Blogging with Parkinson's

A personal perspective on Young Onset Parkinson's


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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…

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Creativity induced by Parkinson’s Drugs?

I really don’t want to believe this, but there is a theory that some drugs used to treat Parkinson’s can increase creativity.

Why don’t I want to believe it? Because it’s my creativity. It’s not Parkinson’s, and it’s not the drug’s. I feel very possessive of my creativity. I had it long before my dopamine levels went haywire and I have long felt that it is an important part of me.

So, without getting any more emotional about this issue, let’s look at the science. (There will be a couple of arty pictures to look at, too, and I shall write a second post describing how I think that this applies to me.) Continue reading


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Rave On: Ecstasy implicated in potential Parkinson’s treatment

I never was a raver. Here's Buddy Holly filtered through Steeleye Span.Health India’s headline is a tad optimistic: “Ecstasy (MDMA), a rave drug could cure Parkinson’s!” (love the ecstatic exclamation mark), but the article itself is more measured. Of course MDMA isn’t going to cure Parkinson’s. A cure is a long way off. MDMA isn’t even going to treat the symptoms of Parkinson’s – but it, or, rather, one of its analogues, might be able to ameliorate the side effects of the ultimate drug for Parkinson’s, levodopa.

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Colonic Interrogation

Colons are boring; here's a semicolon. I know it's not the same type of colon referred to in the post, but dare I suggest that it looks a bit nicer? It's from a font called "Original Garamond".

Half a colon

Scientists at Rush University Medical Center in Chicago have discovered that the bowel may be more closely related to the brain than any of us would have cared to think. Apparently, exceptionally large quantities of alpha-synuclein can be found in the lower bowels of people in the early stages of Parkinson’s. It has also been detected, at higher than normal levels, in the bowels of people who later went on to develop Parkinson’s. The suggestion is that it may be possible to predict the onset of Parkinson’s symptoms by means of a colonic biopsy.

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Two-Faced Dopamine, and the Difference Between Wanting and Liking

This video, which a friend pointed out to me on the Guardian’s Web site, is quite intriguing. Its direct relevance to Parkinson’s is minimal, but it does discuss the role of dopamine in the brain and the psychological and sociological results of an excess thereof. Too much dopamine is, of course, precisely the opposite problem to that posed by Parkinson’s. Continue reading