These are my feet, they have been with me for 42 years soon and they mostly serve me well. However, recently I have noticed an increasing tendency to get freezing-of-gait, an annoying effect of my “flavor” of Parkinson’s disease. For some more information on what freezing-of-gait, watch this film: http://www.youtube.com/watch?v=aaY3gz5tJSk. Although the case in the film is quite severe and I am not even close to having the problems the man in the film has.
I am a firm believer in the ideas of Quantified Self and incidentally currently have the fortune of participating in a study from Psykologifabriken aimed at encouraging everyday creativity. These two things lead to an idea during my walk to work this morning: I will try to quantify my freezing-of-gait and monitor the effects of different interventions on it.
Starting today, the plan is to register when my freezing-of-gait appears, using a scale 1-5 for severity. Let’s see what happens!
To evaluate the effects of my medications, I use an app on my iPhone.
I don’t have the tremor that most people (including myself) associate with Parkinson’s, but instead I have bradykinesia (slowness of movement) and rigidity with a bit of balance and gait problems, just to make it more interesting.
I did know that tapping tests are used to evaluate Parkinson’s clinically so I looked for a tapping test on my iPhone and found “FastFingers”. The app has a window divided in two halves and I think that you are supposed to alternate the tapping between the two halves, but I only use one side. I make sure that the lower part of my palm, thumb, ring finger and little finger are resting against the table, see photo, and tap with my middle finger as fast as I can for 30 seconds. I do this with my right and my left hand a number of times throughout the day and record the results (time and number of taps).
I started collecting baseline data a number of weeks ago and actually found it more difficult than expected to capture enough data in a day to be able to find meaningful patterns. I was able to record enough data for two days, 12th and 13th March, and the results are plotted below with number of taps in 30 seconds on the y-axis and the time for the test on the x-axis. I also included a control, a.k.a. hubby
Thank you Zalamanda and Marten, for your comments on my previous post. Of course, I agree with both of you, two days is far too short a time to expect any kind of significant results. Nevertheless, I did observe some potentially interesting findings in these two days.
The first graph shows the measurements i did on my very first day on the new dose. And the small change I did was that I now take my second dose of the day, a “type A” medication (see a previous post here) at 11 am instead of 11:30 am and have also added a “type C” medication, that hopefully will make this dose last longer and if I’m lucky, the dose will have effect until dose number 3 at 3 pm so I don’t have to take that earlier.
Interestingly enough, the measurements of the very first day on the new dose, indicates that the small shift in time for dose number 2 actually has an effect. Both my right and my left hand scores very high around 1 pm, pointing towards a distinct effect of the changed timing.
At first glance, the results from the second day (second graph) is less optimistic, there is no sign of the peak around 1 pm. However, the observant reader will notice that there are no measurements recorded between approximately 11 am and 3 pm (shame on me…), meaning that the function in my fingers might very well have peaked during that time without me having recorded it.
Mental note to self: Make sure to record frequently, especially between 11 am and 3 pm.
I have compiled the measurements during these last two days, see below. Compared with my base line measurements, they look very random and I will attempt some sort of analysis tomorrow.
The first day on the tweaked dose went OK, no fantastic change, but I didn’t expect that either. Let me try explaining in some more detail, how the different Parkinson’s medication works.
Remember the different types of Parkinson’s medication I mentioned yesterday?
Let’s call the levo-dopa based medication type A. Further, let’s call the kind that imitates the effects of dopamine type B. You might remember that there are two kinds of Parkinson’s medication that inhibits the transformation of dopamine into other chemicals. One type has no effect by itself, but only when taken at the same time as type A, we can call this kind of medication type C. And let’s call the last kind type D. All these different drugs behave differently in the body, they have different uptake rates and biological half-lives (this is where my background in chemical engineering comes very handy). And this, as you might realise, results in an extremely complicated system of different chemical reactions, that in an ideal situation would give me an even concentration of the substances lacking in my brain. Unfortunately, there is no easy way of measuring the concentration of these substances, so instead I try measuring the effect of these substances, meaning that I try to find ways to evaluate my different symptoms objectively, but more about the measurements in a later post.
My “old” medication regimen consisted of:
6 am: A+B+C+D
11:30 am: A
3 pm: A+B+C
6:30 pm: A+B
9 pm: C
10:30 pm: A
As you can see, the regimen is in no way simple, but it has served me very well for the last few years. You might notice that my 11:30 dose consisted of only a type A and if you have been really paying attention, you might wonder why I don’t enhance the effect of the A with a C…. which is exactly what I have done. My “new” regimen is identical with the old one, save dose number 2 of the day. I now take it half an hour earlier and have added a type C. This might sound like a ridiculously small change, but I want to reduce the risk of getting unpleasant side effects. I use my iPhone, iPad and laptop to monitor the effect of the change. More about that later.
These last few days have made me even more aware of how extremely dependent I am of my medications, and if you’re reading this and have Parkinson’s yourself, this is probably very much old news. For people who have not experienced this, I completely understand that this is difficult to understand.
Let me quote an analogue that an experienced and very appreciated neurologist use to describe the process:
Currently, the ruling theory is that the wide range of symptoms falling under the Parkinson’s disease umbrella are caused by a lack of dopamine in the brain. Dopamine is one of a number of neurotransmitters, that together constitutes the signaling system within the brain. (I say currently, because there are theories that other neurotransmitters are also affected). However, the neurologist in question says that dopamine acts like the power steering (“servostyrning” in Swedish), i.e. making movements smoother and less effort-demanding. If the power steering fails, the car can still move and turn, but it takes a lot more effort to do so. For people with a dopamine deficiency, moving around, walking etc, takes a lot more energy when medication levels are low than when they are on a higher level.
Parkinson’s medication come in a few different varieties and these can be combined in a number of ways to achieve the best effect. Very simplified, these varieties are:
- medication based on levodopa, which, once it reaches the brain, is transformed into dopamine
- medication that mimic the effects of dopamine
- medication that inhibits the decomposition of dopamine in two different ways, hence leaving more of this precious chemical to our starving brains
My cocktail of Parkie-drugs consists of one of each of these four types, carefully combined in a collaboration with my neurologist, with whom I am fortunate enough to have developed true Shared Decision Making.
The change in medication is a very small change, barely more than a tweak, but I have learnt over the years, that medicating against Parkinson’s is like balancing a very thin line between wanted effects and unwelcome side effects. I also know that the resulting effect of a change will take weeks or even months to stabilise.
If you want to, you can follow my journey here.
I have found myself really struggling for quite some time now. Struggling to move smoothly, struggling to stay positive, struggling to keep going. And I have realised that it is time to change things. I need to increase my medication. Of course it is a sign that my Parkinson is progressing and of course that insight is not a pleasant one but I knew that this day would come sooner or later and almost 3 years on the exact same dose must probably be regarded as a long time in Parkinson’s.
It never ceases to amaze me, the profound effect that dopamine has on me, or rather, the effect a lack of dopamine has.
The slowness of movement, from the outside probably perceived as me moving in slow-motion and from the inside experienced as every single step requiring an effort of almost ridiculous proportions. The frustration of the mind, not seen from the outside, but from the inside experienced as a storm of thoughts contained in a confined space, stumbling over each other, all trying to find the space they need to develop.
And then the relief when the medication kicks in, the fantastic feeling spreading through my body, when my muscles can relax properly and work in sync again. The surge of joy through my brain when I don’t have to use 90% of my concentration just to keep going in the intended direction any longer but instead actually can walk and talk simultaneously again (Hmmm…. makes me wonder if the body-builders back in the 80′s all had Parkinson’s…..?).
I have been lucky enough to have been very well medicated for such a long time that I had in fact almost forgotten this feeling of hopelessness. And I truly hope that I will be able to forget it again soon. Because starting tomorrow, I plan to increase my medication, and I will monitor the effect very closely using a tapping test on my iPhone. I have spent some time collecting base-line data on the effects of my current regimen, see below, and it will be interesting seeing what the effect of the change tomorrow will be.
Getting close to the end of the second and last day of QS2011 Amsterdam and it has been truly inspirational, extremely intense and a fantastic experience! Today’s highlights from 1/3 of the Stockholm jury:
My first ever day at an unconference and the impressions have been numerous. I love the idea of having the focus of the meeting on the breaks between the presentations, since everybody knows that the really sparking ideas are born over a cup of coffee and some strange looking local speciality (in this case I would call it as the mandarine mousse for the win, or maybe the odd-looking fruit with thorns or spikes…).
Among the ideas/impressions I will take away from today are: