Neuroscience – theory and practice

My extra dopamine
My extra dopamine – on my left arm

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 last few years, I have been increasingly troubled by freezing-of-gait, my least favourite PD symptom. (For more info on freezing-of-gait, see: Bruised knees and bruised ego…Sara Riggare on ‘How Not To Fall’ and Parkinson’s never takes a day off). Imagine my delight when a study was published in The Lancet Neurology in January of this year titled: “Rivastigmine for gait stability in patients with Parkinson’s disease (ReSPonD): a randomised, double-blind, placebo-controlled, phase 2 trial“, and, being the engaged patient I am, I emailed my neurologist, attaching the article, asking him for a prescription. A few days later, I went to the pharmacy and picked up my new medication, Rivastigmine, which is an acetylcholinesterase inhibitor, meaning that it inhibits the enzymes responsible for the breakdown of the neurotransmitter acetylcholine in the brain, thereby increasing the levels of acetylcholine. The article argues that treatment with an acetylcholinesterase inhibitor could improve gait stability in people with Parkinson’s who have fallen during the last year.

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!

The Burden of Tracking

"The quantified self Counting every moment" - The Economist
Image copied from the article “The quantified self Counting every moment”, published in The Economist March 3rd 2012 (http://www.economist.com/node/21548493)

I have called myself a self-tracker since the first time I heard the word. The concept of using technology to collect data about myself and then analysing that data to better understand different aspects of myself and my surroundings has always resonated strongly with me, both as an engineer and as a researcher.

My self-tracking practises have been very useful for exploring how to best manage my Parkinson’s medication and also for other aspects of this challenging disease.

But I don’t track every day. I do however collect data almost every day, mainly relating to my physical activity (steps) and sleep. I don’t consider that tracking though. I consider self-tracking to be a process, and I often use the PDSA-cycle (plan, do, study, act) to explain it, and if not all the steps are addressed, it is not self-tracking.

For self-tracking, I specify the steps as goal-setting, data collection and analysis, reflection, and decision-making and, in my opinion, it is essential that we interact with our data, put our data into a context and reflect on what it means. That is when the magic happens!

When I first learnt about the Quantified Self movement and presented at the first QSEU conference in Amsterdam in November 2011, I thought it was all about the technology, about the gadgets. With time, I have realised that it is not, technology is important, but as a tool, not as the goal itself.

The goal is to use your own data to answer your own questions. 

The collection of data can be facilitated by the use of technology but it is not necessary.

In 2011, I was very optimistic, we probably all were: the emerging technologies would be able to help us better manage our diseases in ways we couldn’t even begin to imagine. I still think we have a lot to gain from using more technology in chronic disease management, but I am significantly less optimistic.

Self-tracking is really hard! 

Firstly, it is very difficult to ask the right questions, like: What do I want to achieve? How can I even measure that? What kind of data do I need? How can I collect it? And how to analyse? and last but not least: What on earth do these results mean? Different questions and approaches are likely to require very different tools, knowledge and skills.

Secondly, it is very, very difficult to design and develop tools for self-tracking that are accurate enough to give correct and valid results but at the same time versatile enough to enable the users to explore their own questions, and not only the ones that healthcare or the device manufacturers thought were the relevant and important ones.

And, finally, self-tracking takes time. A lot of time. And if you are already spending a significant amount of your time on managing different aspects of your disease, maybe you just don’t want to add more chores. In my case for example, I take six different prescription medications, five times per day, in three different combinations, with   four different time intervals. These pills need to be organised, distributed, restocked etc and this takes time. In order to stay as well as I can for as long as I can, I also need to make sure I get enough exercise, which of course also takes time. To add more tasks, like self-tracking, would mean less time with my family.

Self-tracking has to be worth the effort. And to me, most of the time, it is not. I track when I have a good reason, for example when I want to find the best timings for a new medication dose or if I want to investigate a suspected new symptom.

You’ve probably heard the expression: “burden of disease”, frequently used in Public Health as a measure of the impact of health problems, to for example a country or a region. Carl R May, Victor Montori and Frances Mair have proposed the expression “burden of treatment” as a measure of the work we patients have to do to care for ourselves, for example managing treatments and doctor’s visits, lifestyle changes etc.

When discussing the future of healthcare, it is very often predicted that patients will collect a lot of data on their own devices. But will we? Will the effort of tracking pay off in the form of actual health improvements?

I would like to suggest that we start talking about

“the burden of tracking”.