dr Johannes Heimann

Dr. Johannes Heimann, himself suffering from Parkinson's, practiced as a specialist in gynecology and obstetrics until his retirement.

How often do you take your Parkinson's medication?

I recently read this question in a Facebook group and have therefore created a small overview on this topic.

But be careful - without medicine knowledge = pharmacology is not possible. But we also have to know them ourselves, otherwise we feel like a diabetic who has not been explained how to use insulin.

I do not use company names, but the name of the active ingredient. Everyone can find these names on their medication boxes.

1. MAO-B inhibitors: rasagiline, selegelin

Monoamine oxidase is an enzyme in the central nervous system that everyone has. It breaks down the dopamine. If you block this enzyme, dopamine - both what we make and what we swallow as levodopa - remains effective longer.

A drug from this group of effects is the basis for most intake schedules.

2. Dopamine agonists: piribedil, pramipexole, ropinirole, rotigotine (patch), apomorphine (sc injection)

These are active ingredients that act like dopamine, but are chemically clearly different from dopamine. Some of them are also available in a retarded form, which means that the duration of action is longer. Many of us take pills of this type or the patch. In the initial phase of the disease they can postpone the necessary intake of dopa, in the advanced phase they are combined with dopa and help

• to compensate for the peaks and valleys of the dopa.
• keep the dopa dosages lower

3. dopa

Now it's getting harder - watch out!

Dopa, or more precisely the levo-dopa form that turns left, is completely ineffective. It has to be converted into the actually effective dopamine in the brain. Dopamine - that is what we all have too little of. Dopamine is a neurotransmitter. This term tells us something:
A biochemical transmission substance in our brain.
If we still have or are receiving enough dopamine, many of our movement disorders improve. Our psyche also improves a bit - but only partially, because we need two other neurotransmitters against depression, of which most Parkis also have too little:
Serotonin and norepinephrine.

But back to dopa - which has to become dopamine in the brain. There are several hurdles:

• Absorption of the dopa from the intestines into the bloodstream:
  This process is disrupted by a protein-rich food. The amino acids, the building blocks of proteins, compete with the dopa for the transport mechanisms.
• Breakdown of the dopa in the organism before it can even get into the brain.
  This is prevented by benserazide (in Madopar®) or carbidopa. There is no dopa preparation that does not contain one or the other to increase the so-called bioavailability of l-dopa. In addition, some of us take COMT inhibitors, which are also supposed to prevent the premature loss of dopa.
• The dopa escapes from the blood into the brain.
  This process is disrupted by foods rich in protein. The amino acids, the building blocks of proteins, compete with the dopa for the transport mechanisms. And now it gets a little more demanding: The package insert recommends: No dopa 30 minutes before until 90 minutes after Essen! Some patients even recommend 45 minutes before to 120 minutes after eating! A cup of coffee with a sip of milk should only make a small difference. But Madopar plus a cup of yogurt – that could severely limit the effect. But as always, everyone reacts differently and everyone has to find out for themselves together with their neurologist.
  I myself take 5-6 tablets of Madopar. In the beginning it worked quite well: I took 1 ½ - 1 ½ - 1 ½ plus at some point another ½ to 1 tablet. That could be done quite well without too precisely predetermined meal times. But like all of us, I became more demanding over time.
  I noticed - like everyone sooner or later - mountains and valleys, times with high and times with low dopa levels more and more. The well-known fluctuations, which will later be referred to as on and off. With 1 - ½ - 1 - ½ - 1 - ½ - 1 - ½ I had to plan the meal times well.

4. The effect curve

On the picture you can see a curve drawn in black: this is the level of the dopamine level in the brain. For example, someone here takes an L-Dopa preparation, such as Madopar®, four times a day.

After ingestion, it will take a while for the curve to rise. That is quite clear: the swallowed l-dopa must 1. be absorbed by the intestine into the bloodstream 2. passed from the bloodstream through the blood-brain barrier 3. converted in the brain into the actually effective dopamine. (You remember: l-Dopa is completely ineffective, it is a "pro-drug" and must first be converted into the actually effective dopamine.) Points 1-3 take half an hour to a full hour.

The black curve then rises and reaches its maximum after approx. 1½ to two hours.

It then falls again until the next drug intake causes it to rise again with a delay.

Let's imagine that this patient would not swallow a whole tablet 4 times a day, but rather half a tablet 8 times a day. The total amount per day would have stayed the same. But the curve would not have 4 fairly deep valleys and 4 fairly high peaks, but 8 valleys and 8 peaks. And these valleys would no longer be so deep and the peaks would no longer be so high, the curve would be flatter overall.

Unfortunately, the so-called “therapeutic window” in which we are satisfied, drawn in white on the picture, is getting narrower and narrower. This is due to the progressive loss of the corresponding nerve cells that occurs in all of us.

If the black curve is above the white window, i.e. in the area drawn in light blue, we have hypermobility. If the black curve is below the white window, i.e. in the area drawn in dark blue, we have submobility, so we are stiffer, more shaky, less moving.

Here, too, the following applies: Since everyone reacts differently and is in their own individual area of ​​the therapeutic window of action, everyone must work with the neurologist to find the right combination of dose, amount and time of intake. Often this happens during a so-called complex therapy, which is described by many patients as very successful.