Due to the double aging of the population (more older people are living longer), the number of people with dementia will increase significantly in the coming years. The prevalence rate in the general population in 2018 was 1.49% in the Netherlands and 1.69% in Belgium (about 300,000 people with dementia in the NL and about 200,000 in Belgium) and this will increase to a general prevalence rate of 3.15% in 2050 in the Netherlands and 2.95% in Belgium (resulting then in about 540,000 people with dementia in the Netherlands and 350,000 in Belgium). According to the most recent figures from the World Health Organisation (WHO), there are currently 78 million people worldwide with a diagnosis of dementia. By 2050, it is expected that this number will have risen to 139 million.
Age is the greatest risk factor for developing dementia and so prevalence increases with age: less than 5% of all people with dementia are under 65 years of age. Above 65, the prevalence is 10%. At the age of 85, the prevalence is already 35%, and at the age of 95, it is over 50%.
Dementia is a syndrome that can be caused by various diseases. The most common cause, and also the best known, is Alzheimer’s disease. Other known causes are vascular dementia, Parkinson’s dementia, Lewy body dementia, and frontotemporal dementia. In all forms of dementia, motor skills are also affected, as we move with our brains. Even in the prodromal stage (the stage where there is no diagnosis but there are some subjective signs), changes have been observed. Large longitudinal studies show a decrease in physical activity and walking speed as early as 10 to 12 years prior to the diagnosis of dementia.
If we look specifically at the motor problems in the various diseases, we see in Alzheimer’s disease increasing apraxia at an early stage, a slowing down of the motor activity with an accompanying slowing down of reaction time, a slower walking speed, and greater variability in gait parameters. In addition, there is a delay in stimulus processing at an early stage (tested using trailmaking A and B test). In the course of the disease, walking becomes increasingly difficult and movements less fluid. High muscle tension develops, initially as an inability to relax and later to move against the movements of, for example, a carer. The inability to relax and to move with the patient is also called Mitgehen or facilitory paratonia. The opposite movement is called Gegenhalten or oppositional paratonia.
In vascular dementia, motor problems are included in the international criteria. This is mainly because, often as a result of a CVA, the motor system is also affected, with, of course, hemiplegia and spasticity. Walking has a wide gait and is slower. There is often a disturbing static and dynamic balance. Muscle tension is often higher.
Parkinson’s dementia and Lewy Body dementia are two forms of dementia that most likely share a common pathogenesis. Both are caused by the incorrect folding of the alpha-synuclein protein in the cell wall. This causes the formation of inclusion bodies in the cell, which seriously disrupt the cell’s internal processes.
Finally, the motor problems in frontotemporal dementia are visible in the initiation of movements, and disturbances in trunk stability and balance can be observed.
Paratonia was introduced into the medical scientific literature as early as 1828. It is described as an increased muscle tension that can be felt in dementia. In later years, sporadic writings were written about it and the phenomenon did not receive more attention until the end of the 1990s. However, even though paratonia has a devastating effect on the quality of life of people with dementia, and especially in the final phase of dementia, makes care almost impossible, there is surprisingly little scientific research into this phenomenon.
In the early phase of dementia, we find a limited number of observational studies of which 2 are aimed at determining the pathogenesis. Besides a central neurological cause, a peripheral biomechanical process also seems to play a role. This is based on the formation of sugar-protein compounds (Advanced Glycation Endproducts, abbreviated to AGEs) that cause covalent connections in peripheral tissue.