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Parkinson’s disease (PD) is characterized by cardinal motor symptoms of tremor, slowness of movement, and rigidity ^[1]. Symptoms directly affect quality of life and activities of daily living by impeding coordination of multiple limbs and fine dexterity. This can be extremely debilitating, leading to decreased mobility and independence with increased risk for falling.

Current clinical PD therapies are designed to address disease motor symptoms; however, there are limitations associated with these approaches. Drug therapy (e.g., levadopa) effectiveness may decrease over time and lead to side effects such as dyskinesias (involuntary irregular movements) ^[2]. Patients may eventually consider surgical procedures such as deep brain stimulation when increased drug dose side effects outweigh the benefits. This procedure, however, has limitations and risks, such as improper lead placement, decreased effectiveness over time, and not being appropriate for all patients ^[3].

While treatments such as drug therapy and surgical procedures are clinical standards, new research suggests exercise as a potentially less invasive alternative/adjunct treatment. It has been well established that exercise reduces risks of developing chronic diseases such as cancer, obesity, and heart disease ^[4-6]. Such benefits of exercise can also be translated to motor improvement in PD ^{[7, 8].} The general concept behind the benefit of exercise in PD suggests that physical exercise may stimulate specific biochemical changes to induce production of dopamine, a neurotransmitter involved in allowing the body to perform smooth controlled movements ^[9]. The sedentary lifestyle associated with PD promotes further motor symptom impairment through muscle weakness, postural imbalance, and increased risk of falling ^[10]. Thus, there exists an urgency to develop PD-specific exercise regimens early in disease progression in an attempt to break or delay this debilitating cycle.

While tremor is often the most visible symptom of Parkinson’s disease, bradykinesia can be the most impairing to the patient. The term "bradykinesia" literally means "slowed movements"; however, in the literature, the "bradykinesia" is often used synonymously with the terms "akinesia" and "hypokinesia." Technically, "bradykinesia" only refers to slowness of movement; however, lack of spontaneous movement (akinesia) and smaller than desired movements (hypokinesia) are often grouped together as "bradykinesia." This misuse in terminology can result in widespread variability in clinical ratings.

The standard clinical method for evaluating bradykinesia is qualitative assessment by a clinician and score assignment (0 – 4) based on the Unified Parkinson’s Disease Rating Scale (UPDRS). This score is assigned while the subject completes repetitive tasks of finger-tapping, hand opening-closing, and pronation-supination. Evaluators are instructed to account for a wide array of factors such as speed, amplitude, fatiguing, hesitations, arrests in movement, and how these variables change during the task. This is challenging to even the most experienced movement disorder specialist. A given patient could be scored a 2 on the UPDRS finger-tapping task due to slow and large amplitude movements or fast and small amplitude movements. It is difficult to gauge weights that specific clinicians place on different bradykinesia manifestations.

The inconsistency among raters may have implications beyond symptom severity assessments. Recent data have shown that speed and amplitude respond differentially to dopaminergic medication ^[1]. Furthermore, it is unknown if the underlying neural mechanisms that cause the various bradykinesia manifestations are the same. A quantitative understanding of different bradykinesia features could ultimately lead to the development of more targeted treatments for specific patients with Parkinson’s disease.

One of the most difficult aspects of monitoring Parkinson’s disease (PD) motor symptoms, is that the severity of tremor and bradykinesia (slowed movements) greatly fluctuates throughout the day.

When medication is at its peak effectiveness, the patient is said to be “On.” Similarly, when medication has completely worn off, the subject is said to be “Off.” Symptoms are often worst first thing in morning, but improve after the first dose of medication. However, as the medication wears off, symptoms return mid-day. These cycles of waxing and waning motor symptoms continue throughout the day. Controlling these “On” and “Off” cycles can be difficult, as patients with PD are typically evaluated in the neurologists’ office, which only allows the physician to capture a snapshot of motor symptoms. Furthermore, patients typically are instructed to refrain from taking medication the night prior to the office visit. A state of anxiety in this condition may amplify PD symptoms during motor evaluation. Monitoring motor symptoms at home would provide clinicians with improved tracking of these complex motor fluctuations and in-turn optimize medication dose to improve patient quality of life.

Kinesia is a compact wireless system developed by CleveMed to quantify movement disorder symptoms. In clinical trials, Kinesia objectively quantified tremor and bradykinesia in PD patients in the clinic. Objective symptom ratings output by the Kinesia system were highly correlated to clinician ratings. CleveMed has recently begun a clinical study in which the Kinesia system is being used throughout the day, at home, by patients with PD. Preliminary results demonstrate that Kinesia can capture the “On” and “Off” motor symptom fluctuations in a subject’s home. Monitoring PD symptoms on a more continuous basis at a patient’s home should improve clinical outcomes and decrease costs especially for disparate patient populations in areas not in close proximity to movement disorder specialists.

Parkinson’s disease is a neurodegenerative disease of the central nervous system and is primarily characterized by cardinal motor symptoms such as tremor, bradykinesia (slowness of movement), and rigidity. Lower extremity symptoms such as gait and balance disturbances (initiating movement, freezing of movement, improper movement form), especially in advanced patients, can be very debilitating, leading to decreased mobility and independence, decreased quality of life, and an increased falling/hip fracture risk ^[1]. A positive PD diagnosis occurs when a minimum of two cardinal symptoms present themselves. However, less attention is given to gait and balance abnormality as it typically develops in the advanced stages of PD.

Standard clinical assessment of gait and balance based on a 0 (no severity) – 4 (high severity) scale is performed using a subset of the Unified Parkinson’s Disease Rating Scale (UPDRS) motor section. Tasks typically consist of foot stomping while seated, gait assessment while walking, arising from chair with arms crossed over the chest, and balance assessment while being pulled backwards. As gait is particularly sensitive to ON-OFF therapy state changes in PD and incorporates upper extremity function such as arm swing as well as rigidity and bradykinesia in lower extremities, gait analysis may be a reliable method of assessing overall motor function over time in PD ^[2].

When diagnosed with PD, the first line of treatment typically consists of L-Dopa medication to alleviate motor symptoms. However over time, drug effectiveness decreases, requiring the patient to increase dosage. Frequent and stronger side effects such as dyskinesias (uncontrolled arm movement) and unpredictable “on”/”off” episodes are cause for more invasive therapeutic intervention. Deep brain stimulation (DBS) has been widely recognized as an appropriate treatment option when medication no longer adequately alleviates motor symptom severity. Several therapy targets have been established for PD. Subthalamic nucleus (STN) and Globus Pallidus Interna (GPi) stimulation are recognized treatments for sustained improvement in tremor, rigidity, and bradykinesia ^{[3, 4]}. However the effects on gait disturbance are less understood. During DBS lead placement and post-evaluation, neurologists adjust several settings: electrode contact configuration and stimulation parameters (frequency, pulse width, and amplitude). Studies show that while high-frequency/high voltage stimulation improves cardinal symptoms, patients exhibit increased frequency of freezing episodes. However, stimulation at lower frequencies has demonstrated improved gait ^[5].

New PD gait therapies are being researched and developed and existing interventions further established. Another DBS target, the pedunculopontine nucleus (PPN), located near the brain stem plays an important role in locomotion function in animal models, specifically initiation and modulation of gait ^[6-8]. Patients with advanced stages of PD only exhibit mild improvement of freezing with standard medication such as L-Dopa ^{[9, 10]}. Preliminary studies of PPN surgeries off-medication marked a significant improvement of the UPDRS motor exam section III, specifically gait and postural qualities. In addition, the combination of STN and PPN DBS resulted in a further significant improvement. Despite promising results, PPN surgical intervention is currently in its infancy as little is known about the nucleus’ function in humans and how well animal model testing translates to human clinical trials ^[7].