Study links brain atrophy to tremor progression in Parkinson’s
Knowing how tremors will behave could help clinical decision-making
In people with Parkinson’s disease, shrinkage in tremor-related brain areas is associated with the progression of motor symptoms, according to a study.
In the brain’s gray matter, which contains cell bodies of neurons, this shrinkage, or atrophy, of tremor-related regions and the whole brain over two years was associated with less severe kinetic tremors, or those that occur during voluntary movements.
In contrast, atrophy correlated with worsening rigidity and bradykinesia, or slowed movements.
“If future changes in tremor severity can be adequately predicted in individual patients, then this may have implications for clinical practice,” researchers wrote. “For example, medication-resistant tremor is one of the indications for … surgery in relatively early [Parkinson’s] and knowing how the tremor will behave in the next years could help clinical decision-making.”
The study, “Changes in Action Tremor in Parkinson’s Disease over Time: Clinical and Neuroimaging Correlates,” was published in Movement Disorders.
Parkinson’s disease is caused by the progressive dysfunction and death of dopaminergic neurons, the nerve cells responsible for producing dopamine, a chemical messenger involved in motor control. This leads to impaired dopamine signaling in the brain, resulting in motor symptoms, including tremor, which are uncontrollable muscle contractions that commonly affect the hands.
Most frequent form of tremor in Parkinson’s is resting tremors
The most frequent form of tremor in Parkinson’s is resting tremors, when muscles are at rest. While rigidity and bradykinesia worsen as the disease progresses, tremors may worsen, remain stable, or disappear.
Although previous MRI studies showed associations between structural changes in the brain and tremors in Parkinson’s, “the cerebral mechanisms underlying these symptom-specific longitudinal [over time] trajectories are unclear,” the researchers wrote.
To know more, researchers in the Netherlands analyzed data from 520 Parkinson’s patients and 60 healthy controls. The data were obtained from the Personalized Parkinson Project, which is a prospective study of patients living with the disease for a maximum of five years.
Overall, 363 patients had bradykinesia, rigidity, and tremors at baseline (the study’s start), including 247 with resting tremors, 278 with postural tremors (when holding a position against gravity, like holding the arms outstretched), and 279 with kinetic tremors. Postural and kinetic are types of action tremors.
After two years, tremors had progressed at a slower rate than bradykinesia and rigidity, while rigidity progressed slightly faster than bradykinesia. Also, while tremor severity remained constant over time, bradykinesia and rigidity worsened. At follow-up, 41 patients (11%) had no tremors.
In terms of severity of the different types of tremors, resting tremors remained constant, whereas kinetic and postural tremors both were less severe. Within each group, 22% of the patients had no resting tremors, 24% had no postural tremors, and 28% had no kinetic tremors after two years.
Progressive atrophy of gray matter in regions implicated in Parkinson’s tremors
Structural brain changes were evaluated with MRI at baseline and after two years. The analyses focused on four regions implicated in Parkinson’s tremors: thalamus, motor cortex, globus pallidus, and cerebellum. Overall, there was progressive atrophy of the gray matter in these regions. Progressive thinning was also found in total gray matter.
This shrinkage of gray matter in tremor-related regions was significantly associated with less severe kinetic and postural tremors after two years. Total gray matter atrophy was also associated with a progressive reduction of kinetic tremors, but also with progressive worsening of bradykinesia and rigidity.
Whole-brain analyses showed widespread cortex thinning correlated with reduced kinetic tremors, and with worse bradykinesia and rigidity. In addition, atrophy in a brain area called the hippocampus (key in memory and learning) was associated with cognitive decline.
“This study demonstrates that there are symptom-specific longitudinal trajectories in [Parkinson’s] and that the [rate] of these trajectories relates to the speed of gray matter atrophy,” the researchers wrote. Future, large studies should focus on how these findings may be used to predict symptom progression in individual patients.
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