Synonyms in a broader sense
- Shaking paralysis
- Idiopathic Parkinson Syndrome
- Tremble
- Tremor Disease
- Parkinson’s disease
Introduction
This topic is the continuation of our topic Parkinson’s disease. For general information about the disease, diagnosis, and distribution, see our topic: Parkinson’s disease.
Therapy
The therapeutic options for treating Parkinson’s disease can be roughly divided into 3 main categories:
- Drug therapy
- Own measures
- Operations
Drugs
A nerve cell has many dendrites, which are a kind of connecting cable to other nerve cells to communicate with them.
- Nerve cell
- Dendrite
The Parkinson – disease Morbus Parkinson is not yet curable today, but it is treatable. The mechanisms responsible for the symptoms are known, and the following conclusion can be drawn from this: If we now know that Parkinson’s disease lacks the messenger substance dopamine, we should actually be able to assume that all that is needed is to give the patient a little dopamine from the outside and he would feel better.
However, this idea literally encounters a natural limit: the main “transport instrument” for drugs and nutrients in our body is the blood. However, undesirable pathogens (viruses, bacteria, fungi and toxins) also reach almost every part of the body via this route. However, since the brain, as the control center of the body, must be protected in particular against pathogens and the like, it is protected by the natural “blood–brain barrier”.
Many harmful, but also some very useful substances cannot easily pass through this barrier. Dopamine typically cannot overcome this barrier. Nevertheless, all drug approaches revolve around the idea that the body is sufficiently supplied with dopamine.
The theoretical drug approaches here are:
- L-Dopa: L-Dopa is a “biochemical precursor” of the actual dopamine. In contrast to dopamine, it can very well cross the “blood–brain barrier”. One can imagine this mechanism like a fence in which there are gaps, but through which one would never be able to pass with a car.
But if you put the parts through and assemble the car on the opposite side, the car can drive through it. One problem with this type of treatment is that the body does not really know that L-dopa is only to be “rebuilt” in the brain. For this reason, it is important to inhibit the mechanism responsible for the breakdown of the (peripheral) L-dopa not located in the brain.
For this purpose, an enzyme inhibitor (dopa decarboxylase inhibitor) is administered. This inhibitor (benserazide) ensures that the total amount of L-dopa administered is significantly reduced. The patient is thus spared (especially with regard to side effects).
First therapeutic successes are usually visible within days. In addition, L-Dopa is usually well tolerated. As an important tip from the clinical application the following must be considered: L-Dopa should be taken about 1/2 hour before a meal, because taking it at the same time as a meal can hinder the metabolism!
- Dopamine agonists: The group of dopamine agonists are substances that are very similar to the actual dopamine and are able to mimic the effect of dopamine because of this similarity.
An adjustment to such preparations requires some patience. Overall, the onset of action is quite slow. In addition, nausea and dizziness may occur quite often.
In some cases, hallucinations and orientation disorders may also occur. As an advantage of this group of active ingredients, however, it must be emphasized that they usually bring stable improvement over years if well adjusted.
- Catechol-O-Methyltransferase (COMT) – Inhibitors: This complicated name describes a group of active ingredients that inhibits another enzyme (note: the suffix “-ase” actually always means enzyme). As already mentioned, when taking L-Dopa one should take care that it is not “converted” too early and should therefore inhibit the corresponding enzyme.Today, however, we know that, in addition to the enzyme already mentioned (dopa-decarboxylase), there is a second “conversion pathway” for L-dopa, which “branches off” part of the L-dopa, so to speak, and converts it before it reaches the brain through the blood-brain barrier.
This is the enzyme catechol-O-methyltransferase. If this enzyme is inhibited, e.g. with Entacapon (Comtess), the effect of L-Dopa is improved. Without L-dopa, such an inhibitor naturally has no effect on Parkinson’s disease.
- Anticholinergics: As also already mentioned, Parkinson’s disease causes an “excess” of acetylcholine due to the reduction of dopamine, which then leads to rigor and tremor.
The anticholinergics counteract this mechanism. On the positive side, it should be emphasized that there is very good experience in the treatment of tremor. The rigor is also positively influenced.
On the negative side, however, it should be noted that other systems in which acetycholine plays a role are also affected by the anticholinergics. Dry mouth and constipation, but also urinary retention, occur relatively regularly. It must therefore be dosed very carefully.
- Mono-Amino-Oxidase Inhibitors: The suffix “-ase” tells the attentive reader that this complicated name also stands for an enzyme that needs to be inhibited.
The basic mechanism here is as follows: When L-Dopa is finally used at its destination (the brain), it is, like everything organic, broken down into its individual parts again by enzymes after some time to ensure that there are always new, “fresh” and error-free active ingredients and that there is no accumulation. The mono-amino-oxidase inhibitors (MAO inhibitors for short, active ingredient name “Selegelin”) ensure that this breakdown of dopamine is now somewhat delayed and that dopamine can therefore act for a slightly longer period (dopamine expander). As side effects, patients often report sleep disorders and restlessness.
6) Amantadine: The mode of action of this substance is still not fully understood.
It is assumed that amantadine interferes with the above-mentioned imbalance of the messenger substances and in particular influences the effect of glutamate. As safe one knows however today that Amantadin helps! It can positively influence all symptoms of Parkinson’s disease.
Further advantages are that patients usually tolerate it very well and that it can also be administered in liquid form. The disadvantage is that other groups of active substances (especially L-dopa) have a much better and stronger effect. 7th Budipin:Budipin influences a whole range of neurotransmitters.
Particularly to emphasize is however the dopamine-promoting and glutamate-inhibiting effect. It is particularly suitable for the treatment of severe tremor. Unfortunately, side effects such as dizziness, nausea and occasionally cardiac arrhythmia are quite common when using Budipin. In very many cases a doctor will sooner or later suggest a combination therapy of 2 or even 3 different drugs.