Parkinson’s disease is a neurodegenerative condition that primarily affects motor function, leading to symptoms like tremors, stiffness, and slow movement. Beyond these core features, individuals with Parkinson’s may experience other movement challenges. One such complication is dyskinesia, which involves involuntary, uncontrolled movements. Dyskinesia frequently emerges as a side effect of long-term treatment for the disease.
Understanding Dyskinesia
Dyskinesia refers to involuntary movements that can manifest in various ways, ranging from subtle tics to more pronounced, full-body motions. These movements can appear as fidgeting, swaying, head bobbing, writhing, or jerking, affecting any part of the body, including the face, arms, legs, or trunk. While Parkinson’s disease causes slowness, rigidity, and resting tremors, dyskinesia produces excessive, uncontrolled movement.
These movements vary in intensity from mild, barely noticeable motions to severe movements that interfere with daily activities. Unlike the rhythmic oscillations of a Parkinsonian tremor, dyskinetic movements are often fluid, erratic, and dance-like.
Why Dyskinesia Develops in Parkinson’s
Dyskinesia is commonly a complication of long-term levodopa treatment. Levodopa works by temporarily replenishing dopamine levels in the brain, where dopamine-producing neurons have been lost due to the disease. Over time, the brain’s response to this medication can change, leading to fluctuating dopamine levels.
The pulsatile stimulation of dopamine receptors by levodopa, rather than continuous physiological stimulation, contributes to these changes. This can result in an oversensitivity of dopamine receptors, leading to an increased concentration of dopamine when levodopa is administered. This overstimulation of dopamine receptors is a primary factor in the development of dyskinesia. The risk of developing dyskinesia increases with higher doses of levodopa, longer disease duration, and younger age at Parkinson’s diagnosis.
Identifying Dyskinesia
Dyskinesia can present in different forms, often categorized by their timing in relation to levodopa medication doses. The most common type is “peak-dose dyskinesia,” which occurs when levodopa concentration in the bloodstream is at its highest, typically one to two hours after a dose. During this period, Parkinson’s motor symptoms are usually well-controlled, but twisting or writhing movements may appear.
Another type is “biphasic dyskinesia.” This form occurs at the beginning and end of a levodopa dose cycle, as medication levels are rising or falling. These movements tend to be rapid, jerky, and often affect the lower limbs. Finally, “off-period dyskinesia” occurs when medication levels are low and Parkinson’s symptoms are returning. These movements are often fixed, painful, and dystonic, commonly affecting a foot or leg.
Approaches to Managing Dyskinesia
Managing dyskinesia involves strategies aimed at reducing or controlling these involuntary movements while maintaining effective Parkinson’s symptom control. One common approach involves adjusting levodopa medication. This might include lowering the individual dose, administering smaller doses more frequently, or using extended-release formulations to help maintain more stable dopamine levels.
Specific medications can also be added to a treatment regimen to help reduce dyskinesia. Amantadine, for example, is a medication that can help alleviate dyskinesia without necessarily worsening “off” periods. For some individuals, advanced therapies such as Deep Brain Stimulation (DBS) may be considered. DBS involves surgically implanting electrodes in specific brain areas, connected to a device that sends electrical pulses, which can help improve both Parkinson’s symptoms and dyskinesia. In addition to medical interventions, maintaining a healthy lifestyle, including regular exercise, can contribute to overall motor control and may help in managing dyskinesia.