Parkinson’s Symptoms–Not Only A Movement Disorder
Parkinson’s is known for the shuffling gait, the masked face, the stooped posture, the soft, almost inaudible voice, the slowness of movement, the trembling and rigidity. These motor or movement symptoms manifest when a portion of the brain called the basal ganglia has significantly decreased levels of dopamine, a neurotransmitter that is necessary for both initiating and controlling movements. By the time of diagnosis, it is estimated that the pigmented, dopamine-producing cells in the substantia nigra of the midbrain are operating at 50-60% of their capacity.
Non-motor symptoms such as loss of the sense of smell, constipation, depression, anxiety, fatigue, restlessness, irritability, and sleep difficulties may appear 20 years or more ahead of the motor symptoms. They do not improve with dopamine-enhancing medications. They contribute to a diminished quality of life as Parkinson’s progresses. Researchers are examining whether non-motor symptoms could lead to earlier diagnostic criteria, and strategies to prevent the decline of dopamine production.
60-75% of people with Parkinson’s may exhibit a characteristic personality pattern, going back as far as many can remember into childhood, although those memories are subject to recall bias. The most common traits identified by clinicians, family members, and PD patients are: suppression of pain or stoicism or denial in the face of pain; cynicism or anticipation of negative outcomes; avoidance of illicit pleasure-seeking or risky behaviors; diminished novelty-seeking; and difficulty with self-love or self-compassion–even though the person may be altruistic or compassionate towards others. Are these Parkinson’s symptoms, or consequences of dopamine depletion?
Dopamine circuits motivate people, animals, even insects to move towards perceived benefits or rewards and away from threats. Could traits of avoiding pleasure, not seeking rewards, contribute to the shutdown of the dopamine circuits, on the principle of use it or lose it? Most researchers assume that this personality pattern is a consequence of dopamine depletion. A few research studies suggests it may precede dopamine loss, including one that identified a genetic dopamine receptor deficit in people with cautious, cynical and stoic personalities. However, people may have these personality patterns who don’t have Parkinson’s. And people with other Parkinson’s symptoms may be cheerful and optimistic. Could it then be classified as an increased risk factor?
There is no single known cause, but there are several factors associated with a higher risk of developing Parkinson’s: a familial pattern, multiple head injuries, early childhood or in utero infection, and toxic exposures of pesticides, herbicides, or industrial chemicals. Some sources suggest that specific kinds of childhood trauma may also be a factor.
What can prevent decline?
Decades of the most promising laboratory research has failed to find any medication or treatment that can slow the progression of Parkinson’s or that shows a neuroprotective benefit. Movement or intensive exercise that demands focus and concentration, such as tango, Irish dance, boxing, dancing to upbeat music, forced exercise cycling, and Tai Chi seem to show the most hopeful neuroprotective benefit. The consistency of symptom stabilization or improvement has elevated these activities to “highly recommended” status for newly diagnosed.
The dopamine circuits have an emotional component, as they interact with the limbic system. Parts of the brain previously thought to be incapable of healing have shown amazing neuroplastic changes. With continuous, deficit targeted, intensive therapy, people are walking after spinal cord injuries, regaining use of a limb after strokes, controlling seizures in epilepsy, and recovering from obsessive compulsive disorder. The emotional or mind-body or personality component in Parkinson’s may be a significant limiting factor. However emotional and personality traits can also be changed.
People with Parkinson’s, when they know they are engaged in a placebo-controlled trial actually show less benefit from the medication, dubbed the Lessebo effect, for the anticipation of negative benefit. It seems plausible that changing the personality pattern to stimulate positive motivation, self-love, and anticipation of benefit might also positively impact the dopamine circuits.
Mindfulness, Neuroplasticity, Massage & Research?
Intentional personality changes, changes of belief in what is possible, changes to anticipate positive benefits have been documented in neuroplasticity research for other conditions and in mindfulness meditation MRI imaging. Massage and body-based therapies can contribute to relaxation, relief of depression, anxiety, stiffness and rigidity, and improve kinesthetic body awareness. They can stimulate dopamine, oxytocin, and serotonin, two other neurotransmitters deficient in PD. Mindfulness-Based Stress Reduction has been taught to over 20,000 patients through the University of Massachusetts Medical Center, and people improved in measures of mood, anxiety, stress, pain, self-efficacy, and self-confidence. Could mindfulness training, intentional personality changes, feedforward principles, movement programs and body-based therapies activate the motivation/reward/movement system and regulate dopamine circuits while they relieve non-motor symptoms?
Neurofeedback and Motor Imagery Study: Improvement of Parkinson’s Symptoms1
There was one clinical trial of 2 sessions of neurofeedback training with fMRI (functional, real-time MRI feedback) of the brain’s motor cortex when a person was moving their hand, and then seeing if they could activate the same part of the brain by imagining moving the hand. They continued the imagery at home between trainings. Compared to controls of people with Parkinson’s, matched by symptom severity and time since diagnosis, they showed significant improvement in Parkinson’s symptoms–up to 37% improvement on the movement portion of the UPDRS, a well-established PD rating scale. The authors were cautiously optimistic that this treatment might benefit people with Parkinson’s in slowing the progression of the condition and in decreasing the need for medications in people with early-stage PD. The authors have been funded by an NIH grant to follow up with a larger study.
1Subramanian, et al. (2011). Real-time functional magnetic resonance imaging neurofeedback for treatment of Parkinson’s disease. J. Neurosci. 31 16309–16317. http://www.ncbi.nlm.nih.gov/pubmed/22072682