Blogging with Parkinson's

A personal perspective on Young Onset Parkinson's


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Could it really be so simple?

My problems with sleep have been going on for more than two years, but they seemed to get significantly worse at the end of last year (2016), when I stopped taking Ropinirole. I had thought that the lack of Ropinirole might be the cause; my consultant had said that it could cause hyperactivity, which I thought might have been masking the effects of poor sleep, allowing me to run on empty …

But now I have a new theory. A very simple one: I was undermedicated. And I’m amazed that it took me this long to figure it out.

In June, I was bitten by an insect and had an impressive (but not dangerous) allergic reaction to the bite. More seriously, the bite became infected and I ended up in hospital overnight on intraveneous antibiotics. The time in hospital was a pause, a break from normal life: a time to think. I realised that I needed to do something about my sleep. I decided to try over the counter medication (with advice from my GP and pharmacist).  Unfortunately, it didn’t work (I think mainly because my problem was not going to sleep in the first instance, but staying asleep).

I also got in touch with my Parkinson’s nurse specialist and asked for help.  She wanted me to speak to the consultant, but that wasn’t possible at the time (I now have an appointment for September).

It felt like I was unavoidably on my own, at least for the duration of the summer holidays.

After struggling through a nasty cold that was all the nastier (or so I presume) for my poor sleep, it suddenly occurred to me to try adding an extra Sinemet CR tablet into my day.

Sinemet CR is a controlled release form of Sinemet, a widely-prescribed levodopa vehicle that contains 50mg caridopa as well as 200mg levodopa. It is currently my main anti-Parkinson’s drug. I also take 1mg Rasagiline (Azilect) daily for its supposed protective function, and have a supply of Sinemet Plus (half the dose of the CR, but potentially faster acting because it isn’t controlled release) that I use as a sort of boost to the CR.

I was taking four CR daily, starting at 7 am and finishing at 8:30 pm. I would go to bed and wake in the wee small hours, typically between 3 and 4:30 am. If I went to bed late, I would often wake earlier. Going back to sleep was difficult. Often I would start to notice my Parkinson’s symptoms getting more prevalent as I got more and more impatient with being awake; I tried taking Sinemet Plus, and it seemed to help, often giving me another two hours of sleep, about an hour after taking it.  It wasn’t reliable, but it was the only thing that seemed to have any effect at all. This was one of the reasons that I decided to try a new regime.

I am now taking five CR daily, starting at 7am and finishing at 11pm. They are a little closer together.

It has only been a few days – six, to be precise – but the effect was apparent the first night and has remained constant: I sleep longer (I’ve been waking at 6am). I feel better during the day. I have not needed to “boost” myself with Sinemet Plus so much. I am still, I think, recovering (from the cold as well as from prolonged lack of sleep), but things are definitely looking better.

I have also noticed that, when my sleep was interrupted in the early hours, I invaribly woke in the same position that I had gone to sleep in. I don’t know if that is, or was, “normal” for me or not – I had never scrutinised my sleep that closely before. But a couple of times over the last week, I have woken in a different position – both times on my back, instead of on my right hand side. One of those awakenings was in the middle of the night. I woke enough to register it, and to turn onto my side, and then… I went back to sleep.

 

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Downside

Happy Christmas

Happy Christmas

[This post relates to my last-but-one post, “Don’t it always seem to be…”]

I spoke to my consultant. Apparently this tiredness could be part of the withdrawal from Ropinirole, which can  make you “a bit hyperactive”. I think that’s what she said (I think I was, at times). But she also said that it will pass, and that I will reach an equilibrium.

And I’m going to try a modified release Sinemet, which should help to even out what they call the “on” and “off” states.

I refuse to stay down here for long. I’m looking for the UP escalator. Anybody know where it is?

 


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Don’t it always seem to be…

You don’t know what you got ’til it’s gone.

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Joni Mitchell’s song, drawn in a sketchbook by me in 2014

I’m really missing sleep. I used to sleep very heavily (it’d take me a while to get there sometimes, but I didn’t used to wake up worth noticing before I had to, and even then I was very good at sleeping through alarms). Now I wake up in the wee small hours and I can’t get back to sleep.

It isn’t as bad as is has been, but it’s still not great. Last year, when I started taking Sinemet, I was waking up at 3am on a regular basis. Tired but not sleepy.

My consultant supposed that it might be an interaction between the two drugs, Sinemet and Ropinirole. You need to be careful coming off Ropinirole, as with all dopamine agonists, and do it gradually. There are horror stories of eternal depression as a result of DAWS (Dopamine Agonist Withdrawal Syndrome); it seems to be a greater risk if you experienced a severe impulse control disorder as a result of taking the dopamine agonist. I’m very glad to say that my artistic impulse was not unduly increased by the Ropinirole I was taking (coincidence of timing might have made it seem so from the outside) and that I have not had any trouble coming off Ropinirole.

The Ropinirole is gone. I’m not taking it any more. It’s been gone for three or four weeks and I don’t miss it.

But I do miss that sleep. Like I say, it’s not as bad as it was. It’s usually 5am that I wake up at at the moment. And when I do wake up, it’s blatantly obvious what’s wrong – my muscles are stiff and I’m shaking and it’s really uncomfortable. My medication has worn off. I know that I need to get up in around two hours and so taking a “bedtime” medication isn’t a good idea. I can either get up and start my day early (and slowly), or I can try and tough it out without fidgeting too much (my husband is a light sleeper and is also suffering from my lack of sleep).

I think it’s time to talk to the consultant again.

 


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Morality and Parkinson’s

I recently had cause to take a good hard look at my own behaviour, and the way in which I was reacting to other people.

It’s difficult to accept that you might be selfish or careless of other people’s feelings. It’s also far too easy to blame it on an illness – or the drugs used to treat that illness – especially if you are aware that this is a possibility.

Which it is…

In July 2015, a study was published that suggested levadopa (the most prevalent treatment for Parkinson’s, and the key ingredient in the Sinemet that I take) made healthy subjects more selfish. The same study also looked at an antidepressant drug that increased serotonin levels, and that drug was found to make people more caring.

To my mind, the study was based on a simplistic and fairly extreme premise, probably out of necessity – morality is difficult to measure. The study used the choice to deliver a painful but not intolerable electric shock to either oneself or another person (not present in the same room). In both cases, cash could be paid to prevent the shock. The amount that people were prepared to pay to avoid harming themself, and to avoid harming another, was monitored and compared. The findings can be summarised as follows:

  • those whose serotonin levels were increased were willing to pay significantly more to avoid harm to another than to avoid harming themselves
  • those whose brain chemistry was unchanged (because they took a placebo) would still pay more to avoid harm to others, but not as much as the increased-serotonin group
  • those whose dopamine levels were increased paid equal amounts to avoid harm to others and to avoid harm to themselves

I would like to think that, even with levadopa, my judgement would err towards the altruistic avoidance of harm to another. And perhaps it would – the results were, after all, averages. However, I have never, to my recollection, found myself in that sort of situation.

But what if the situation was more subtle? If it were more a matter of insensitivity, not paying full attention to what others were doing, increased focus on the self? If it were a matter of taking opportunities without paying heed to the limited nature of the opportunities and to other’s desires to take the same opportunities? I think I have been guilty of these things. I’m not sure that it is entirely down to drugs, either; at least some of it is inherent in my personality (I know that I am quite good at some things, and I also know that I can come across as patronising or condescending as a result of the first knowing without meaning to; I try to guard against this tendency, but I do not always succeed). At least some of it must be due to Parkinson’s itself – the difficulties in doing things that didn’t ought to be difficult, that didn’t used to be difficult, and the self-awareness that comes with the process of constant adjustment (because the effects of Parkinson’s vary from day to day, from hour to hour, and gradually become more frustrating over weeks and months). And another part, again, is a result of the knowledge that, because I have Parkinson’s, my timescales are reduced.

Interestingly, I have recently started taking an antidepressant called mirtazapine. This is not the same drug that was used in the study (that was citalopram); it is described as “an atypical antidepressant” because it only targets one type of serotonin receptor in the brain. But it does still increase serotonin levels.

I take mirtazapine to counteract the excessive wakefulness that sinemet causes (that is, it helps me sleep). Might it also go some way to counteract the apparent selfishness that sinemet causes?


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Motivation

_20151104_083956A few weeks ago, my local Parkinson’s UK group welcomed a speaker. Dr. Masud Husain, who described his work at Oxford University on Motivation related to Parkinson’s.

Not only was the talk fascinating, it also felt very relevant. The behaviour patterns he described were uncomfortably familiar (in broad outline, although the lines were bolder and blacker for the people Dr. Husain was talking about than they are for me).

There was a man who had a stroke, affecting – very specifcally – the dopamine-producing regions of his brain. He recovered. But he didn’t want to do anything. He didn’t want to not do anything, either. He wasn’t depressed. He was inert. Apathetic. Completely unmotivated. He lost his job. He lost his home. His friends took him in, then they took him to the doctor. “He’s boring,” they said, “he didn’t used to be. He doesn’t do anything at all unless you tell him to do it.” The doctor referred him to Dr. Husain. Dr. Husain gave him Parkinson’s medication, and the man regained some of his lost motivation.

We were shown a video of a couple. She had Parkinson’s. He had gripes. “She doesn’t do anything”, he said. “Except watch television.” She agreed, but she looked uncomfortable. She didn’t want not to do anything – not in the abstract – she wanted to be her former, busy self. But she wasn’t. She couldn’t. Her get up and go had got up and gone.

Dopamine, explained Dr. Husain, has been associated primarily with motor functions, especially in Parkinson’s patients – but that isn’t its only function. It is also associated with pleasure, rewards, and motivation. Basically, it isn’t just the carrier for the signal from brain to muscle to do something.  It’s what gets you moving. What gets you out of bed in the morning. What makes you send the signal in the first place.

I was particuarly intrigued by a couple of graphs, which can be seen in Fig. 4 of a “Note” published in Cortex, Volume 69, August 2015, Pages 40–46. The note, by Trevor T.-J. Chong, Valerie Bonnelle, Sanjay Manohar, Kai-Riin Veromann, Kinan Muhammed, George K. Tofaris, Michele Hu and Masud Husain is entitled “Dopamine enhances willingness to exert effort for reward in Parkinson’s disease”.

I have linked the graphic below. The caption is taken from the note.

from

Effort indifference points plotted as a function of stake for patients and controls. (A) Regardless of medication status, patients had significantly lower effort indifference points than controls for the lowest reward. However, for high rewards, effort indifference points were significantly higher for patients when they were ON medication, relative not only to when they were OFF medication, but even compared to healthy controls. Inset: For clarity, PD data are replotted against control performance for patients (B) ON medication and (C) OFF medication. Shading denotes effort indifference points being greater for patients than controls (orange), or less for patients than controls (yellow). Error bars indicate ±1 SEM.

My take on this is to observe that, with or without medication, the person with Parkinson’s is likely to find it harder to do something they aren’t very interested in than a “normal” person. Without medication, with greater interest, they will eventually reach the same level of motivation as normal (but it’s got to be a really interesting thing!).  With medication, they reach “normal” sooner – and then exceed it. So if that really interesting thing comes along, the medicated person with Parkinson’s is not going to let it get away!

Everybody has different interests, and it goes without saying that painting a landscape is not going to float every Parkie’s boat, but relatively few will get excited about doing housework…