The therapy of Parkinson's syndrome is individually adapted to each patient depending on the course of the disease and the symptoms present. Drug treatment, physiotherapy, speech therapy (speech and swallowing training) and surgical interventions are applied and combined depending on the degree of the disease.
Furthermore, the choice of therapy is strongly influenced by the age of the patient. Likewise, occupational and social circumstances have an influence on the Parkinson's patient's need to combat the symptoms as much as possible. It is therefore important that patients and their relatives are involved in the decision-making process as to which therapies should be carried out.
In order to adequately assess the efficacy of a drug and avoid overdose, Parkinson's therapy involves changing the dose only in small increments. There is a high risk of overdose when trying to suppress all symptoms of the disease with medication.
To date, there is no form of therapy in which the dopamine-producing cells in the brain can be prevented from dying. The current treatment approach is therefore to compensate for the lack of dopamine by means of drug therapy. Since dopamine itself - when administered as a tablet, for example - is unable to penetrate the areas of the brain affected by the disease due to the blood-brain barrier (natural barrier between the bloodstream and the central nervous system), other active substances are used in the therapy:
- Levodopa: Levodopa (L-dopa) is a precursor to dopamine that is able to cross the blood-brain barrier to enter the affected areas of the brain. There, L-dopa is subsequently converted into dopamine and in this way compensates for the lack of dopamine. However, L-dopa is sometimes broken down in the bloodstream before it reaches the brain, causing the drug to lose effectiveness.
To prevent this premature degradation, L-dopa is combined with other agents. Levodopa itself can cause movement disorders after several years of treatment, making it primarily used in patients after age 70.
- Dopamine agonists: These agents are most commonly used in Parkinson's patients under the age of 70. These are substances that are chemically different from dopamine but have similar effects. They can easily cross the blood-brain barrier and subsequently bind to the same receptors in the nerve cells as dopamine. Unlike L-dopa, there is less risk of developing movement disorders over time. However, the dopamine agonists are less effective.
- MAO-B inhibitors: these drugs increase the amount of dopamine in the brain by inhibiting dopamine breakdown. Normally, after dopamine binds to its receptor, it is broken down by the enzyme MAO-B (mono-amino oxidase-B). MAO-B inhibitors - such as rasagiline or selegiline - now inhibit this enzyme, increasing dopamine concentrations. However, MAO-B inhibitors are less effective than levodopa and than the majority of dopamine agonists.
- NMDA antagonists: NMDA antagonists (N-methyl-D-aspartate antagonists) are drugs that block the action of the neurotransmitter glutamate in the brain. Since blocking the effect of glutamate improves the effectiveness of dopamine, dopamine deficiency can be compensated for somewhat in this way. NMDA antagonists can be used in combination with other medications to help treat Parkinson's disease. The main active ingredient is called amantadine.
- COMT inhibitors: COMT (catechol-O-methyl transferase) is the name given to an enzyme responsible for breaking down L-dopa in the body. COMT inhibitors can therefore be used to prolong the duration of action of L-dopa, as the breakdown of this active substance is inhibited. COMT inhibitors are therefore always administered together with L-dopa.
- Anticholinergics: These agents have no direct effect on the dopamine balance. Their effect is based on inhibiting the overreactive neurotransmitter acetylcholine in Parkinson's syndrome. In this way, a slight improvement in symptoms such as a reduction in tremor and increased saliva production can be achieved. Old people usually do not tolerate anticholinergics, so these agents are primarily used in younger patients.
Deep brain stimulation (tHS)
In deep brain stimulation, a pulse generator (also called a brain pacemaker) is surgically implanted in the Parkinson's patient, which electrically stimulates certain brain areas (subthalamic nucleus, globus pallidus or the anterior thalamus). The stimulation influences the activity of the brain area, which can lead to an improvement in the symptoms of Parkinson's syndrome. Deep brain stimulation is the most common surgical procedure performed for Parkinson's disease.
Using tHS, good results can be achieved against off-phases (phases of complete immobility) and dyskinesias (over-movements). Tremor (trembling at rest) can be improved by electrical stimulation of the thalamus (a specific brain nerve nucleus).
The surgery is performed in only a few, highly specialized centers.
- Seek information from doctors and Parkinson's associations about the disease.
- Regular physical activity can help maintain the best possible state of health. Physiotherapy, occupational therapy and the practice of light endurance sports are highly recommended.
- In many cases, patients with Parkinson's eat and drink too little because they find it difficult to eat due to the motor impairment and tend to avoid going to the toilet. Therefore, special attention should be paid to a balanced diet and adequate fluid intake. Dopamine preparations should not be taken together with a protein-rich diet, as the active substance is then less easily absorbed in the intestine.
- In the case of symptoms such as so-called freezing (the patient can hardly move during this phase), visual stimuli on the floor, such as footprints stuck on the floor, help. Acoustic rhythm stimuli also improve the situation.
- Parkinson's patients should not be urged to hurry, as this prolongs rather than shortens the phase of freezing.