Before my Parkinson’s had evolved into the kind with “freezing-of-gait”, or FOG for short, that now is far more familiar than I would like, I had a very hard time to wrap my head around the phenomenon: “Why do they just stand there? Why don’t they just lift their feet and walk like they did just a second ago?” Well, these days I know better…
(If you want to learn more about FOG, I have written about it before, here, here and here with a short film clip of me in a “FOG-episode” here.)
On any given day, my ability to walk will vary immensely over the course of the day, mostly relating to my medication intakes: the longer from the previous dose, and also a bit after my next dose, the more effort I will have to use for walking and moving in general and the more likely I am to end up in a “FOG-episode”. But, to add some spice to the mix, my FOG can also be triggered at any time by anything unexpected, like a sudden movement or a sudden noise. That kind is very difficult to prepare for, because how do you prepare for the unexpected…
I can imagine that people around me are just as puzzled as I was a couple of years ago when I saw someone freezing: “Why does she just stand there? Why doesn’t she go through this door that I am holding up for her? Oops, did she just fall???” I have come to realise that falling is a very “social” thing. Let me explain: a couple of hours ago, I was crossing a small street on my way to the grocery store. Someone behind me called out unexpectedly and, of course, I wobbled, stumbled and ended up with my right knee on the ground. The person who called out came up to me with his two buddys, all equally inebriated and on the way to the store. I would guess, judging by their “atmosphere”, that it had been several days since either of them was sober and they all displayed the classical broad-stance walking of a longtime alcoholic. They put me gently but unsteadily back on my feet and didn’t leave my side until they had made sure I wasn’t going to fall again. When I went on my way, I had a number of annoying questions twirling in my head, the most powerful one of course being: “What is it with this f***ing disease???” But also: “How kind of them to help me! I wonder if I would have done the same for them?”.
And this is where the social aspects come in. Think about it: someone falling quickly becomes the centre of attention. People come to help, lift the person to their feet, brush of their clothes, etc. And as a person who increasingly find myself on the receiving end of such kindness, I can tell you that it evokes mixed feelings. Don’t get me wrong, of course I appreciate the kindness of people, but at the same time, the FOG itself often makes me wish that I could just sink through the ground and disappear.
If there is one thing that Parkinson’s teaches you, it’s humility
Last week was a week of contrasts for me. On Tuesday I left Stockholm for New York City and the purpose of my trip was to attend a workshop at The White House in Washington DC. The workshop was on a topic very close to my heart: engaging participants as partners in research and it was organised jointly by the conference Stanford Medicine X and the Office of Science and Technology Policy at The White House. The intention from the organisers was to, by using design principles, 1) identify what’s working, 2) strengthen the community of innovators in the area, and 3) accelerate progress.
And if a reference to the Declaration of Human Rights is not enough
to convince you, consider this: In the ‘dark ages’, before the Internet, knowledge was scarce. If you wanted to learn medicine, you had to go to university to study. Sure, you could pick up bits and pieces in books at the library but on the whole, (medical) knowledge was difficult to come by on your own. Times are very different now, we can all learn literally everything we want, using the tools and information available to us online. And in my opinion, it is a good thing that knowledge is democratised and available, it offers us plenty of opportunities but also a few significant challenges. One of the most exciting opportunities, and if you ask me, probably the best thing since sliced bread, is that we are now so many more people that can access the knowledge necessary to collaborate to solve the many remaining medical mysteries, like how to cure cystic fibrosis, cancer or genetic prion disease, or how to design better cardiac defibrillators or closed-loop-glucose-monitors-insulin-pumps or stoma bags and also how to enable us all to communicate across obstacles caused by injuries or diseases. Slightly more discouraging is that we are basically still doing research in the same old way as we did in the not-so-long-ago pre-internet days. Why are we doing that? Wouldn’t you say that it is an extreme waste of great minds with so much to give to NOT engage participants as partners? Who can be in a better position to help tease out which issues research should focus on than we, who are living with these diseases every hour of every day?
When I returned to Sweden, I went straight to our place in the Swedish countryside (see pic below), where my family owns a few houses right by a lake in the beautiful area of Bergslagen. The red house is my absolute favourite place in the whole world and as I was enjoying “fika” with my family, telling them about my travels, I was struck by the extreme contrast between The White House and the red house and that I am very fortunate to be able to experience such a wide range of environments. The work we all did at that workshop in The White House is a step in the right direction. My hope is that the work we started in The White House will lead to scientific progress so that many more of the Emilys, Hugos, Erins, Michaels, Danas, Sonias, Matts, Corries, Annes, Dougs, Jelicas, Cliftons, and Saras of the world can spend more time in their “red houses”. And I think it is possible, because these issues are too important not to deal with. These issues matter to people both in The White House and in the red house!
I’m sure most of you have seen me write once or twice before that PD is a very complex disease, but it bears repeating:
PD is a very complex disease!
Let me explain to those of you lucky enough not to know first hand (or by proxy, like my husband and daughter do). If you’ve followed my work, you probably know about my complicated medication regimen, not unusually complicated if you have PD but very much key to my health and well-being. There are essentially four major types of PD meds: L-dopa (or levodopa), which goes into the brain and transforms into dopamine, the neurotransmitter that PD “steals” from us, dopamine agonists (or DA’s for short), which “imitates” some of the effects of dopamine in our brains, COMT inhibitors, which when taken simultaneously with L-dopa, lengthens the active period of the L-dopa, and MAO-B inhibitors, which helps to block the natural breakdown of dopamine in the brain. All of these act to increase the levels or effects of dopamine in our brains, which in turn restores some or even most of our normal patterns of movement as well as addresses, to a varying degree, the non-motor symptoms that comes with reduced levels of dopamine in the brain, such as for example depression, autonomic dysfunction, pain or sleep issues. My medication regimen consists of one of each of these types of PD meds, in different combinations throughout the day.
Neurotransmitters are chemicals that that help transmit signals in our brains, from one nerve call to another nerve cell, muscle cell or gland cell. There are plenty of different neurotransmitters, each with different chemical compositions, purposes and functions in our nervous systems. Dopamine is one of the most important for controlling our movements and is also involved in the reward system in our brains. Another important neurotransmitter is acetylcholine, which interestingly also is involved in our movement, it helps control our muscles. Acetylcholine also plays an important role in attention and motivation.
So why am I giving you a crash course in neuro science? Well, apart from the fact that the brain is the most sexy organ there is (look up the word “sapiosexual”), as a person with PD, my curiosity in neurotransmitters has very recently been key in my successfully managing an increasingly difficult disease.
During the following weeks I followed the scheme my neurologist had given me for introducing this new medication, while trying to find a constructive balance between objectively observing the potential effects and living life as usual. After a rather terrifying experience when I went from 3 to 6 mg in my morning dose, I tapered it off again. The terrifying part meant that I found myself more or less unable to move, literally, a few hours after taking this higher dose. I felt almost like a statue and it would have been very interesting if I hadn’t felt so scared. I was very glad to get hold of my PD friend, who also is a neuroscientist at that time. He gave me a bit of a lecture about neurotransmitters and assured me that the effect was likely to wear off and my mobility return to normal (for a Parkie). Later that day, I could confirm his theory, at which point he was kind enough to point out to me that I couldn’t know for certain that the Rivastigmine was responsible for the effect I experienced unless I repeated the experiment. I haven’t. Yet.
I went back to 3 mg per day and over the last few weeks, I have found myself really struggling with moving and walking. I usually say that living with PD takes an olympic gold in stubbornness, but over these last few weeks, it has been much tougher than I probably have been prepared to admit to myself. Thinking back, I have not been able to do much more than doing my daily dose of exercise, working, falling asleep on the couch, watching TV and then going to bed. And with PD, you can’t really be sure what’s wrong until you’ve done a fair amount of troubleshooting:
First, observation: “Hmmm, I don’t feel well today… my whole body is heavy, my back hurts, my hands move slowly… even more slowly than usual…. I wonder what’s wrong…?”.
Then, hypothesis testing: “Am I coming down with something…? Do I have a pinched nerve in my back or lumbago….? Or did I forget to take my meds….? Have I been stressing too much… or sleeping badly….? Or…., the worst fear: is my PD suddenly progressing faster…?”
This kind of troubleshooting takes some time, as you can imagine… But I am very happy to tell you that I feel much better today! So, what is different today? I’ll tell you: My neuroscientist friend with PD told me that our movements are really controlled by the balance between dopamine and acetylcholine (this is of course an extremely simplified explanation) and in simple terms: the Rivastigmine was likely to somewhat cancel out the effect of my dopamine enhancing medication. When this crucial piece of information had reached its way into my brain, I formed a new hypothesis which I tested this morning: this morning, I took more L-dopa than I usually do and what a success it was! It was such a relief to be able to move effortlessly again (well, effortless by PD standards anyway…)! My family and colleagues will tell you that I have been smiling the entire day from the pure joy of moving!
This approach enables me to keep living as well as I can with this very complex disease!