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Compensation by healthy parts of the brain alleviates complaints in Parkinson’s disease – the cerebral cortex takes over after the loss of cells that make dopamine

Compensation by healthy parts of the brain alleviates complaints in Parkinson’s disease – the cerebral cortex takes over after the loss of cells that make dopamine

September 29, 2023

In Parkinson’s disease, the cerebral cortex can take over from the deeper part of the brain that has been damaged and in which cells that make dopamine have been lost. The degree of compensation by the cerebral cortex determines the number of complaints people have. This is clear from a publication issued by the Radboud University Medical Center. Patients can stimulate this compensation by exercising, for example, and thus slow down the disease process.

It was already known that in Parkinson’s disease the brain cells that produce dopamine slowly disappear. This is why patients receive an additional amount of dopamine as medication. But only a limited relationship has been found between the loss of these cells and the degree of complaints in Parkinson’s disease. Even if all the cells are already damaged, one person will have mild symptoms, while another person will have much more symptoms. Researchers from Radboud University Medical Center investigated whether something else was going on.

They discovered that the outer part of the brain, the cerebral cortex, can continue to compensate for the loss of cells that make dopamine. In this way complaints are postponed. The severity of complaints seems to be clearly related to cortical compensation. The more actively you take on tasks, the milder your inertia and the better your thinking. Doctors have suspected for some time the existence of this compensation mechanism, but it has now been scientifically proven for the first time.


These conclusions are based on a study conducted on 353 people with Parkinson’s disease and 60 healthy volunteers. They all had their brains tested while in the MRI scanner. The test was a kind of computer game, where participants had to make easy and difficult choices, which puts a lot of pressure on the brain. The researchers were able to use an MRI scanner to find out exactly which areas of the brain were active during the game. They expected that making difficult choices stimulates compensation, and that the use of compensation varies between people.

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They have seen for the first time that the brain structure that contains a lot of dopamine, the basal ganglia, is actually damaged and shows much less activity in people with Parkinson’s disease than in healthy volunteers. These basal ganglia are located deep in the brain, under the cerebral cortex. This brain area ensures that people are able to move and think smoothly. Therefore, damage to this area leads to slow movement and thinking in Parkinson’s disease.

Enhance compensation

Moreover, it has been shown that in people with Parkinson’s disease there is a very clear relationship between the severity of complaints and the activity of the cerebral cortex. Doctoral candidate Martin Johansson: “People with mild complaints showed much greater activity in the cerebral cortex, especially in areas involved in movement control. These areas were more active than those in healthy volunteers, indicating that compensation had occurred. In the case of severe complaints The cerebral cortex was much less active than in healthy volunteers.

This discovery offers new starting points for treatment and lifestyle. “In Parkinson’s disease we solve the problem of dopamine deficiency with medications. But we will now look more closely at how we enhance this compensation through the cerebral cortex,” says Rick Helmich, a neurologist at Radboud University Medical Center. “We have previously seen that exercising three times a week It helps in treating complaints and prevents shrinkage of the cerebral cortex. Thanks to the current study, we now know why the cerebral cortex is important.

About the post

This research was published in brain: The clinical severity of Parkinson’s disease is determined by decreased cortical compensation. Martin E. Johansson, Evan Toney, Roy BC Kessels, Bastian R. Blom, Rick C. Helmich.

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