Parkinson’s disease is a neurodegenerative disease 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 slowed movements (bradykinesia).
Parkinson’s is treated with medications that increase the levels of dopamine in the brain, called dopaminergic treatments. Over time, these medications may cause side effects like dyskinesia (uncontrollable, erratic movements) that can interfere with daily life.
Dopamine is a chemical messenger in the brain known as a neurotransmitter. Neurotransmitters are responsible for communicating between brain cells (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 Parkinson’s disease, the dopamine neurons in the substantia nigra begin to die off. After the neurons begin to die, they cannot send signals properly and movement is affected.
Dopamine neurons in the substantia nigra may die due to the presence of Lewy bodies in this brain region. Lewy bodies are clumps of a type of protein called alpha-synuclein, which can interfere with the neurons’ function.
Treatments for Parkinson’s motor symptoms work by increasing dopamine levels in the brain or mimicking dopamine. These drugs are sometimes referred to as dopaminergic treatments. Over time, dopamine treatments can become less effective, and higher doses may be required.
Dopamine is a chemical that is normally created in the brain. 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 drugs that mimic the shape and function of dopamine. Unlike levodopa, dopamine agonists aren’t converted to dopamine. Dopamine agonists are not as effective as other treatments, but they alleviate symptoms for longer periods. They are also thought to make brain cells more receptive to dopamine. Examples of dopamine agonists include pramipexole (Mirapex) and apomorphine (Apokyn).
Monoamine oxidase inhibitors (MAOIs) 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 safinamide (Xadago) and rasagiline (Azilect).
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The 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. Below are examples of side effects you may experience when taking Parkinson’s medications.
Dyskinesia is a common side effect of Parkinson’s medications. Dyskinesias are uncontrollable, erratic movements of the arms, legs, torso, or face. These movements include muscle spasms, fluid dancelike motions, or rapid jerking. While they may be mistaken as symptoms of Parkinson’s, they are due to the medication.
Dyskinesia often develops after 4 to 10 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 can have severe symptoms. The most common type of dyskinesia is known as peak dose. This occurs from one to two hours after you take levodopa, or when the medication is at its peak dose in the bloodstream.
“On” and “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. This is called diphasic dyskinesia.
“On” and “off” periods can be addressed by changing the dosage or timing of your levodopa, or by taking an extended-release form of the drug. Lifestyle habits — including physical activity and good sleep hygiene — may also help manage these 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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