Does cycling cadence affect interlimb symmetry in pedaling power in individuals with 1

Parkinson’s disease? 2

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Student Name, Harsh H. Buddhadev, Jun G. San Juan, David N. Suprak 4

Department of Health and Human Development, Western Washington University, Bellingham, 5

Washington, United States of America 6

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Conflict of Interest Disclosure: None 8

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Correspondence Address: 10

Harsh H. Buddhadev, PhD 11

Department of Health and Human Development 12

201H Carver Academic Facility, MS 9067, 13

516 High Street, Bellingham, WA 98225 14

Telephone: +1 (360) 650-4115 15

Fax: +1 (360) 650-7447 16

Email: harsh.buddhadev@wwu.edu 17

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Running Title: Parkinson’s disease and asymmetry during cycling 20

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Abstract 24

Cycling at higher pedaling rates leads to symptomatic improvement in patients with Parkinson’s 25

disease (PD). However, these patients show inter-limb asymmetry in pedaling power when 26

cycling at their slow self-selected cadence. The effects of higher pedaling cadence on symmetry 27

of effort between limbs is unknown. We compared the effect of pedaling cadence on symmetry 28

of crank power output in individuals with PD versus healthy controls. Fifteen participants with 29

PD and 15 healthy controls performed 2-minute bouts of stationary cycling at three cadences (50, 30

65, 80 rpm) at 60W and self-selected workload. Power output contribution of each limb towards 31

total crank power output was computed over 60 crank cycles from the effective component of 32

pedal force, which was perpendicular to the crank arm. 33

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Keywords: Ergometer, neurorehabilitation, UPDRS 39

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Word Count: 41

Introduction 42

Parkinson’s disease (PD) is a common progressive neuromuscular condition affecting 43

more than 10 million individuals worldwide 1-3 and costs the healthcare system in the United 44

States 14 billion dollars annually 4. In patients with PD, degeneration of the dopaminergic 45

neurons within the substantia nigra leads to substantial reduction in dopamine production 5-6 46

resulting in symptoms such as resting tremors, bradykinesia or akinesia, rigidity, and postural 47

imbalance 7-11. These symptoms adversely affect the ability of these patients to perform activities 48

of daily living such as maintaining balance and walking. In addition, these clinical features in 49

patients with PD are generally more pronounced on side compared to the other, thereby leading 50

to asymmetry in performing motor tasks such was walking and cycling 12-13. 51

Cycling at is a commonly prescribed mode of neurorehabilitation for patients with PD 9, 52

13-14. Generally, patients with PD are prescribed stationary cycling at high cadences (i.e. 80-90 53

rpm) three times per week with sessions ranging from 30-60 minutes 9, 15-16. Post-cycling 54

sessions, patients experience immediate and long terms improvements such as decrease in resting 55

tremor, bradykinesia, and rigidity 9, 17-18, and enhancement in executive function 19. Cycling 56

cadence is a very critical variable for effectiveness of pedaling as an intervention for patients 57

with PD. Several studies have shown that symptomatic improvement is only observed at higher 58

and not lower preferred cadences of patients with PD 9, 14, 17, 20. Researcher have speculated that 59

cycling at higher cadences alleviates symptoms of PD by promoting changes in neural drive by 60

increasing both motor output and sensory input 14, 16. 61

Penko et al.13 found that individuals with PD are asymmetrical when pedaling at their 62

self-selected cadences. Specifically, these individuals exerted lesser power with their more 63

affected leg and compensate by exerting greater power with their less affected side. Generally, 64

self-selected cadence of patients with PD were low (59 ± 13 rpm) 9, 14, 16-17, 21, whereas 65

symptomatic improvements were observed at higher pedaling cadences (80-90 rpm) 9, 14, 16-17, 21. 66

Previous research in healthy subjects has shown that pedaling at higher cadences reduces 67

asymmetry in power output. However, no previous research has investigated whether asymmetry 68

of power output between lower limbs in cycling changes when pedaling at higher compared to 69

lower cadences in patients with PD. Similar to healthy subjects, pedaling at higher cadences 70

could also reduce interlimb asymmetry in power output for patients with PD. However, this 71

hypothesis has not yet been tested. Interlimb asymmetry in effort would place asymmetrical 72

stresses on the lower extremity joints on each side 22, 23. By reducing interlimb asymmetry in 73

cycling, effectiveness of pedaling could potentially be improved for rehabilitation of patients 74

with PD. 75

The purpose of this study is to examine the effects of pedaling cadence on interlimb 76

asymmetry in crank power output in patients with PD compared to healthy control. We 77

hypothesize that: 1) interlimb asymmetry in power output will be greater for patients with PD 78

compared to healthy controls, and; 2) interlimb asymmetry in power output will decrease at 79

higher cadences. 80

Methods 81

Study design: In this cross-sectional, case-controlled study differences in interlimb 82

asymmetry in crank power outputs at different cadences were assessed during low-intensity 83

stationary cycling between patients with PD and age-and-sex matched control subjects. All 84

experimental data were collected in single data collection session. 85

Participants: Sixteen individuals with idiopathic PD and twenty age-and-sex matched 86

healthy controls were recruited from the surrounding community. Sample size was calculated 87

using GPower 3.1 software based on index of asymmetry data reported by Penko et al.13. A total 88

sample size of 16 participants (8 per group) was needed to achieve a statistical power of 0.8 to 89

detect a large effect size (Cohen’s f=0.53) 24 for group main at an alpha level of 0.05. 90

A local neurologist screened the individuals with PD. Only individuals with Hoehn and 91

Yahr stage II-III when “off” anti-parkinsonian medication were eligible to participate 13. These 92

individuals were also assessed by the neurologist on the day of their testing using the Movement 93

Disorders Society’s revision of Unified Parkinson’s Disease Rating Scale (UPDRS) while “off” 94

anti-parkinsonian medication for at least twelve hours prior to examination 13. UPDRS is a 95

reliable and valid test to assess the severity of Parkinson’s disease 25-26. This scale was used to 96

determine which lower extremity was more affected based on UPDRS motor examination of 97

tremor, rigidity, and leg agility score on each side. These tests were scored on a scale from 0-4. 98

A score of 0 indicates a normal, unaffected individual, where a score of 4 indicates a high 99

severity of PD 15. These data were used to identify the limb that was more affected by PD. 100

All of the participants completed a health history and physical health questionnaire to 101

screen for exclusion criteria and obtain information about their current physical activity status 102

and cycling experience. Exclusion criteria included any muscular, orthopedic, neurologic, and/or 103

cardiovascular disorders that limited an individual’s ability to pedal on an ergometer at low to 104

moderate intensities. The Western Washington University Institutional Review Board approved 105

the study, and all participants gave written informed consent before participating. 106

Data Collection: In a single test session, participants completed 8 three-minutes pedaling 107

trials at cadence of 50, 65, 80 rpm at an experimentally controlled power output (i.e. 60 W) 13 108

and self-selected power output 9, 14, 16 in a random order. These chosen cadences fell within the 109

range of self-selected cadences (i.e. 50-70 rpm) 9, 14, 16 and therapeutically prescribed cadences 110

(i.e. 75-90 rpm) 9, 14, 16, 21 of individuals with PD. 111

All pedaling trials were conducted on an electronically braked Velotron Dynafit 112

ergometer cycle ergometer (Racer-Mate Inc., Seattle, WA) which is shown to be accurate and 113

reliable for measuring power output during cycling 27, 28. Power output of each leg was 114

determined using an instructed force pedal system (Sensix, Poitiers, France) which 115

synchronously measures pedal forces in all planes of motion via strain gauges and pedal and 116

crank orientation via optical encoders. Prior to arrival of participants, the calibration of the 117

Velotron ergometer was verified by performing the Accuwatt calibration check test (Racer-Mate 118

Inc., Seattle, WA) and instrumented force pedals were initialized to ensure they were calibrated 119

accurately with respect to manufacturer settings. 120

Subjects were then asked to change into spandex clothing and shoes provided by the 121

researchers. The subject’s weight and height were measured in pounds and inches, respectively, 122

using a standard balance beam scale with stadiometer. Subjects then completed a five-minute 123

warm-up at 20 W resistance and a self-selected cadence on the Velotron cycle ergometer 13, 15. 124

Three to five minutes of rest followed the warm-up where participants sat on the cycle 125

ergometer. Following this warm-up, participants completed three-minute trials under each of the 126

three randomly ordered workload-cadence conditions (60 W 50 rpm, 60 W 65 rpm, 60 W 80 127

rpm). Following the fixed power output pedaling conditions, participants repeated the three 3-128

minute trials of the same cadences in random order at self-selected power output. A rest interval 129

of three to five minutes separated each condition. 130

During these six cycling conditions, data were synchronously captured for bilateral pedal 131

forces and orientation, and crank position using instrumented force pedals at a sampling 132

frequency of 240 Hz during the last two minutes of each three-minute experimental condition. 133

Verbal encouragement was provided along with a visual screen that participations could look at 134

to maintain their assigned cadence. Participants finished with a five-minute cool-down at 20 W 135

resistance and a self-selected cadence 13, 15. 136

Data analysis: The crank position, pedal orientation, and pedal force data were low pass 137

filtered at 4 Hz using a fourth order recursive Butterworth filter. The pedal forces were 138

transposed to the crank coordinate system using pedal force and orientation, and crank position 139

data using the Sensix I-Crankset software (Poitiers, France). The anterior-posterior and normal 140

components of pedal forces were then used to compute resultant sagittal pedal forces. Effective 141

component of force is the only component of force that creates the angular impulse to rotate the 142

crank. The effective force was computed as the component of the resultant force perpendicular to 143

the crank arm using trigonometric methods described in previous studies 29, 30. Effective crank 144

torque on each side for a complete crank cycle was computed as a product of the component of 145

the effective pedal force and length of crank arm (0.1725 m). The crank power on each side was 146

computed as a product of effective crank torque and crank angular velocity. The data for crank 147

power on each side were then averaged over 60 crank cycles. 148

Based on the average crank power output measured for each limb, the Symmetry Index 149

(SI) was calculated for each 360-degree crank cycle. The equation to compute symmetry index is 150

based on previous research 13, 31 and it is as follows: 151

𝑆𝑦𝑚𝑚𝑒𝑡𝑟𝑦 𝐼𝑛𝑑𝑒𝑥 (𝑆𝐼) = (𝑈𝑛𝑎𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝑙𝑖𝑚𝑏 − 𝐴𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝑙𝑖𝑚𝑏

(𝑈𝑛𝑎𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝑙𝑖𝑚𝑏 + 𝐴𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝑙𝑖𝑚𝑏)/2) 152

Values from this equation can be used to quantify the magnitude of contribution from each limb. 153

A positive value indicates a greater contribution from the unaffected limb, while a negative value 154

indicates a greater contribution from the affected limb 13. This equation can be modified to 155

evaluate the contribution of left versus right lower extremity contribution, or dominant versus 156

non-dominant leg power. For the control group, leg dominance was determined by asking which 157

leg they preferred to kick a ball 32, 33. 158

𝑆𝑦𝑚𝑚𝑒𝑡𝑟𝑦 𝐼𝑛𝑑𝑒𝑥 (𝑆𝐼) = (𝐷𝑜𝑚𝑖𝑛𝑎𝑛𝑡 − 𝑁𝑜𝑛𝑑𝑜𝑚𝑖𝑛𝑎𝑛𝑡 𝑙𝑖𝑚𝑏

(𝐷𝑜𝑚𝑖𝑛𝑎𝑛𝑡 𝑙𝑖𝑚𝑏 + 𝑁𝑜𝑛𝑑𝑜𝑚𝑖𝑛𝑎𝑛𝑡 𝑙𝑖𝑚𝑏)/2) 159

Statistical analysis: Two-factor mixed model analysis of variance (ANOVAs) (limb 160

condition (4) x cadence (4)) with repeated measures on cadence were used to test the effects of 161

limb condition on index of asymmetry and total, average, and relative crank power output. For 162

between group contrasts, limb condition for the Parkinson’s disease group (i.e. more affected and 163

less affected leg) was not equivalent to the limb condition for healthy controls (dominant and 164

non-dominant leg). Therefore, limb condition variable with four levels (PD-more affected, PD-165

less affected, control dominant, and control non-dominant) was used for the between group 166

contrast. The statistical design used in the current study is identical to the one used by Hunt et 167

al.10, contrasting interlimb asymmetry in ACL-deficient individuals and healthy controls. Alpha 168

was set at .05. Significant main effects and interactions were further analyzed using univariate 169

ANOVAs and t-test, respectively. Effect sizes (Cohen’s f) are reported for primary dependent 170

variables. Small, medium, and large effect sizes correspond to Cohen’s f-values of 0.1, 0.25, and 171

0.40, respectively 24. All statistical procedures were performed using SPSS (Version 21). 172

173

Review of literature

Cycling at higher pedaling rates leads to symptomatic improvement in patients with

Parkinson’s disease (PD). However, these patients show inter-limb asymmetry in pedaling power

when cycling at their slow self-selected cadence. The effects of higher pedaling cadence on

symmetry of effort between limbs is unknown. This chapter will introduce the reader to relevant

information about PD, neurorehabilitation via cycling, assessment of symmetry in cycling, and

cycling cadence (a mechanical variable that affects both symptoms and symmetry in cycling).

This pertinent review of literature provides evidence to support the testing protocol and

procedures used in the current study.

Overview of Parkinson’s disease

Etiology

Parkinson’s disease (PD) is the second most common, progressive neuromuscular

condition, after Alzheimer’s disease, affecting more than 10 million individuals worldwide 1-3, 34.

Both the prevalence and the incidence of the disease increases with age. For individuals age 60

years or higher, the incidence of PD is 1-2% 34-35. Though the prevalence rates compared

between sexes has shown to be insignificant, more males have been reported to have the disease

34, with incidence showing significance in the age range of 60-69 and 70-79 36. The exact cause

for the disease is unknown, but studies have shown that both genetic and environmental factors

play a role in the development of PD 34-35, 37-38.

Neurophysiology

Parkinson’s disease is characterized by changes in the brain, more specifically the basal

ganglia. The basal ganglia are a group of subcortical nuclei that are highly connected with many

areas of the brain including the cortex, thalamus, and brain stem. These nuclei are associated

with many functions of life including voluntary movement, cognition, and emotion. Synaptic

pathways between the basal ganglia and the cortical systems are affected by dopaminergic status,

and dysfunction in these connections may lead to Parkinson’s disease symptomology 5, 38.

Within the basal ganglia is a structure known as the substantia nigra, which plays a role

in movement and reward. Degeneration of the dopaminergic neurons within the substantia nigra

pars compacta leads to as much as a 90% reduction in dopamine in the striatum, depriving the

basal ganglia of the dopamine that it requires to initiate and facilitate movement and postural

control required of daily living. Thus, leading to many of the motor and non-motor signs and

symptoms observed in PD 3, 6, 34, 37. de Lau et al. 1 speculated that dysfunction at the muscular

level, such as mitochondrial dysfunction, oxidative stress, and protein mishandlings, may play a

role in the pathogenesis of PD.

Symptomology

PD is characterized by motor and non-motor symptoms. As the disease progresses, it

becomes an increasing social and economic burden on those affected. Four cardinal motor

symptoms associated with PD are resting tremors, bradykinesia or akinesia, rigidity, and postural

imbalances. Resting tremors are an involuntary oscillatory movement produced when a limb is

fully supported against gravity and the muscles involved are not active 7. Bradykinesia or

akinesia are defined as a slowness or absence in movement initiation and execution. There is also

an observed reduction in its amplitude of movement up until complete cessation of the

movement 8. Diminished levels of dopamine and associated reduced motor control output in

patients with PD, is suggested to influence bradykinetic movements and impaired sensory

integration 9. Rigidity refers to an increase in resistance when passively stretching a muscle 10.

As PD progresses, patients begin to exhibit abnormal body posture, including an increase in

flexion of the head and cervical spine, an increase in thoracic kyphosis, and other postural

imbalances that greatly affect daily life 1, 11. Even though these symptoms are very common in

patients with PD, some of these symptoms are not always observed. The current criteria for the

diagnosis of PD includes the presence of at least two of these motor symptoms 1. The non-motor

symptoms include sensory deficits, insomnia, and emotional problems such as depression, lack

of facial expression, a slowing of gastrointestinal function, and reduction in the sense of smelling

39-40.

Diagnosis and Classification

Unified Parkinson’s Disease Rating Scale

Though there lacks a reliable and valid tool for these assessments, the Unified

Parkinson’s Disease Rating Scale (UPDRS) has been widely used to assess many factors of PD

including activities of daily living (ADLs), motor symptoms, mentation, and treatment

complications in these patients 25-26. Ramaker et al. 25 reports high internal consistency, inter-

rater reliability, and a moderate construct validity. The UPDRS has specific use in PD, covers

many arrays of the widespread scope of PD in differing severities, as well as clinimetric

properties, especially in ADLs, and motor examination. In 2009, the release of the Movement

Disorder Society-UPDRS (MDS-UPDRS) improved the older version of the test to cover

multiple groups at differing levels of severity 41. The MDS-UPDRS consists of four parts: I: non-

motor experiences of daily living; II: Motor experiences of daily living; III: Motor examination;

IV: Motor complications. Patient and caregiver or administrator complete questions in each

section on a rating scale of zero to four, with zero being normal, one being slight, two being

mild, three being moderate, and four being severe 42. The MDS-UPDRS rates sixty-five items,

taking the patient and caregiver approximately thirty minutes to complete 42.

Hoehn and Yahr scale

The Hoehn and Yahr scale has been widely accepted and utilized in the research of PD 18,

43-44. In a research setting, the Hoehn and Yahr scale is primarily used to define

inclusion/exclusion criteria 43. The scale consists of five stages, with each stage increasing in the

severity of the disease.

The modified Hoehn and Yahr scale is as follows: 41

Stage 0: No signs of disease

Stage 1.0: Symptoms are very mild; unilateral involvement only

Stage 1.5: Unilateral and axial involvement

Stage 2: Bilateral involvement without impairment of balance

Stage 2.5: Mild bilateral disease with recovery on pull test

Stage 3: Mild to moderate bilateral disease; some postural instability; physically independent

Stage 4: Severe disability; still able to walk or stand unassisted

Stage 5: Wheelchair bound or bedridden unless aided

Pharmacological management with Levodopa

Since PD remains a progressive and thus far, a non-curable disease, rehabilitation has

focused on decreasing the rate of progression as well as aiding in alleviating the side-effects that

are common from the debilitation disease. For nearly the past half century, the use of the drug

Levadopa (L-dopa) has been used to help alleviate the symptoms of PD. Further research found

that administration of L-dopa in lab animals led to an excretion of dopamine in the urine,

suggesting that dopamine levels were elevated 9, 45-46. As the disease progresses though,

complications arise from Levodopa including either inadequate dopaminergic tone, where the

drug wears-off or there are dose failures, or excessive dopaminergic tone that can cause

levodopa-induced dyskinesia 46. Though alternative medication can be used once L-dopa begins

to have negative side-effects, alternative medications are used when tolerance increases 46.

Neurorehabilitation for PD

PD is identified as a dysfunction in sensorimotor integration, leading to common

symptoms such as bradykinesia and other atypical movement. Alternative rehabilitation methods

have been researched and how they can positively elicit changes in the symptoms seen in PD 2-3,

8-9, 14. Neurorehabilitation programs are an increasingly favorable method for the rehabilitation of

PD 47. Huang et al. 47 also stated since the mechanism for the symptoms of PD, including

weakness and fatigue, are unknown and often subjective, challenges arise when constructing

neurorehabilitation programs. Though exercise has shown to combat other side-effects such as

sleep deprivation and depression, finding a regimen that can improve kinesthetic deficits as well

can be difficult 17. Many studies have shown an increased attention to interventions that promote

changes in neural drive 9, 13. These studies have shown that an increase in not just motor output,

but sensory input may play a role in these motor improvements, and since drugs like levodopa do

not improve these kinesthetic deficits, neurorehabilitation interventions like these are greatly

needed 14. High intensity exercise has been highly suggested as a method to increase neural drive

and promote neural plasticity as well as neuroprotection against dopaminergic cell loss 14.

Though the exact method is still undetermined, non-invasive trans-magnetic stimulation has been

used to show a decrease in the dysfunction of corticomotor excitability in people with PD 48.

These changes in corticomotor excitability could be at the base of symptomatic improvements.

Neurorehabilitation through cycling

An increasing interest in cycling specifically has occurred in researches studying the

effects of neurorehabilitation interventions for PD 16. Penko et al.13 stated that pedaling is a

bidpedal motor task, similar to walking, that requires the same principles of lower extremity

coordination, so quantifying pedaling kinetics can give a more precise measurement of lower

extremity function. The exact protocol for cycling has been studied largely by researchers hoping

to find a protocol that improves kinesthetic deficits the most 9, 13-14, 16. Alberts et al.16 stated that

in order for the patients to gain a benefit from exercise, the rate of the exercise must be increased

to trigger a release of neurotrophic factors and possibly dopamine.

Mode of cycling

A wide array of protocols has been looked at regarding cycling, and can be classified into

three distinct categories; Active, active-assisted, and passive. Active, also known as voluntary

cycling, is performed by the patient alone, usually at a self-selected pace 49. Though individuals

do see some improvements in symptomology from an active protocol, the other modes of

exercise have been shown to elicit greater improvements 9, 13-14, 16, 49. Active-assisted cycling

involves the individual biking with the assistance of an able-bodied assistant on a tandem

bicycle. The exact mechanism for a greater response in this mode is unknown, but it is

hypothesized that patients in this mode cycle at a cadence higher than their preferred speed, and

this intervention promotes an increase in afferent input to the central nervous system 50. Ridgel et

al. 14 found that patients in an active-assisted group showed a 13% greater increase in UPDRS

scores than compared to a voluntary group. In a practical sense, active-assisted cycling may not

be the best mode in terms of resources as well as at-home protocols. Not every individual will be

able to have an able-bodied assistant help them during at-home sessions. Passive cycling, or

forced exercise (FE), has been researched to work around these limitations. During FE, the

individual is assisted through a motorized bike that is set at a specific cadence. Patients are told

to cycle with the cadence of the motorized bike, so it is not passive in the sense that the patient

isn’t cycling, but they do not need to exert the force need to increase the cadence past their

comfortable range 14, 16. It has been proposed that FE promotes angiogenesis and synaptogenesis

which begin to degenerate in Parkinson’s disease. Acute aerobic exercise, in this case through a

forced-cycling regimen, has been shown to release neurotrophins such as brain-derived

neurotrophic fact (BDNF) and glial-derived neurotrophic factor (GDNF) as well as dopamine,

which aids in supporting neuroplasticity as well as protect against cell loss in the basal ganglia.

The key to this difference between FE and VE is the increase in intrinsic feedback, given by the

higher pedaling rate 16.

Mechanical variables critical for cycling performance assessment

Cadence

The specific modality of the cycling training program has been extensively studied as to

which modality is the most beneficial, and there has been an increasing interest in speed-based

training. Uygur et al. 18 examined the effects of an acute cadence-derived protocol primarily on

the symptoms of bradykinesia in Parkinson’s disease patients. Three groups were looked at; no

exercise, voluntary cycling, and high cadence-low resistance (HC:LR) cycling. For the HC:LR

group, the cycled at a self-selected pace, similar to the voluntary group, but during the first 15-

seconds of minutes 5-24, they pedaled at a self-selected fast cadence. They found that subjects in

the HC:LR group had significant improvement during a 4-square step test and 10-minute walk

test, primarily in walking velocity. It is suggested that this exercise facilitates locomotor central

pattern generators, which are generally impaired in the Parkinson’s disease population.

Power output

Power output as well as lower extremity function can be quantified using pedaling

kinetics. Power output can be a direct measurement of lower extremity asymmetries by

examining crank torque produced on the pedals 13. Penko et al.13 studied the effects that power

output has on common asymmetries seen in PD subjects. They tested their subjects by having

them cycle on a cycle ergometer beginning at 20W for three minutes at a self-selected pace.

They then increased the power by 20W every two minutes until the fourth stage (eighth minute),

when 40W increases were made until exhaustion. A symmetry Index was calculated to determine

whether the affected limb was contributing more or less as power increased. They witnessed a

decrease in the symmetry index as workload increased, indicating that symmetry was increasing.

The results of their study helped support a claim for a therapeutic intervention that provides

higher quality and quantity afferent information through the use of augmented pedaling motion,

as seen in forced exercise.

Measurement of cycling and its importance in rehabilitation

Asymmetry

As PD progresses, individuals experience a decrease in gait function, postural stability,

and coordination of voluntary movements. Every human exhibits some degree of asymmetry that

mostly goes unnoticed throughout the gait cycle 51, but individuals with PD exhibit a greater

degree of asymmetry that affects their activities of daily living. Asymmetry can be directly

quantified by measuring the crank torque of a modified cycle 13. Identifying asymmetry in

Parkinson’s disease patients would therefore provide a baseline to be later used to measure the

effectiveness of an intervention 13. Primary goals of exercise regimens for PD individuals should

be in reducing asymmetry, thus improving normal daily activity.

Index of asymmetry

Researchers have used the Symmetry Index as a method of evaluating the lower

extremity kinematics and degree of asymmetry in cyclers. Penko et al. 13 calculated the

symmetry index using the equation below:

𝑺𝒚𝒎𝒎𝒆𝒕𝒓𝒚 𝑰𝒏𝒅𝒆𝒙 (𝑺𝑰) = Unaffected limb − Affected limb

(Unaffected limb + affected limb)/2

Using this equation, the researchers could evaluate the degree of contribution from each limb,

with a positive value indicating a greater contribution by the unaffected limb, and a negative

number indicating a greater contribution from the affected limb 13. These variables could be

modified to evaluate left versus right leg contribution. Penko and colleagues 13 found that as the

power increased during a maximal cycle ergometry test, the symmetry index decreased,

indicating an increase in symmetry.

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