Parkinson’s disease is a neurodegenerative disorder leading to a range of motor and non-motor symptoms. These symptoms progress gradually, impacting movement control. Dyskinesia, a common motor complication, involves involuntary, erratic movements that can emerge in individuals with Parkinson’s.
Understanding Dyskinesia
Dyskinesia refers to involuntary movements that can affect various body parts, including the face, arms, legs, or trunk. These movements manifest as fluid, dance-like motions, rapid jerking, or sustained muscle spasms. The intensity and appearance of dyskinesia vary widely among individuals.
One common manifestation is choreiform dyskinesia, which presents as flowing, dance-like movements that can be either slow and wriggling or quick and jerky. Dystonic dyskinesia involves sustained muscle contractions, leading to twisting or repetitive movements and sometimes unusual body postures. Myoclonic dyskinesia, a less common type, involves brief, shock-like jerks or twitching movements across the body.
It is important to distinguish dyskinesia from the core motor symptoms of Parkinson’s disease, such as tremor, rigidity, and bradykinesia (slowness of movement). While both involve involuntary movements, dyskinesia is a side effect linked to medication, whereas tremor is a symptom of the disease itself. Dyskinesia frequently appears when Parkinson’s symptoms are well-controlled by medication, a period known as “on” with dyskinesia. It can also occur when medication levels fluctuate, as seen in peak-dose dyskinesia (when levodopa concentration is highest) or diphasic dyskinesia (as medication levels are rising or falling).
The Link to Parkinson’s Treatment
Dyskinesia commonly develops in people with Parkinson’s disease due to long-term levodopa therapy. Levodopa is considered the most effective medication for managing Parkinson’s motor symptoms, converting to dopamine in the brain, replacing lost dopamine. This complication, known as levodopa-induced dyskinesia (LID), often emerges after a few years of treatment.
The underlying mechanisms of LID are complex, involving changes in brain chemistry, particularly dopamine. In Parkinson’s, dopamine-producing cells are lost, decreasing dopamine levels. Levodopa temporarily restores dopamine. However, taken intermittently, brain dopamine levels fluctuate, rising and falling. This pulsatile stimulation, rather than continuous delivery, contributes to changes in proteins and genes, promoting dyskinesias.
Disease progression also plays a role. Continued loss of dopamine-producing cells makes it challenging to maintain steady dopamine levels, contributing to dyskinesia. Not everyone on levodopa develops dyskinesia; however, over 50% of long-term levodopa patients eventually experience it. Factors such as younger age at Parkinson’s onset, longer disease duration, and higher levodopa doses can increase the risk of developing LID.
Managing Dyskinesia
Managing dyskinesia involves strategies to reduce involuntary movements while maintaining Parkinson’s symptom control. Medication adjustments are a primary approach. This may include lowering levodopa doses, increasing the frequency of smaller doses, or switching to extended-release formulations like Rytary or Duopa to maintain more stable dopamine levels.
Specific anti-dyskinesia medications are used. Amantadine is an established treatment that can reduce dyskinesias without worsening “off” periods, where Parkinson’s symptoms return. An extended-release formulation, Gocovri, is approved for levodopa-induced dyskinesia in Parkinson’s, often taken once daily at bedtime for sustained levels.
For individuals whose dyskinesia or motor symptoms are not adequately controlled by medication, Deep Brain Stimulation (DBS) may be considered. DBS is a surgical procedure where electrodes are implanted into specific brain areas involved in movement control (e.g., subthalamic nucleus (STN) or globus pallidus interna (GPi)). These electrodes connect to a neurostimulator, similar to a pacemaker, implanted under the skin. This device delivers electrical pulses to modulate abnormal brain activity and reduce dyskinesia. DBS can reduce dyskinesias, often by about 60-80%, and may allow for a reduction in dopaminergic medication.
Lifestyle adjustments and supportive therapies can improve quality of life for individuals with dyskinesia. Regular physical activity, including walking, swimming, gardening, or dancing, can improve muscle strength, flexibility, and balance, and help reduce anxiety and depression. Stress management techniques, such as breathing exercises, massage therapy, or meditation, are beneficial, as stress can worsen Parkinson’s symptoms, including dyskinesia. Dietary considerations like increasing fiber and fluid intake can help manage constipation, a common non-motor symptom.