What is Parkinson’s Disease?
Parkinson’s Disease (PD) is a neurodegenerative brain disorder (degeneration means cell death) in which clusters of nerve cells, or nuclei, die inside the basal ganglia. The basal ganglia are clusters of neurons (nuclei) situated deep within the forebrain that control body movements. That is, they allow your muscles to move and function in unison.
In people without PD, the nerve cells in the basal ganglia produce an essential brain chemical called dopamine. Dopamine is the primary pleasure-reward-seeking and feel-good chemical. It also fine-tunes voluntary movements through direct and indirect pathways from the basal ganglia and other brain areas.
However, when the neurons in the basal ganglia die or become impaired, they can no longer produce dopamine, which accounts for the movement difficulties of Parkinson’s.
What Are the Signs and Symptoms of Parkinson’s Disease?
The criteria for the diagnosis of Parkinson’s Disease requires the presence of at least two of the following clinical features:
- Resting tremor: trembling/shaking mainly of the hands, but can also involve the legs, jaw, or head
- Bradykinesia: slowness of movement
- Rigidity: severe muscle stiffness, or tightness, of the limbs
- Poor balance and coordination, which can lead to falls
Interestingly, these telltale symptoms of Parkinson’s disease sneak up when 80% of the dopamine-producing neurons are already dead.
Definite warning signs may begin as early as 12–14 years before the actual hallmark symptoms of PD. These include:
- Rapid eye movement (REM) sleep behavioral disorder: This is a sleep disorder experienced during the REM stage of sleep in which a person acts out his dreams with sounds and sudden, often violent arm and leg movements.
- Loss of smell: More than 90% of people with Parkinson’s disease may lose their sense of smell long before the onset of the movement-related symptoms.
- Constipation
- Depression
- Urinary incontinence, or inability to hold urine
What Causes Parkinson’s Disease?
Scientists still do not know what causes nerve cells to die in the brain region producing dopamine.
With that said, they have identified a few potential genetic and environmental influences.
Environmental influences found to be associated with Parkinson’s disease include:
- Smoking
- Pesticide and herbicide exposure
- Lower caffeine intake
- Exposure to certain chemical solvents, primarily trichloroethylene (TCE) and perchloroethylene. TCE is a common groundwater contaminant. PERC is a frequently used chemical in garment dry-cleaning.
What is the Treatment for Parkinson’s Disease?
The treatments designed to treat PD are mostly those that replenish dopamine.
The commonly used treatment for PD is a medication called Levodopa (L-DOPA), which crosses your brain and is converted to dopamine. L-DOPA, however, produces nausea and vomiting. Doctors, therefore, combine it with carbidopa to prevent this adverse effect.
Despite this combination, L-DOPA has many side effects in the long run. Other medications approved for treating Parkinson’s disease also carry side effects as severe as hallucinations and compulsive behaviors like gambling, binge eating, shopping, and hypersexuality.
Hence, various new treatment modalities are being developed and studied for treating the symptoms of Parkinson’s disease more effectively.
Real‐time electroencephalography (EEG)‐based neurofeedback is an emerging intervention as a highly promising therapy. It helps improve movement problems in everyday life by allowing patients to train brain areas involved in controlling body movements.
How Does Neurofeedback Benefit Parkinson’s Disease?
Neurofeedback treatment makes the patient see the brainwave patterns detected through sensors stuck to the scalp. It teaches the patient to speed up or slow down the brainwaves. If the brain does what is required, the patient gets a reward. If not, they don’t get any reward.
This rewarding feeling is associated with a specialized pathway in the brain known as the “mesolimbic pathway.” This pathway is responsible for releasing dopamine — a deficient chemical in people with Parkinson’s disease. The mesolimbic pathway is thus the fancy term for the “dopamine-reward pathway.” It connects an area in the midbrain to the basal ganglia in the forebrain. And as mentioned above, the basal ganglia are those clusters of neurons in your brain that control movement — with their nerves releasing dopamine.
Thus, this EEG-mediated self-regulation may help adjust the brain waves of the basal ganglia where they need adjustment. In addition, the EEG sends a continuous loop of information about the brain’s electrical activity, so people with PD can learn to control parts of their brain and its networks consciously.
Moreover, evidence suggests that neurofeedback boosts the compensatory activity of a pathway in a specific motor area in PD brains. This eventually improves motor speed in patients with Parkinson’s disease.
In addition, patients with Parkinson’s disease display abnormal beta wave activity in a segment of the basal ganglia dubbed the subthalamic nucleus (STN). These patients can voluntarily control beta waves in their deep brains via neurofeedback.
Research indicates an indirect connection between the β-band power in the STN and movement difficulties in Parkinson’s disease. However, if a direct link exists between this beta brain activity and movement problems in PD has yet to be ascertained.
A research group at Osaka University revealed the effect of real-time neurofeedback training on beta wave activity. Furthermore, the group showed that neurofeedback could help control the β-band power in the STN. This eventually induces plastic changes in the STN in individuals with Parkinson’s disease.
While the researchers didn’t notice an improvement in patient symptoms, they concluded that their study set the stage for addressing Parkinson’s disease. What’s more? By possibly mitigating the parkinsonian symptoms, neurofeedback can also help lower the dose of L‐DOPA and minimize its side effects. This is why scientists are now considering neurofeedback as an add-on therapy to L‐DOPA in patients with Parkinson’s disease.
