Journal of Biomechanics 121 (2021) 110366

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Journal of Biomechanics
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Levodopa facilitates improvements in gait kinetics at the hip, not the

ankle, in individuals with Parkinson’s disease
Sidney T. Baudendistel a,⇑, Abigail C. Schmitt a,b, Ryan T. Roemmich c, Isobel L. Harrison a, Chris J. Hass a
a
Applied Neuromechanics Laboratory, Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, USA
b
Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR 72704, USA
c
Center for Movement Studies, Kennedy Krieger Institute, Baltimore, MD, USA. Department of Physical Medicine and Rehabilitation, Johns Hopkins University School of
Medicine, Baltimore, MD, USA

a r t i c l e i n f o a b s t r a c t

Article history: Parkinson’s disease symptoms impair gait, limit mobility, and reduce independence. Levodopa improves
Accepted 1 March 2021 muscle activation, strength, and coordination; thus, facilitating increased step length, but few studies
have evaluated the underlying forces associated with medication-induced gait improvements. Here,
we assess the effects of levodopa on gait kinetics in persons with Parkinson’s disease. Over two sessions,
Keywords: 13 participants with Parkinson’s disease walked on a treadmill while both optimally medicated and after
Gait a 12-hour medication withdrawal. Walking was analyzed for spatiotemporal parameters, ranges of
Parkinson’s disease
motion, anterior-posterior ground reaction forces, joint torques, and powers using an instrumented
Kinetics
Levodopa
treadmill and motion capture system. When on medication, participants increased gait speed by signif-
icantly improving step length (p = .009) and time (p = .004). Peak propulsive force (p = .001) and hip flex-
ion torques (p = .003) increased with medication while hip extensor and ankle plantarflexor torques did
not. While differences in joint power were not significantly different, the optimal medication condition
showed medium to large effects, with the largest effect at the hip (dz = 0.84). Our findings suggest the
underlying forces responsible for the increases in gait speed are primarily due to increases at the hip, with
limited change at the ankle. Disproportionate use of muscle force may be a limiting factor for levodopa’s
use as an intervention for walking. Future interventions should consider targeting force production def-
icits during gait in those with Parkinson’s disease.
Ó 2021 Elsevier Ltd. All rights reserved.

1. Introduction
Persons with Parkinson’s disease (PD) often experience gait dys-
function that impairs ambulation and independence. Difficulty
walking can have a considerable impact on daily life; for example,
the average individual with PD walks too slowly to traverse a street
within the programmed crosswalk time (Ellis et al., 2016). Symp-
toms of postural instability, rigidity in the lower extremity, and
impaired muscle activation contribute to limited range of motion
(ROM), reduced muscle power production, and diminished limb
advancement, significantly impairing mobility (Albani et al.,
2014). At the joint level, those with moderate-to-severe PD (Hoehn
& Yahr Stage (H&Y)
II) display a pattern of redistributing muscle
force away from the ankle and toward the hip as a potential com-
pensatory strategy to improve stability (DeVita & Hortobagyi,
⇑ Corresponding author at: 1864 Stadium Road University of Florida Gainesville,
FL 32611, USA.
E-mail address: sbaudendistel@ufl.edu (S.T. Baudendistel).
2000; Kuhman et al., 2018; Winter et al., 1990) compared to those
with mild PD (H&Y < II), even though this strategy may increase
energetic cost (Albani et al., 2014; Donelan et al., 2002). Collec-
tively, these features negatively affect spatiotemporal gait mea-
sures, reducing step length and gait speed (Albani et al., 2014;
Nieuwboer et al., 1998). Indeed, walking is 30% slower in those
with PD compared to age-matched peers and declines markedly
faster with disease progression than normal aging (Ellis et al.,
2016).
Gait speed is recognized as a clinical vital sign and predicts
community independence and mortality (White et al., 2013). How-
ever, speed is a single measure that can be modulated by several
strategies including changes in step length and/or frequency. Since
reduced step length is the primary contributor to slowed gait speed
in PD (Albani et al., 2014; Morris et al., 1994), focusing on the
biomechanical basis for improving step length is of particular
importance. Levodopa - the gold standard treatment for PD -
results in faster walking driven by increased step length, while
temporal parameters, such as stride time and double support time,

https://doi.org/10.1016/j.jbiomech.2021.110366
0021-9290/Ó 2021 Elsevier Ltd. All rights reserved.
S.T. Baudendistel, A.C. Schmitt, R.T. Roemmich et al.
show varied results and may not improve (Blin et al., 1991; Bryant
et al., 2011; Mirelman et al., 2019). Even when optimally medi-
cated, PD walking remains slower than healthy controls (Ellis
et al., 2016). Thus, the addition of physical rehabilitation to phar-
macological interventions are common (Nijkrake et al., 2007). For
example, treadmill walking has been shown to significantly
improve gait, with increased step length and reduced variability
of stride time and swing time (Frenkel-Toledo et al., 2005;
Krystkowiak et al., 2003; Pohl et al., 2003). An improved under-
standing of the biomechanical mechanisms underlying changes
in step length could influence physical rehabilitation techniques,
including treadmill interventions, to better complement pharma-
cological treatment.
Step length, and consequently speed, is improved by increasing
the propulsive ground reaction forces (GRF), due primarily to
increased muscular force generation at the ankle and hip (Judge
et al., 1996). Although it is currently unknown how levodopa alters
the kinetic pattern in those with PD, differences in hip kinetics may
act as a main contributor to the differences in speed between older
adults with and without mobility deficits (Graf et al., 2005). When
older adults with higher and lower physical performance, as deter-
mined by Short Physical Performance Battery (cut-off score: 9),
walk at similar speeds, ‘‘low-performance” older adults walk with
reduced ankle power, and increased hip extensor power in early
stance (Graf et al., 2005). Even when the ‘‘low-performance” group
increased speed, further increasing step length, ankle power
remained unchanged. While levodopa improves muscle activation,
coordination, and overall strength (Cioni et al., 1997; Vaillancourt
et al., 2006), there are no studies to our knowledge on non-
surgically treated (no deep brain surgery/stimulation (DBS))
patients that investigate the impact of medication on kinetics dur-
ing walking. We hypothesized that the effect of levodopa on gait
would be driven by changes at the more proximal joint, and those
with PD would exhibit increased hip joint torques–resulting in
improved gait performance (e.g., increased step length and
selected speed) -compared to following a 12-hour withdrawal.
2. Methods
The current study represents a secondary analysis from an orig-
inal dataset and detailed methodology can be found in (Roemmich
et al., 2014). Thirteen participants with idiopathic PD, whom were
being treated with stable doses of orally-administered levodopa,
were recruited. University Institutional Review Board approved,
written informed consent was obtained. Participants came for test-
ing at the same time of day on two days, so that on day 1, half of
the participants were ‘‘On medication” (ON) and the other half
were ‘‘Off medication” (OFF) with the opposite on day 2. During
ON, participants came in their self-reported, optimally medicated
state and during OFF were at least 12-hours withdrawn from any
anti-parkinsonian medication (time since last dose: 15 ± 2 h). Par-
ticipants disease severity was assessed using the Unified Parkin-
son’s Disease Rate Scale motor section (UPDRS-III) and H&Y via
video-recordings scored by a movement disorders neurologist
blinded to medication condition. The videographer scored rigidity
in-person to complete the exam.
Thirty-five retroreflective markers were placed on participants
according to the Plug-in-Gait full body marker system. A 7-
camera motion capture system (120 Hz; Vicon, Oxford, UK) with
instrumented treadmill (1200 Hz; Bertec Corporation, Columbus,
OH) generated kinematic, including spatiotemporal parameters
(STP), and kinetic data. Participants walked on the treadmill at
their comfortable, preferred speed for 5 min while holding the
handrails (Dingwell and Marin, 2006). Handrails do not signifi-
cantly alter the kinematics in those with PD (Ambrus et al.,
2
Journal of Biomechanics 121 (2021) 110366
2019; Bello et al., 2010), but it is unknown how handrail use alters
kinetics in PD or how levodopa affects use of handrails in PD.
Treadmill speed was chosen independent of medication status or
overground walking speed. Participants were naïve to their self-
selected speed. Overground comfortable pace across a 12-m walk-
way was recorded before the protocol.
The last minute of walking was analyzed and gait events (foot-
strike and foot-off) were identified. The following STP were calcu-
lated: step length, time, width, and single support (percentage of
the gait cycle). Kinematic and kinetic data were computed using
the Plug-in-Gait model and filtered using 4th-order, low-pass But-
terworth filters with cutoff frequencies of 10 and 20 Hertz, respec-
tively (Roemmich et al., 2014). Variables of interest included:
sagittal ROM of the ankle and hip, as well as peak GRF braking
and propulsive force, peak plantarflexion torque and power, and
peak hip extensor and flexor torques and powers. The knee was
not included in this analysis since it does not meaningfully con-
tribute to forward progression (Judge et al., 1996). All kinetic vari-
ables were calculated as the peak value during stance (foot-strike
to foot-off). To ensure consistency of peak power generation of
the hip, hip power generation was limited to early stance (H1),
hip extensor power generation (Eng and Winter, 1995; Winter
et al., 1990). ROM was calculated as the difference between the
maximum and minimum angles between foot-strike to the subse-
quent ipsilateral foot-strike.
Normality was verified (Kolmogorov–Smirnov test) and paired
t-tests were performed between medication status for UPDRS-III,
H&Y, overground speed, and average vertical GRF on the more
affected limb. Considering PD is a movement disorder character-
ized by asymmetric motor symptom onset and progression, this
investigation focused on the more affected limb, designated by
UPDRS-III. Four repeated multivariate analysis of variance tested
differences between medication state on each set of variables: 1)
STPs, 2) ROMs, 3) force components (GRF and torques), and 4)
force–time components (powers). Multivariate significance was
set at p < .05. For univariate follow-up, Dunn-Bonferroni adjust-
ments were used (STP: p = .01, ROM: p = .025, force components:
p = .01, powers: p = .017). Cohen’s dz estimated the within-
subject repeated-measures effects using 0.2, 0.5, and 0.8 as a small,
medium, and large effects, respectively.
3. Results
Thirteen participants were analyzed (height: 1.74 ± 0.07 m,
mass: 74.1 ± 8.4 kg). H&Y stage was not different between collec-
tions (Table 1; t(12,1) = 1.897, p = .082). UPDRS-III scores improved
ON levodopa (t(12,1) = 2.891, p = .014) and preferred overground
walking speed was significantly faster ON (t(12,1) = 3.015,
p = .011).
STP: Multivariate results revealed a significant effect of medica-
tion (Table 2; k = 0.810, F(5,8) = 5.109, p = .021). The ON condition
increased preferred speed (F(1,12) = 16.995, p = .001), increased
step length (F(1,12) = 9.574, p = .009), and reduced step time (F
(1,12) = 12.336, p = .004). Step width and single support percent
were not different between conditions (p
0.783).
ROM: Medication significantly affected ROM at the ankle and
hip (k = 0.401, F(2,11) = 8.203, p = .007). ROM at the ankle (F
(1,12) = 8.13, p = .015) and hip (F(1,12) = 14.07, p = .003) increased
with dopaminergic therapy.
Force based kinetics: Medication significantly changed the
kinetics of individuals walking on the treadmill (k = 0.174, F
(5,8) = 7.581, p = .007). Peak hip flexion torque in stance (F
(1,12) = 14.08, p = .003) and peak propulsive force (F
(1,12) = 21.009, p = .001) significantly increased in magnitude. Peak
hip extension torque (p = .059), peak plantarflexion torque
S.T. Baudendistel, A.C. Schmitt, R.T. Roemmich et al. Journal of Biomechanics 121 (2021) 110366

Table 1
Demographic and disease severity ratings for each participant.

ID M/F Age (years) LEDD (mg/day) Disease duration (months) H&Y UPDRS-III Overground Treadmill
Speed (m/s) Speed (m/s)
OFF ON OFF ON OFF ON OFF ON
1 M 79 800 24 3.0 3.0 47 43 0.94 0.89 0.65 0.80
2 M 69 825* 72 2.5 2.5 39 42 0.94 1.14 0.81 0.81
3 M 76 1250 n/a 3.0 3.0 58 46 1.31 1.35 0.89 1.26
4 M 65 488* 48 2.5 2.5 31 28 0.98 1.03 0.85 0.97
5 M 65 1100 60 2.5 2.5 40 38 0.99 1.29 0.93 1.03
6 M 65 413* 48 2.5 2.0 40 39 1.07 1.22 0.78 0.80
7 F 54 380* 28 2.5 2.5 29 27 1.07 1.12 0.81 1.01
8 M 66 750 60 2.5 2.0 45 39 0.82 1.3 0.81 1.08
9 M 77 500* 36 3.0 3.0 46 41 1.36 1.36 1.04 1.04
10 F 49 1775* 60 2.0 2.0 24 23 1.16 1.17 1.11 1.35
11 M 65 n/a 36 3.0 3.0 44 40 0.96 1.08 0.95 0.95
12 M 70 n/a 108 3.0 2.5 32 34 1.00 1.02 0.74 0.82
13 M 72 642* 120 2.5 2.5 41 37 1.02 1.35 0.68 0.96
Mean 67.1 975 58.3 2.65 2.5 39.7 36.7 1.05 1.18 0.85 0.99
SD 8.5 239.8 29.8 0.32 0.38 9.0 6.8 0.16 0.15 0.13 0.17

ID – Participant Identification, LEDD – Levodopa Equivalent Daily Dose, H&Y – Hoehn & Yahr stage, UPDRS-III - Unified Parkinson’s Disease Rating Scale Motor Score (III),
Overground Speed – preferred pace of walking overground, n/a – not available, *dopamine agonist in addition to levodopa

Table 2
Gait Parameters for ON and OFF at preferred Treadmill speed. Mean (Standard Deviation).

OFF ON p-value Cohen’s dz

Spatiotemporal*
Selected Treadmill Speed (m/s) y 0.85 (0.13) 0.99 (0.17) .001 1.15
Step Length (m) y 0.51 (0.08) 0.55 (0.08) .009 0.85
Step Time (s) y 0.66 (0.07) 0.61 (0.05) .007 1.07
Step Width (m) 0.22 (0.03) 0.22 (0.03) .872 0
Single Support (% cycle) 37.7 (2.0) 37.5 (1.9) .783 0.08
Gait Cycle Range of Motion*
Ankle (Degrees) y 24.0 (5.5) 27.9 (8.8) .015 0.80
Hip (Degrees) y 41.3 (3.8) 44.3 (5.5) .003 1.02
Peak Force Based Kinetics*
Propulsive Force (%BW) y 0.13 (0.02) 0.15 (0.03) .001 1.31
Braking Force (%BW) 0.07 (0.03) 0.09 (0.06) .041 0.57
Ankle Plantarflexor Moment (Nm/kg) 1.29 (0.14) 1.26 (0.18) .549 0.22
Hip Flexor Moment (Nm/kg) y 0.45 (0.24) 0.74 (0.36) .003 1.03
Hip Extensor Moment (Nm/kg) 0.85 (0.19) 1.14 (0.46) .059 0.60
Peak Force-time Based Kinetics
Ankle Power Generation (Watts/kg) 1.48 (0.45) 1.87 (0.59) .017 0.79
Hip Power Generation (Watts/kg) 0.71 (0.12) 1.31 (1.01) .053 0.59
Hip Power Absorption (Watts/kg) 0.40 (0.22) 0.73 (0.43) .009 0.84

*Significant at Multivariate Level, ySignificant at Univariate Level with Dunn-Bonferroni Correction Note: Hip Power Generation is limited to early stance.

(p = .549), and peak braking force (p = .041) were not significantly
different after corrections.
Force-time based kinetics: Although the multivariate level was
found to be not significant for medication changes in power
(k = 0.551, F(3,10) = 2.719, p = .101), univariate p-values can be
found in Table 2.
4. Discussion
Unsurprisingly, optimal medication status increased preferred
speed on the treadmill with corresponding changes to reduced step
time and increased step length. The underlying kinetic changes
included increased propulsive force and increased hip flexion tor-
que in stance with no significant change in hip extensor or plan-
tarflexor torque. Yet, the medium effect size between the ON and
OFF conditions for hip extensor torque further suggests that the
hip extensors in early stance potentially contributes more effec-
tively than the ankle toward maintaining position on the treadmill
and progressing forward. No statistically significant differences
were found in the variables of joint power when analyzed together,
but all variables showed medium to large effects eluding to poten-
3
tially meaningful effects. These findings are consistent with the
distal-to-proximal redistribution found in healthy older adults
(DeVita & Hortobagyi, 2000; Graf et al., 2005; Kuhman et al.,
2018). Collectively, these results identify further gait-related mea-
sures that are resistant to anti-parkinsonian medication that could
be specifically targeted with supplementary interventions.
The underscaling of amplitude of movements in PD is thought
to be more affected than the regularity or timing (Albani et al.,
2014), therefore improvements in gait speed are primarily exhib-
ited by increased step length (Albani et al., 2014). Yet similar to
Krystkowiak et al., 2003, optimal medication state improved both
temporal and spatial parameters of walking with significant
increases in joint ROM with large effects. Additionally, the coordi-
nation of phasic action, shown with single support percent, was
nearly identical between medication states and was within the
normative values for healthy control subjects, further supporting
that underlying control for gait may remain intact in PD
(Hollman et al., 2011; Morris et al., 1994). The use of the treadmill
may further aid in controlling coordination as a constant speed is
required, as shown with the lack of differences in single support
and improvement of both step length and time. As all participants
used the handrails, we expected no differences in step width and
S.T. Baudendistel, A.C. Schmitt, R.T. Roemmich et al.
the present observations confirmed this. While the kinematic vari-
ables support the use of levodopa to improve gait performance
through increasing amplitude of steps, multiple variables including
selected speed, step length and time are still below healthy control
norms suggesting additional improvement may be possible
(Hollman et al., 2011).
The biomechanical changes related to the increase in speed
were driven primarily by a large effect of hip flexor torque
increases accompanied by a slightly decreased ankle plantarflexion
torque. Joint power was statistically unchanged, similar to the
results found by DeVita and Hortobagyi, 2000, perhaps due to
the large variability within group. While our conservative statisti-
cal approach limits the interpretation of the univariate effects, the
differences showed medium to large effects, including peak ankle
power, warranting further exploration of joint power. While we
analyzed peak hip extensor power generation, which stabilizes
the trunk and aids propulsion, the hip flexors also provide consid-
erable power absorption to decelerate the limb during extension
and power generation to forward motion during pre-swing (Eng
& Winter, 1995; Winter et al., 1990). Interestingly, optimal medica-
tion state increases activation of distal leg muscles better than
proximal muscles (Cioni et al., 1997), this pattern is not reflected
in the kinetic changes observed, as ankle joint moment slightly
decreased. While Ferrarin et al. tested overground gait associated
with both medication and DBS, their levodopa-specific results
match ours, with increases in hip torque and power with no change
in ankle torque or power when speed increased (Ferrarin et al.,
2005). Of note, all subjects in the mentioned study (Ferrarin
et al., 2005) had DBS and thus, even in the OFF medication and
OFF stimulation condition, participants had surgical lesions that
may improve symptoms of PD (Siegel & Metman, 2000; Walter &
Vitek, 2004). No participants in the current study had DBS. While
anti-parkinsonian medications may improve neuromuscular activ-
ity of the distal musculature (Cioni et al., 1997), optimally-
medicated individuals with PD still display reduced triceps surae
activation and increased proximal muscle activation compared to
healthy older adults (Cioni et al., 1997; Dietz et al., 1995; Islam
et al., 2020). Although we did not analyze joint redistribution or
muscle activation, medication may result in disproportionate reli-
ance on the hip flexors and extensors to improve propulsion and
speed, regardless of the gains provided with dopaminergic therapy
(Cioni et al., 1997). As this proximal redistribution may be an adap-
tive compensation (Kuhman et al., 2018), hip and ankle function
during walking should be further investigated in this population
to better understand the potential positive or negative impacts
associated with this gait pattern. Improved gait continues to be
an outcome of importance for those with PD and future studies
should specifically target impaired force production, in conjunc-
tion with joint kinetic redistribution, to deliver novel therapeutic
interventions that could improve mobility.
Acknowledgements
We would like to thank the patients, clinicians, and volunteers
at the Fixel Institute for Neurological Diseases. This project was
partial funded through an NIH Pre-doctoral Training Grant (NIH
T32-NS082128). This funding source had no direct involvement
or role in this study.
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