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Parkinson’s disease is caused by low levels of dopamine and improper signaling in the brain, which leads to movement symptoms. Parkinsonism is a set of movement disorders characterized by tremors, muscle stiffness, coordination issues, and bradykinesia (slowed movements). Parkinson’s disease is one of the most common movement disorders that affect the central nervous system.
Parkinson’s is treated with dopaminergic treatments. Over time, these medications may cause side effects like dyskinesia (uncontrollable, erratic movements) that can interfere with daily life.
Dopamine is a specialized chemical messenger in the brain known as a neurotransmitter. Neurotransmitters are responsible for communicating between cells in the brain called neurons. Some neurons are responsible for sending signals with specific neurotransmitters. For example, neurons that communicate using dopamine are known as dopamine neurons or dopaminergic neurons.
Dopamine neurons are found in specific areas of the brain, including the substantia nigra and basal ganglia. These areas of the midbrain work together to control your muscular and skeletal movements. The substantia nigra makes dopamine to send signals to the basal ganglia and other areas of the brain to cause movement.
In neurodegenerative disorders such as parkinsonism, the dopamine neurons in the substantia nigra begin to die off. This may be due to the presence of Lewy bodies in this brain region. Lewy bodies are clumps of the protein alpha-synuclein, which can interfere with the neurons’ function. After the neurons begin to die, they cannot send signals properly and movement is affected.
People with Parkinson’s disease have low levels of dopamine in their brains. Dopaminergic treatments are used to increase dopamine levels or mimic the chemical to improve symptoms. These drugs are mainly used to address motor problems, such as tremors or difficulty walking. Over time, dopamine treatments can become less effective, and higher doses may be required.
Dopamine is a specialized chemical that is normally synthesized in the brain. To mimic this process, dopaminergic drugs are taken orally or are infused using a pump system, which allows the drugs to enter the bloodstream. They then travel to the brain and are broken down into dopamine, increasing levels of the neurotransmitter.
Some examples of dopaminergic treatments include levodopa/carbidopa, which is sold under the brand names Sinemet, Parcopa, and Rytary. Levodopa contains a natural chemical that is able to enter the brain and is converted into dopamine. Carbidopa is used to help prevent levodopa from being converted into dopamine outside the brain.
After levodopa is converted into dopamine, it can then interact with dopamine receptors in the brain to improve motor symptoms. Specialized enzymes known as catechol-O-methyltransferase (COMT) inhibitors can also be used to increase the amount of levodopa that reaches the brain.
Dopamine agonists are a type of drug that mimics the shape and function of dopamine. These are not as effective as other treatments, but they alleviate symptoms for longer. They are also thought to make brain cells more receptive to dopamine. Examples of dopamine agonists include Mirapex (pramipexole) and Apokyn (apomorphine).
Monoamine oxidase inhibitors (MAOIs) are a class of antidepressant drugs which are thought to work by preventing the breakdown of dopamine. This increases the amount of dopamine in the brain, which can treat some symptoms of Parkinson’s disease. Examples of MAOIs include Xadago (safinamide) and Azilect (rasagiline).
The overall goal of Parkinson’s disease treatment is to alleviate the symptoms as much as possible with as few side effects as possible. No medication is perfect, but treatment should improve quality of life, and the benefits should outweigh the risks. Dyskinesia usually occurs when taking levodopa, but it can also occur with dopamine agonists, MAOIs, and COMT inhibitors.
A common complication with Parkinson’s medications is the development of dyskinesia. Dyskinesia results in uncontrollable, erratic movements of the arms, legs, torso, or face. These movements include muscle spasms, fluid dance-like motions, or rapid jerking. While they may be mistaken as symptoms of Parkinson’s, they are due to the medication.
Dyskinesia often develops after two to three years of levodopa treatment, and it can usually be addressed through medication adjustments or by adding a new treatment. Every person with dyskinesia will experience it differently. Some people may have mild symptoms, while others’ symptoms can be severe. The most common type of dyskinesia is known as peak dose. This occurs between one to two hours after you take levodopa, or when the medication is at peak dose in the bloodstream.
Diphasic dyskinesia, or dyskinesia-improvement-dyskinesia (D-I-D) syndrome, can occur as you are beginning “on” or “off” periods. “On” or “off” periods are caused by the rise and fall of dopamine levels, which become difficult to manage after several years of levodopa treatment. As a result, symptoms like dyskinesia may develop.
“On” and “off” periods can be addressed in a few different ways. One way is by changing the dosage or timing of your levodopa, or taking an extended-release form of the drug. This will help control the fluctuation of dopamine levels in the brain, reducing the chances of “on” and “off” periods. Learn more about managing “off” periods.
Dopaminergic treatments can cause nonmotor side effects, including hallucinations, delusions, and compulsive behaviors such as gambling or excessive shopping. Hallucinations and delusions can also be symptoms of Parkinson’s disease — they are not exclusively medication side effects.
Side effects like nausea, dizziness, or sleeping problems can also occur with Parkinson’s medications.
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