Why I fired one of the UK’s top neurologists
As a scientist, experimenting with both botulinum toxin (Botox) and beta-blockers seemed to me a sensible avenue of research in order to develop more effective approaches for managing the uncontrollable repetitive jerking of my legs (clonus).
Botox injections laser-in on particular muscles and, for a few months at a time, completely relax them – and only them. That, of course, is why some people have Botox injections in their face to try and make some lines and wrinkles less obvious. Botox seemed to me to be a far more focused approach than a general-acting oral drug like baclofen.
The point is, even if I hadn’t suffered from the very-common side-effects of higher doses of baclofen (I suffered even worse with tizanidine), prescribing a muscle relaxant for someone whose problem is weakening muscles, seemed to me a dubious first line of attack. Worse, prescribing a general muscle relaxant that will affect every muscle in the body seemed like a predictably counterproductive overkill – given that it is predominantly my calf muscles alone that are causing the trouble. The words ‘sledgehammer’ and ‘nut’ spring unbidden to mind.
What is more, in the field of System Dynamics it is well understood that it is rare to find a single ‘magic bullet’ that solves systemic problems. And if you try to use one, you tend to invoke major unintended consequences (such as making me feel weak all over rather than just in my legs). Instead, the approach that does often work is to nibble away at the problem from different directions.
So, also attacking the clonus with an utterly different approach than just beta-blockers seemed sensible – in a ‘belt and braces’ sort of a way. Given that it seemed as if there was some form of fight-or-flight mechanism at work with the overly-sensitive triggering of my clonus, maybe that was a good direction for a pincer-movement to be set up. Beta-blockers reduce the effect of adrenaline, so, my logic went, maybe a beta-blocker might help.
This multi-pronged approach is exactly the direction our research eventually took.
I carefully titrated off all baclofen and was then injected with Botox at six points on each calf. Within a week, the toxin had killed off enough nerves to both reduce my spasticity and lessen the associated clonus. But it didn’t prove to be enough to significantly lessen the fight-or-flight overreaction. And much more Botox would mean my legs would be weakened sufficiently as to impact my already-very-limited ability to walk. Instead, we needed to try cutting off the source of the overreaction.
Non-selective beta-blockers such as propranolol reduce the effect of adrenaline throughout the whole body, whereas a selective beta-blocker such as bisoprolol focuses its effects on the heart.
I initially suggested to my cross-disciplinary network of clinical-care specialists that I try bisoprolol. Being a selective beta-blocker, it has less side-effects, so is a good first-line approach to try. However, bisoprolol seemed unlikely to have much impact on my leg muscles – only my heart – and so it turned out.
I then suggested we try propranolol, which is generally well-tolerated, and which also has long been used to treat a form of uncontrollable shaking known as Essential Tremor. This worked much better. Indeed, for me its effect was instant, transformative, and sustained. Not only did the propranolol immediately cut down the number of times my clonus was triggered by external stimuli, but it also appeared to reduce the degree of clonus itself. For instance, I found that with a low dose of propranolol I could sustain a particular level of activity on a recumbent bike with no clonus; without propranolol, I could not. Consistently. It is a nicely objective measure.
In conclusion, Botox with propranolol turned out to have a transformative effect on my clonus. From the beginning, for the reasons I’ve outlined, it was a reasonable working hypothesis that the combination might work. We experimented. Botox injected directly into the most-offending muscles helped, but not enough. A supplementary approach of bisoprolol failed to have an impact, but propranolol worked well. That’s the Scientific Method for you.
So, given their logical underpinning, wouldn’t you have thought that any Neurologist worthy of the title would at least have agreed that those experiments were worth conducting?
In November 2017, my London-based consultant at UCLH, one of the most senior MND Neurologists in the UK wrote to my GP advising against my proposed direction of research: “I do not think that he needs to be concerned about [beta-blockers]. Botox is more concerning. This drug can increase weakness and does not really have an indication in treating spasticity in motor neurone disease.” Instead of an open mind, let alone a curious mind, this authority in the field seemed wedded to the scientifically-unjustifiable One-Size-Fits-All approach of treating spasticity only with baclofen.
This is the same person who got a bit hot under the collar when I explained that I wanted to be steadfastly proactive in my overall clinical care, and intended to always remain ‘well-ahead of the curve’. “I refuse to become involved in that,” he surprisingly-angrily broke in. “MND follows no rules. You cannot be proactive. I utterly refuse to be anything other than completely Reactive!” I politely answered that I found that a very interesting viewpoint, but was there no way that I could at least tap into his unparalleled experience to anticipate the most likely range of scenarios of how my current condition might evolve so that I could best prepare. “Absolutely not!” Followed by the insightful clarification: “After all, if we did that for you, we’d have to do it for everyone with MND!”
Hmmm, personalised Clinical Care. A radical idea…
Purely from a scientific (and logical) standpoint, I fundamentally diverge from this gentleman’s attitude. Usually, I’m extremely tolerant of scientific disagreement. But in this case I don’t believe we have different valid viewpoints, I actually believe that on this one he’s demonstrably just plain wrong. And dangerously wrong. There are some developments in MND that if you wait to react to changed symptoms then you’ve left things too late – Voice Banking and having a Feeding Tube inserted are classic examples. I suspect that, given his senior position of authority, his patients and medical colleagues tend to unquestioningly follow all his (to my mind, rather cavalier) rulings on Clinical Care. In my case, that would have significantly diminished my quality of life. Hopefully, I’m the only one potentially affected in this way.
Fortunately, everyone in my cross-disciplinary MND team – each of them day-to-day responsible for practical on-the-ground Clinical Care across the South-West of England – fundamentally disagreed with this world expert pontificating from a Teaching Hospital in the Capital; they have a refreshingly different mindset than I experienced at UCLH. They’re happy to question Orthodoxy for a start. If an authority figure resorts to unsubstantiated dogma, anyone in the team may query it by asking for supporting evidence. They choose Science over Habit. UCLH could learn a great deal from them. Don’t get me wrong: I found the London consultant to be a lovely guy, an excellent diagnostician, despite my views on being proactive he was very happy to remain in overall charge of my clinical care, and I liked him. So, I won’t actually name him here (only his institution). But he didn’t appear to have a scientific bone in his body. I quietly fired him from any further involvement in my case.