Sara Riggare

Not patient but im-patient

Tag: medication

  • Managing medication in PD – both complex and simple?

    Managing medication in PD – both complex and simple?

    Medication management is probably the absolutely most important part of my Parkinson’s disease (PD) selfcare since without my pills, my body would not function. During the day I take meds approximately every three hours to be able to move around, take care of myself and be able to work. When I wake up in the morning, I have not taken any meds for at least 7 hours and my movements are REALLY slow and stiff.

    My approach to PD is that I try to take my meds at the same times every day. I know that other persons with Parkinson’s (PwP) have other approaches and no-one really knows which approach is best, since there has been no research conducted (or at least not published) comparing different approaches (which is actually one of my main reasons for writing this post).

    When I occasionally make changes to my medication regime, I note down dates of the change and what I changed (for example types of meds added/taken away, changes in timings for intakes, and/or changes in combinations of meds for each intake). For example, a few months ago I noticed that I tended to get slightly dyskinetic (a side effect of PD meds, see here) around lunch so I decided to push my second dose of meds 30 minutes and started taking it at 10:00 am instead of 9:30 am. This changed resolved my dyskinesia. These notes are for myself, none of my neurologists have ever asked about changes I have made between visits, they have only shown an interest in my current regimen at the time of the visit. I can completely understand this, they have enough work to do as it is and don’t need more tasks to complete. Of course there is plenty that could be learned from systematically recording individual medication regimes for a large number of persons with Parkinson’s (PwP) including following up the effects of that regimen on an individual level but I have long since accepted that that is probably not the best use of healthcare resources.

    In my role as an academic researcher, I have applied for funding many times over the past decade to address different aspects of how to optimise PD meds on an individual level. Unfortunately my funding applications have not really succeeded despite the fact that this area is extremely under-researched. I think there are several reasons for this apparent disinterest in the field of medication optimisation in PD and I will mention the three at the top of my mind:

    1. Complexity

    PD is SUPER COMPLEX! We have heard this so many times but what does it actually mean? The complexity of PD is multi-layered and there is so much we currently don’t know. We don’t know how and why the condition starts on an individual level, we are not sure about what processes makes the condition progress, and we don’t know why some medications work well for some but do not work as well for others.

    On the level of individual neurologists, I think that many of the clinicians who have made it their profession to help us actually think that medication intakes are already optimized based on available guidelines and their clinical experience. Those guidelines are however based on group-level data, and do not often translate well to individual patients. There is a huge gap between what is measured in research trials (which subsequently forms the basis of guidelines) and what PwP experience in their daily lives.

    One aspect that is often overlooked is that taking medication is not as simple as just swallowing a pill at the right time. It requires remembering (which, ironically, can be difficult when you have a neurodegenerative disease), carrying medication with you at all times, for some PwP also planning around meals, and adjusting for unpredictable factors such as stress, sleep quality, and physical activity. Even something as basic as getting water to take a pill can be a challenge in certain situations. The effort required to consistently take PD medication is far greater than many neurologists or researchers realize.

    Another factor adding to the complexity is that we living with PD are not really interested in taking the pills, we actually have zero interest in the actual pill taking itself. The reason we take them is to get the effect the pills (hopefully) have on reducing our symptoms. But what does healthcare use to evaluate this process? They use medication adherence, meaning if we take our pills in the way our neurologists have prescribed. As far as I know, there are no standardized adherence scales available that take into account the complexity of finding your individual best timings for intakes of meds to achieve the optimal effect.

    And since this complexity doesn’t directly influence the work of neurologists and researchers, it’s not strange that they don’t see the need for research into how to best optimize PD meds.

    2. Money

    The reality is that the use (and non-use) of pharmaceuticals is (almost) entirely driven by money. And currently there is no money to be gained on a corporate level from helping the approximately 10 million PwP in the world getting a better effect from the many pills we take.

    The pharmaceutical industry mostly hinges on developing new drugs, not on optimizing the use of existing ones. This means that the funding available for research favor the discovery of new molecules over the fine-tuning of treatment regimens for individual patients.

    3. Simplicity

    As a person who has spent more time thinking about this A LOT over the past 10 – 15 years, probably more than is healthy…, I have come to the conclusion that the main problem with the issue of medication optimization in PD actually is simplicity. More precisely, the illusion of simplicity. Medication adherence and effectiveness in PD are mostly treated as simple, binary issues: “Did you take your medication? Yes or no?” But in reality, it’s much more complex. Timing, food intake, stress levels, sleep quality, and countless other factors can influence how well our meds works.

    Yet, our healthcare system is not set up to systematically track and adjust for these variables. Instead, PwP are mostly left to figure it out themselves, with trial and error as our primary tool.This means that many PwP, myself included, spend years fine-tuning our medication regimens without structured support. Some of us get lucky and find a pattern that works well; others struggle for years with inconsistent results.

    In conclusion

    For this area to develop, we need a better understanding of how PwP actually take their medication in daily life and not just how they are prescribed to take it. We need more research that focuses on the real-world challenges of medication adherence, from remembering doses to managing side effects and adjusting for the unpredictability of daily life with PD. We need a more nuanced discussion of what is working, what isn’t, and why. Until then, PwP will continue doing what we have always done: adapting, experimenting, and trying to make the best of an imperfect system.

    It’s ironic that while Parkinson’s medication is one of the most researched aspects of the disease, the actual experience of taking it—the daily struggles, the trial and error, the constant balancing act—is still largely unstudied. The truth is, many PwP are experts in managing their own meds out of necessity, yet our knowledge remains anecdotal and undervalued in clinical settings. If we truly want to improve Parkinson’s care, we need to start acknowledging the experiential expertise of us who live with it every single day.

    And no, there is nothing simple about managing PD meds – it’s complex all the way!

  • My 5 top learnings from tracking my Parkinson for over a decade

    I have more than a decade of experience from tracking my Parkinson’s disease (PD) and I want to share my 5 most important learnings. Hopefully this can contribute to the increasing interest in tracking for PD by adding a bit of nuance to the, often very data- /research- /doctor-centric discussions. Do let me know what you think by commenting on this post!

    (more…)

  • A small round white pill

    One of my containers for my morning doses with one morning dose laid out.

    Every morning I have my phone alarm set to ring at 6 am. Every morning, weekday or weekend, workday or holiday, because at 6 am I take my first dose of medication. I take six different pills for my Parkinson’s disease, one to make up for not having a thyroid and one contraceptive. I prepare my morning doses a few weeks at a time in containers with one compartment for each day of the week (see photo) and keep next to my bed together with a bottle of water. That way I can take my meds while still in bed and more often than not, I will go back to sleep for a while longer before getting up. This way the meds will have kicked in when I rise and moving will be a bit less difficult. (more…)

  • 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!