After four decades leading revolutionary advances in acute stroke care, Perth neurologist Dr David Blacker AM received his own life-changing Parkinson’s disease diagnosis in 2018.

For more than two years before seeking help, he watched his symptoms progress, wrestling with the same delays and rationalisations he’d seen in countless patients.

In this exclusive extract from his new book, My FIGHT with PD, he reflects on why even doctors struggle to cross the line from clinician to patient, and what he learned about living with Parkinson’s only after experiencing it himself.

Readers might ask why I took so long to seek an independent consultation and commence treatment. It was more than two years after the slowness and stiffness became problematic that I sought help. In some public health systems (including Australia’s), people with similar symptoms can wait this long for a specialist appointment.

I have a whole host of reasons for the delay, which all sound like weak excuses now. The first was that it had all started so slowly and insidiously. I had hoped that the exercise induced dystonia would remain just that, and symptoms of PD would not emerge.

The tremor was only intermittent and short lived, and not a consistent problem. I also had the fear that I was being a paranoid hypochondriac and was imagining symptoms. I didn’t want to put Kirsten and the boys through the stress that I knew a formal diagnosis would bring, unless it was a certainty.

Clinical Professor David Blacker

A big factor of course was my career. At first, I was confident I was still managing, and in no danger of harming patients. Thankfully, not being a surgeon or a proceduralist, my work was almost entirely cognitive and I had found ways to compensate for the deficiencies.

The handwriting issue was becoming a problem, and becoming more and more energy sapping. I gradually came to be certain that I wasn’t imagining things and this was really looking like PD. This made me feel guilty that I was deceiving people when they noticed a change in me, and I denied there was anything wrong.

There was also the debate about when to commence treatment with medications, with concerns that early commencement with drugs, particularly L-dopa, could lead to the earlier appearance of medication complications. Over the last few years these concerns have been dispelled, and many movement disorder specialists are now advocating earlier treatment, particularly to optimise the PD patient’s ability to participate in exercise – the one thing that seems to slow progression.

In retrospect, I wish I had commenced symptomatic treatment with L-dopa earlier; I regret missing out on the benefits it has provided. So finally, my increasing symptoms, which were interfering with several aspects of my life, drove me to overcome the procrastination and seek help by getting a formal diagnosis and starting treatment.

I thought I should start with an MRI of the brain. While this is not necessary for the diagnosis of PD in classic cases, I felt I should do this, and then get on and see a neurologist colleague. I’d had MRIs before, once when I was a control subject in some work on developing functional MRI protocols. (I went on to co-author a paper where we worked with speech pathologists to develop a protocol for localising the language areas of the brain and later did a small study of stroke patients with dysphasia [impaired language]). So, I was familiar with being inside the MRI tunnel.

This one seemed to be a bit different; again, there was anxiety, and the right sided tremor appeared. The MRI staff were fantastic and the neuroradiologist called me the next day, reassuring me the scan was entirely normal. He said, ‘It looks like you’ve been looking after your brain.’ I recall staring at my MRI, and feeling strangely frustrated that it looked so normal, but clearly wasn’t working properly.

I had heard patients talk about this frustration, and had been unable to understand it; I thought they should be grateful to have normal anatomy. But now, confronted with a clear scan, I too felt this paradoxical disappointment at having no visual evidence to explain my symptoms.
The next task was to choose a colleague to see.

Perth neurologists are a very small group, and there are a limited number of movement disorder subspecialists. Given that I didn’t think there was any diagnostic difficulty, my choice was based around some other complex factors. I wanted someone a little separate from my day-to-day work, someone I respected, and I also didn’t want to stress out one of my previous trainees by asking them to look after me.

I wrote a referral letter, briefly outlining many of the symptoms I have previously described here. I made an appointment, as the last patient, late on a Friday afternoon. Kirsten and I went in together. I was surprised at how nervous I was, and again the right sided tremor was there for us all to see. I could feel the rigidity as he carefully examined my limbs, and my slowed finger-tapping on the right all made the clinical diagnosis straightforward.

The diagnosis should not have been a surprise, but it still hit me hard, and there were some tears. On the positive side, he gave me a script for Madopar, which I was happy to try. He was independently of the opinion we should go straight to L-dopa. I was not keen to start with a dopamine agonist such as pramipexole; I have seen patients get sleepy on this, and suffer impulse control disorders. I already have obsessive tendencies and don’t enjoy any feeling of sedation, so am probably not a good candidate for these medications.

I vividly recall taking my first dose of Madopar one afternoon, and testing my right-hand finger tapping. After about forty-five minutes I could feel a clear difference, with the movements becoming smoother and quicker. A few further doses confirmed that I was indeed responding to the medication.

I was pleasantly surprised by this. For some reason my expectations were low. I had waited so long to start, it seemed almost too good to be true. Even though I had seen good responses in patients before, I have also seen patients with little improvement, so I felt very lucky to be obtaining benefit. My walking also improved, and in the days and weeks to follow, I enjoyed a new sense of freedom of movement.

The only downside was nausea. It took me a few weeks to get into a regular routine of taking it three times a day, and it took about that long for the nausea to settle. Nausea is such a horrible feeling. When you are dealing with the emotional stress of a new diagnosis, and starting a new treatment, nausea is the last thing you need.

Oral L-dopa crosses into the brain and then is metabolised to dopamine. L-dopa is usually combined with another agent, either benserazide (in the brand Maopar) or carbidopa (in Sinemet and Kinson).

They are the second part of the dose written on the medication labelling. For example, the 25 milligrams in Madopar 100/25. These components inhibit the breakdown of L-dopa into dopamine in the blood outside the brain. This allows more L-dopa to reach the brain, and reduces nausea that results from L-dopa being metabolised into dopamine outside the brain.

Probably 75–100 milligrams of benserazide or carbidopa is required to counter the nausea, so when starting off at a low dose, such as one 100/25 milligram tablet three times a day, there is only just enough of this. Reassurance that the nausea will abate is important.

It took me a while to get the rhythm of the medication regimen going. Just like any patient, I had a bit of trouble remembering doses, and had the frustration of thinking ‘have I taken it or not?’

In that situation I might take half a tablet, so I wouldn’t be too far off the mark either way. I had never thought of recommending that until I had to take them myself! Another strategy was to carry a day’s supply with me, so I could avoid the uncertainty.

Pretty soon I started carrying the number I needed, plus an extra, in case I dropped or lost one. I arranged a supply of tablets all over the place, including a bottle in the kitchen, my car and one at work.

I have numerous small plastic containers that were initially for ear plugs, each filled with about eight capsules. On weekends or when going out I usually have one in my pocket. At work and at golf I have so much other stuff in my pockets there is not enough room, so I keep a supply in my small black neuro exam bag from the Mayo clinic (one of my precious possessions), and my golf bag; my favourite bag.

I am paranoid about running out, because the feeling of being ‘off’ is terrible, so I am fastidious about keeping my scripts up to date. I prefer the Madopar capsules because they are easier to swallow than the tablets. The advantage of the tablets is that they can be broken into smaller pieces in order to make dose adjustments, whereas capsules cannot.

When I travel I usually pack an extra bottle of tablets. I do this in case I lose my main supply while in a location where I couldn’t easily obtain a script, having tablets that I could break apart and ‘ration’ the supply out.

I doubt I would have ever imagined these nuances if I wasn’t taking this medication myself.

Dr Blacker’s book, My FIGHT with PD, can be purchased online through Parkinson’s WA