Parkinson’s disease is a progressive disorder in which it is assumed that an active lifestyle and structural physical exercise contribute to reducing that progression (KNGF 2004). We know that through the close interaction of the extrapyramidal system with the frontal lobe, executive functioning of the Parkinson’s patient is impaired. As a consequence of this cognitive limitation, the Parkinson’s patient will take fewer initiatives to undertake activities. Insight into this is very important both for the physiotherapy care and for the patient and his family and friends. If the reason for why the Parkinson’s patient takes little initiative to undertake activity is known, that cannot be attributed to unwillingness, demotivation, or depression. It also indicates that external motivators may be needed to stir the Parkinson’s patient into action. This can be his family and friends but also, for example, a diary in which the weekly events are noted.

If you have come across Parkinson’s patients, this description will probably be familiar to you (see also ◘ Fig. 2.1).

In the literature a number of causes can be found for the occurrence of Parkinson’s disease. These are based only on assumptions. The following hypothetical causes are named:

In contrast to CVA, Parkinson’s disease (as well as the pathologies that are described in the following two chapters) is a progressive CNS disorder. The speed at which it develops differs per individual and is partly dependent on the activity level of the Parkinson’s patient himself (KNGF 2004).

Parkinson’s disease is divided according to the Hoehn and Yahr scale into different stages. Within these stages, a five-point scale is used:

Parkinson’s disease is caused by a disruption in the substantia nigra. The substantia nigra is located in the basal ganglia and forms part of the extrapyramidal system. Dopamine is produced here and then transported to the corpus striatum (◘ Fig. 2.2).

The dopamine produced is stored in the end of the axons. An axon is a part of a nerve cell, which outside the actual cell body consists of two components:

In the end of the axon, there are vesicles with a special substance: the neurotransmitter. In this case they contain the neurotransmitter dopamine. When the dendrite makes contact with the opposite axon end, this forms the signal for the release of the neurotransmitter. This process repeats innumerable times and this way the signal spreads further.

If less dopamine is produced in the substantia nigra, then the signal transmission described above between the ends of the axons will stagnate. The flow of information between the globus pallidus and the thalamus therefore is poorer (◘ Fig. 2.3). Because of this, the extrapyramidal system will be, via the globus pallidus, be more dominantly present. This result in inhibition predominates excitation and leads to the stereotypical symptoms that we can observe in Parkinson’s disease.

This only becomes apparent when there is more than 80% reduction in the production of dopamine. The first area to be less well supplied with dopamine will be the putamen, followed by the nucleus caudatus. This could be an explanation for why motor problems occur initially and cognitive problems only appear at a later stage. In practice, this makes the case for early learning of strategies. As soon as the nucleus caudatus is supplied with less dopamine, the learning of motor skills becomes less easy, because cognitive problems can arise resulting in a reduction in the ability to learning.

The diagnosis of Parkinson’s disease is made on the basis of clinical findings. Bradykinesia should be found in combination with the following primary symptoms: tremor, rigidity, or the presence of balance problems that are not caused by specific dysfunctions.