite television programme is "You've Been Framed", and for half an hour a week I am completely incapacitated by home video funnies.

It's only because of the brilliant support of Mr. Kizzy that I'm able to fully appreciate the show, though. In our house, it's Mr. Kizzy who looks after the video recorder, and always makes sure we get You've Been Framed on tape, even though he doesn't like it himself at all. The problem is that, once a particular clip has got me going, my head drops and my eyelids droop, so I don't get to see the next couple of clips, even though I can hear the soundtrack. By having a copy on tape, I can watch it again to see the bits I missed the first time.

Sometimes, I've thought that what I need is a soft neck brace, so that I can keep my head upright when I know that I'm going to laugh, but that still leaves the problem of trying to keep my eyelids open.
Then I found this device. It's called the "Lundie Loop", and I actually found it through the website of the Myasthenia Gravis Association.

Myasthenia gravis is a much more serious and debilitating condition than narcolepsy, and is characterised by - as the phrase translates from the Latin - excessive muscular fatigue. Its cause is entirely different to cataplexy, and affects a much greater range of muscular groups.
As with cataplexy, though, one of the signs is involuntary drooping of the eyelids. The Lundie Loop is designed to help sufferers to keep their eyes open, even when the muscles are too weak to lift the lids themselves. Whether it works or not, I don't know. I just found it rather intriguing and highly ingenius. I might try to get hold of one, and see how it works for me.

I am, of course, only being semi-serious, although I'd genuinely be prepared to wear almost anything that works - Lundie Loop included, if for example I'd paid for tickets to see a favourite comedian perfom live. I'd love to have the joy of laughing uninterrupted through the whole show, and without missing any of it.

There is a line that I'd draw, though. I cannot tell you how wonderful this "Pillowig" concept by Joon Youn Park looks to me, but I'd never wear it. Even for a person like me who is relatively unconcerned about what other people think, it's a step too far.

Even so, it just looks so wonderful - whenever I get one of my sudden, crushing, sleep attacks (and I'm talking about sleep now, not cataplexy) this photograph has the same effect on me as I think a picture of Willy Wonka's factory would have on a chocoholic. It is genuinely only a concept design, anyway.


This Sleeping Jacket, on the other hand, is just brilliant, and be ideal for both sleep and cataplectic attacks. As far as I can tell, it's genuine, too, from a designer called Matthew Gale. Finally, it brings me to my wonderful, newly discovered Latin word of the day...



...Excubo. I sleep outside.

SCIENCE, SLEEP AND SSRIs

In an earlier post, I mentioned that I have narcolepsy with cataplexy, which is a very odd condition, and becomes odder all the time. One of the recent discoveries about it involves the identification of orexin producing cells in the hypothalamus, and their depletion in narcolepsy. Hence there is a diagnostic test which involves a lumbar puncture to take a sample of cerebro-spinal fluid and analyse it for orexin concentration. In narcoleptics, the level is either abnormally low, or undetectable.

I was very worried about having the test. Notwithstanding the unpleasantness of the test itself, it has taken me more than half my life to find a sympathetic neurologist who would agree that my symptoms might be narcolepsy with cataplexy, and the diagnostic validity of this test is taken to be so strong that I was terrified the outcome. What if the orexin count was not low? It would leave me wondering if my symptoms were psychiatric all along, and perhaps my neurologist would think that too.

Photograph by MegElizabeth

Anyway, I needn't have worried. I was honest with my neurologist about my apprehension, and he said that whatever the outcome, he felt strongly that something neurological was going on, and that nothing would alter his standard of care to me. You can see why I didn't want to lose him! As it turned out, my orexin levels were, as he put it, "barn door abnormal".

I take modafinil for the narcolepsy, and venlafaxine for cataplexy at the moment, although I used to take prozac for the latter. Over at Ben Goldacre's brilliant Bad Science blog, there's a discussion going on about the quality of research into the effectiveness of selective seratonin re-uptake inhibitors, SSRIs, like prozac. Most particular to the confusion as to their effectiveness seems to be the selective reporting of positive trials, and mis-reporting of some that had less favourable results. Venlafaxine is a selective seratonin-norepinephrine reuptake inhibitor (SNRI), and I don't know how well its trials and their fair publication compare.

One thing that is always interesting about psychoactive drugs is that there are high variations from individual to individual in their effect, dosage and efficacy. They also seem to act differently for different conditions. For example, fluoxetine (prozac), when prescribed for depression, usually takes a couple of weeks to start taking effect. When I was prescribed it for cataplexy, the effect was within 48 hours. It seems to me that it must be acting through different channels in each case. The human nervous system is an enigmatic and complex machine, and I don't think our current understanding is adequate to explain these differences. It is interesting, for instance that Parkinson's patients can develop secondary narcolepsy, and exhibit the full range of narcolepsy and cataplexy symptoms, although the primary defect is in the dopamine system. Recent research has seemed to indicate that REM sleep behaviour disorder (RBD) is strongly associated with later development of Parkinson's Disease, unless it is associated with narcolepsy, in which such a progression is not expected.

It all makes me wonder whether depression is really a single illness at all, when it has many different triggers (and none) and manifests itself differently from person to person in its extent, prognosis and response to treatment. When the brain and its workings are so difficult to understand, then any medical trial has the problem that even in the patient group, we may not be comparing like with like. Faced with the difficulties in trials of comparing an active drug accurately with placebo, and the added difficulty of comparing placebo to no treatment at all, the possibility that very similar symptoms may arise from different organic mechanisms within the study group makes any inferences very tricky indeed.

I'm not arguing against trials - on the contrary, I think we need to know far more. But we also need to better understand the nature and origin of the illnesses before we can make hard pronouncements. We need well organised, well reported trials, but we also need to be willing to challenge all underlying assumptions openly and honestly, and not censor or prejudice any possible debate.

BAD SCIENCE

Perhaps I've just had too good a Christmas, and my normal bad temper is on rebound, or perhaps some things are just remarkably annoying. I usually make a point of not watching programmes like "The Wright Stuff" on UK Channel 5, but my other half is off work with the 'flu today, and put it on.

As the programme went to an advertisement break, the teaser question we were left with was:

In what year was MRSA first discovered?
a) 1880
b) 1950
c) 1980

It's often possible to answer these questions on a psychological basis rather than actual knowledge; they are almost always designed to surprise. Now, I don't mind the intellectual superiority that people intend to show by asking these kinds of questions, as long as the answer is actually correct, and illuminates the subject in some way. However, it was all too easy to predict that the given answer would be - and indeed was - 1880.

Since MRSA is methycillin-resistant Staphylococcus Aureus, it doesn't take a genius to suppose that MRSA cannot have been discovered until after methycillin was developed. This was by Beecham, in 1959. It was first reported in the UK in 1961 that certain Staphylococcus Aureus had been found to be resistant to methycillin.

The bacterium itself was discovered in 1880. It resides perfectly normally on human skin, nose, throat and the colon, and doesn't necessarily indicate the presence of infection. It usually responds to methycillin, among other antibiotics.

Why does this wind me up so much? Because what it does to the watching population is give the impression that MRSA has been around for over 100 years, and has not been a problem until now. I think the average viewer may conclude that all the recent concern is merely scaremongering, and will also find the conflict with what they thought previously will add to a sense that science is not to be trusted, and that scientists change their advice according to political expediency.

Staphylococcus Aureus in itself is not a worry. MRSA is a big concern. It may well have been caused to thrive today by continued overuse of antibiotics. It is very hard to see how we can get back from this position, but disinformation is unlikely to help.