Research Report

Lower Limb Neuromuscular Function and

Blood Flow Characteristics in AFO-Using
Survivors of Stroke
Kyle A. Sherk, MS, CPO1,2; Vanessa D. Sherk, PhD1; Mark A. Anderson, PT, PhD3;
Debra A. Bemben, PhD1; Michael G. Bemben, PhD1
ABSTRACT
Background and Purpose: Ankle-foot orthoses (AFOs) and gait
aids are commonly used by survivors of stroke to ambulate,
but they have not been used as inclusion or exclusion criteria
for physiological studies. The purpose of this study was to
examine differences in neuromuscular function and blood
flow characteristics between the lower limbs of ambulatory,
AFO-using survivors of stroke (n = 9).
Methods: The subjects were, on average, 14 years poststroke
and had used an AFO for about 7 years. We used the following
measures to assess both lower limbs: quadriceps muscular
strength (manual muscle testing, 1RM), calf muscular endurance (single-leg heel raises), lower limb soft tissue composition and muscle cross-sectional area, calf resting blood flow
(strain gauge plethysmography), and central neural drive of
the plantar flexors (nerve stimulation). The sound limb was
defined as the control.
Results: Quadriceps strength, triceps surae endurance, and
calf cross-sectional area all were greater in the sound limb than

in the affected limb (relative differences: 76.3% 16.6%,

146.4% 24.6%, and 25.6% 5.7%, respectively). In addition, resting blood flow, peak torque, and central neural drive
of the plantar flexors were significantly greater (relative differences: 38.7% 5.9%, 94.4% 17.9%, and 43.6% 12.0%,
respectively) in the sound calf.
Discussion: Our findings confirm that significant decrements
in muscle performance, size, and blood flow persist in the
affected limb many years after stroke despite a resumption
of ambulation.
Conclusions: This cohort of ambulatory AFO users exhibited
large variations in functional abilities. We recommend that
future studies in stroke survivors consider AFO use in their
research designs.
Key Words: ankle-foot orthosis, blood flow, manual muscle
test, stroke, twitch interpolation
(J Geriatr Phys Ther 2015;38:5661.)

INTRODUCTION
1Department

of Health and Exercise Science, University of

Oklahoma, Norman, Oklahoma.
2Hanger Orthotics and Prosthetics, Oklahoma City,
Oklahoma.
3Health Science Center, University of Oklahoma, Oklahoma
City, Oklahoma.
Kyle A. Sherk transferred from the Oklahoma City, OK
office, to the Englewood, CO office of Hanger Orthotics
and Prosthetics in July 2011 after completing his MS degree
at the University of Oklahoma.
Vanessa D. Sherk is now with the University of Colorado
Denver, Division of Geriatric Medicine.
This study was performed at the Department of Health
and Exercise Science in the Neuromuscular Laboratory,
University of Oklahoma.
No data from this study has been publicly presented.
Kyle A Sherk is employed by Hanger Orthotics and
Prosthetics, a nation-wide provider of orthotic and
prosthetic devices.
The authors declare no conflicts of interest.
Address correspondence to: Kyle A. Sherk, MS, CPO, Hanger
Orthotics and Prosthetics, 3535 S Lafayette St, Suite 100,
Englewood, CO 80113 (kylesherk@hotmail.com).
Richard W. Bohannon was the decision editor.
DOI: 10.1519/JPT.0000000000000017
56

Residual foot drop after a stroke is clinically defined as

paresis or paralysis of the tibialis anterior muscle, resulting
in decreased toe clearance through the swing phase on the
affected side.1 Weakness of the peroneal muscles, the evertors of the foot, may also be present. These neuromuscular
deficits are easily overcome by using an ankle-foot orthosis
(AFO). An AFO functions to aid muscular control of the
affected limb to increase dorsiflexion during the swing
phase and to provide mediolateral stability of the foot and
ankle during terminal swing for proper foot positioning
during the stance phase.2 Replacing the function of these
muscles with an external device commonly limits the range
of motion (ROM) of the plantar flexors.3-5 This restricted
ROM, however, may contribute to atrophy of the plantar
flexors independent of decreases in central neural drive.6,7
There are approximately 460 000 new survivors of stroke
each year who will require some level of rehabilitation
services,8 and a conservative estimate is that 50% of these
individuals would need an AFO. Even with this incidence
of AFO use, muscle function has not been well characterized in survivors of stroke who use AFOs.
It is also currently unknown whether AFO use is associated with changes in lower limb blood flow characteristics.1
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Edema is commonly observed in the affected limb in survivors of stroke, and is indicative of poor venous return.9-11
Reductions in venous return may be partly due to neurologic deficits of the plantar flexors that result in a reduced
muscular pump effect during ambulation. Because AFO use
can alter muscular activity of the lower limbs,7,12,13 venous
return may be altered in AFO users compared with other
survivors of stroke.
Interlimb differences in neuromuscular and vascular
function after stroke in AFO users are unknown because
previous studies of stroke survivors have not differentiated between gait aids (canes, walkers) and orthoses.1,14
Therefore, the purpose of this study was to quantify differences in lower limb muscular size and function and vascular
function between the sound and affected limbs in ambulatory survivors of stroke who use an AFO for gait assistance.

METHODS
This study was approved by the University of Oklahoma
Institutional Review Board, and potential volunteers were
contacted through local orthotic providers. Individuals
were considered for participation if they survived a stroke,
were male or postmenopausal female, were aged 55 to
75 years, used an AFO (unilaterally) for ambulation and
activities of daily living for at least 6 months, and were at
least 2 years poststroke. We excluded persons on the basis
of the following criteria: weight greater than 300 lb, nonambulatory status, and AFO use before the stroke. Nine stroke
survivors met the study criteria, gave written informed consent, and obtained medical approval from their physicians
for participation in this study. Participants performed all testing procedures in a minimum 2-hour postabsorptive state.
The right limb was tested first for all outcome measures.

Testing Procedures
Seated manual muscle testing (MMT) of the quadriceps
muscles was performed on both lower limbs before
1-repetition maximum (1RM) testing. A score of 3+ on
the 5-point MMT scale was defined as full ROM against
gravity and minimal resistance applied by the investigators index finger at the anterior aspect of the ankle.
Participants who did not score at least 3+ (fair plus) out
of 5 (normal) did not perform the 1RM test on that limb
and a weight of 0 lb was recorded. Quadriceps strength
was assessed by 1RM: the largest amount of weight that
could be moved through the full range of knee extension,
on a seated knee-extension device (Cybex International,
Medway, Massachusetts). Each participant warmed up by
performing 1 set of 10 repetitions at a self-selected weight.
The load was then gradually increased until the participant
was unable to extend the knee through the full ROM while
verbal encouragement was provided. The last successful
lift was recorded as the 1RM for that limb, and then the
contralateral limb was assessed.

Muscular endurance testing of the plantar flexors of

each leg was performed by balance-supported, singleleg heel raises.15 Participants were first tested in seated
MMT,16 then were familiarized with this test to ensure that
they could raise their heel off of the floor under full weightbearing, and to determine the maximum height that the
participant could raise the heel off of the floor while standing. Participants held a fixed, horizontal bar with both
hands to provide balance support only. A reference block
was set to 80% of the maximum heel height and placed
beside the heel for objectivity of measurement. Successful
repetitions, defined as lifting the heel off of the floor to the
marked height without using the arms for assistance, were
counted until participants failed to reach the established
height or stopped of their own volition. Verbal encouragement was provided during the testing.
Total and regional bone-free lean body mass (BFLBM)
and fat mass were quantified from a full-body dual energy
x-ray absorptiometry scan (DXA, GE Medical Systems,
Lunar Prodigy, version 13.50.086). Total cross-sectional
area (tCSA), muscle CSA (mCSA), and fat CSA (fCSA) of
each calf were measured by peripheral quantitative computed tomography (pQCT, XCT 3000 Stratec Medizintechnik
GmbH, Pforzheim, Germany). Muscle and fat density of
each calf were determined as an exploratory measure of
muscle quality and presence of edema. The scan site was at
66% of the total length of the tibia from the distal end of
the tibia, and scans were analyzed according to previously
published methods (voxel size of 0.4 mm, a slice thickness
of 2.2 mm, and a scan speed of 20 mm/s).17
Resting blood flow rate and postischemic reactive
hyperemia were measured by strain-gauge plethysmography in both calves before the muscle testing. Participants
were instructed to lie quietly for 10 minutes on a plinth
in a temperature-controlled room (22 and 24C) to
obtain stable resting heart rates and blood pressures. A
mercury strain gauge was then placed around the largest circumference of the calf, and pneumatic cuffs were
placed around the ankle and distal thigh. The ankle cuff
was inflated to 240 mm Hg to minimize arterial flow into
the foot, and the thigh cuff was inflated to 50 mm Hg to
limit venous return from the calf to the thigh and was
deflated after a minimum of 4 pulse waveforms being
recorded. The ischemic stimulus was created by inflating
the thigh cuff to 300 mm Hg for 3 minutes. Postischemic
recordings were taken at 1 and 3 minutes after the release
of the thigh cuff pressure, and the slope of the peaks of
the waveforms was used to calculate the rate of blood
accumulation in the calf. Detailed descriptions have been
published previously.11,18,19
Central neural drive was determined by the twitch
interpolation technique and a KIN-COM dynamometer
(software version 5.16; Isokinetic International, Harrison,
Tennessee). Briefly, a transcutaneous electrical stimulation
of the tibial nerve was evoked during and after a maximal
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volitional isometric contraction of the triceps surae. The
stimulation amperage for each participant was determined
by increasing the amperage by 5 mA above the previous
trial until there was no change in torque production across
2 successive amperage levels. The supramaximal amperage was defined as 110% of the maximal amperage, and
maximal amperage was confirmed when no additional
torque was generated by the supramaximal amperage.20-22
Torque output from the KIN-COM was determined from
custom LabVIEW software (National Instruments, Austin,
Texas).20 Participants preformed 2 trials with each leg and
were encouraged to give a maximal effort for each trial. A
successful trial was defined by reaching a plateau in torque
where the superimposed stimulation was applied. The percentage of voluntary activation was defined by the following equation: 100 (peak torque/maximum total torque).
The peak torque was defined as the torque plateau value
before the supramaximal stimulation, and the maximum
total torque was the highest torque value obtained immediately after the supramaximal stimulation.

Statistics
Data are reported as mean (standard error). Statistical analysis was performed with SPSS v18 (IBM Corp, Armonk,
New York). We used paired t tests to compare the affected
limb to the sound limb for continuous variables. The percent difference between the affected and sound limbs was
calculated as 100 (XS XA)/[(XA + XS)/2]. The Wilcoxon
signed-rank test was used to compare categorical variables.
Statistical significance was set at P 0.05.

RESULTS
Participants (n = 9) were 64.2 (1.9) years old and 13.5 (4.4)
years poststroke. Self-reported AFO use was 6.5 (1.4) years.
They were 172.7 (3.2) cm tall and weighed 85.1 (7.1) kg. No
participants reported walking more than 1 mile per day, and

4 reported walking less than 1 block per day. The average

lapse of time from the stroke to returning to walking was
11.8 (5.7) weeks.
Knee extension 1RM was significantly lower (76.3%
16.6%) in the affected lower limb (P < 0.001). The
affected side quadriceps MMT scores ranged from 3 to 5
and the 1RM scores ranged from 6.25 to 50 lb, whereas
the sound-side quadriceps MMT scores were all 5 out of
5 and the 1RMs ranged from 31.5 to 87.5 lb. Muscular
endurance and MMT scores of the plantar flexors were
significantly lower for the affected calf (P < 0.05). The
calf MMT scores ranged from 2+ to 5 for the affected leg,
and the number of heel raises performed ranged from 0 (n
= 5) to 16 (n = 1). All sound plantar flexor MMT tests
were scored as 5, and the number of heel raises performed
ranged from 3 to 100.
Soft tissue composition and CSA measures for both legs
are reported in Table 1. BFLBM (difference: 6.2% 1.3%;
P < 0.05), but not fat mass (difference: 6.2% 1.4%;
P > 0.05), was significantly lower in the affected limb.
There was a 25.6% (5.7%) difference in mCSA (P < 0.01)
between the calves, but no significant interlimb differences
in fCSA or muscle or fat density (all P > 0.18).
Resting calf blood flow was lower on the affected side
(n = 9; 1.57 (0.24) mL/dL/min vs 2.38 (0.39) mL/dL/min;
P < 0.01) (Figure 1). Reactive hyperemia testing was successfully completed bilaterally on 6 participants (3 participants were unable to tolerate the ischemic stimulus). There
were no significant limb differences for the 1- or 3-minute
postischemic stimuli.
Figures 2 and 3 show voluntary activation and peak
torque results. The percentage of voluntary activation was
significantly greater in the sound limb (76.9% 9.6% vs
51.6% 10.0%; P = 0.021) as was peak torque (206.1
(47.7) Nm vs 76.5 (23.1) Nm; P = 0.008). Peak torque relative to mCSA was also greater for the sound limb (0.029
(0.005) Nm/mm2 vs 0.013 (0.003) Nm/mm2; P = 0.008).

Table 1. Leg Sizes, Masses, and Clinical Strength Measures (n = 9)

Affected Side
Means (Standard Error)

Variable

Sound Side
Means (Standard Error)

Total leg BFLBM, g

7733 (693)

8148 (761)

0.017

Total leg fat mass, g

5330 (790)

5476 (785)

0.197

mm2

9745 (643)

11098 (712)

<0.001

3264 (635)

3040 (511)

0.592

8.09 (2.93)

1.32 (5.86)

0.181

Calf total CSA,

Calf fat CSA,

mm2

Calf fat density, mg/cm3

mm2

5850 (520)

7453 (554)

0.002

75.34 (1.55)

78.26 (2.35)

0.218

Calf raises

5.8 (2.5)

27.2 (9.8)

0.042

Quadriceps 1RM, kg

28.4 (5.3)

59.1 (6.4)

<0.001

Calf muscle CSA,

Calf muscle density, mg/cm3

Abbreviations: BFLBM, bone-free lean body mass; CSA, cross-sectional area; 1RM = 1-repetition maximum.

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Figure 1. Resting blood flow in each limb for each participant.

Figure 2. Percentage of voluntary activation responses for individual participants.

Figure 3. Plantar flexion peak torque responses for individual participants.

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DISCUSSION
To our knowledge, this is the first study to document that
survivors of stroke who are ambulatory AFO users have
significant interlimb differences in neuromuscular and
vascular function more than 2 years after their stroke.
Specifically, the affected lower limb had reductions in total
limb BFLBM and calf mCSA, lower quadriceps strength
and endurance of the plantar flexors, decrements in percentage of voluntary activation of the plantar flexors, and
lower resting calf blood flow rate. These characterizations
are an important first step for generating hypotheses about
the effects of AFO use on functional and physiologic outcomes after stroke.
We expected side-to-side differences in strength on the
basis of the clinical presentation of the participants and
previous studies of stroke survivors.6,7,14,20-24 Knee extension 1RM results from this study, and others illustrate the
large strength variations found within each MMT grade.25
Five of the participants were unable to perform the MMT
test for the plantar flexors as described by Daniels and
Worthingham.15 One of these participants was able to
withstand a break test (5 out of 5), as defined by Kendal
et al,16 on the affected side but could not maintain balance while attempting a heel raise. In addition, the large
variation in heel raise performance by the sound limb was
greater than previously reported for healthy individuals in
this age group.26
The differences in total limb BFLBM and calf mCSA
agree with previous studies that reported decreased
muscle mass and area in the affected limbs after a stroke.
We hypothesized that fat mass and area would be larger
in the affected limb, but this was not observed.6,23,24,27,28
The pQCT-based attenuation coefficients are calibrated
such that fat has a density of 0 mg/cm3 and water has a
density between 50 and 60 mg/cm3; therefore, elevated
density values indicate that there may be an accumulation
of fluid in the limb. Calf fat density was highly variable
in the sound limb, but was consistently elevated in the
affected limb, suggesting that edema may be present in
many of the affected limbs, but only in a portion of the
sound limbs.
Inconsistencies in the literature about whether resting
blood flow is reduced in the affected calf likely stem from
differences in study inclusion criteria.10,11,18 Potential confounders may include differences in autonomic neurologic
effects of the stroke for hemiplegic versus hemiparetic survivors of stroke,11 time since stroke, and AFO use. In contrast to previous studies, we did not include all survivors
of stroke since we were particularly interested in characterizing AFO users because of the potential for AFOs to alter
the ability of the calf muscles to adequately provide the
muscle pump action needed to effectively return fluid to the
heart.1,12 Although there were no interlimb differences in
reactive hyperemia in those who were able to complete testing, interpretations of these data must be made cautiously
60

because of the proportion of participants who were unable

to tolerate the occlusion stimulus. Further testing of the
reactive hyperemia in survivors of stroke may provide
greater insight into autonomic neurological effects in this
clinical population, and longitudinal studies to determine
whether changes in blood flow after stroke are affected by
AFO use are warranted.
Little is known about expected differences in percent
voluntary activation of the plantar flexors between the
limbs in survivors of stroke. Previous studies on survivors
of stroke observed interlimb differences in quadriceps
activation of 12% and 15%.20,21 Our observed differences in voluntary activation of the plantar flexors are
similar to survivors of stroke who were ambulatory with
AFOs or gait aids.28 Large interlimb differences in the
percent activation of the calves in survivors of stroke with
plantar flexor paresis have been reported22; however, we
did not include or exclude on the basis of plantar flexor
muscle control on the affected side. The 63% difference
in the peak torques between calves is comparable to previous observations (62%, 72%).22,28 Differences in peak
torque remained when normalizing peak torque values to
mCSA. Significant interlimb differences in the percentage
of voluntary activation and mCSA, combined with the
lack of interlimb differences in muscle density, suggest
that strength differences were the result of differences in
muscle size and neuromotor drive, rather than by a difference in the quality of the muscle fibers, as previously
suggested.6,27 Because stroke and AFO use likely have
independent effects on these outcome variables, controlled
trials to determine whether AFO use has a positive or
negative effect on neuromuscular function after stroke are
needed.
The generalizability of these findings is limited by the
small sample size. There was a large heterogeneity in limb
differences despite limiting enrollment to ambulatory AFO
users. Although all participants were able to ambulate with
their AFO and appropriate gait aids, not all were able to
negotiate low barriers or climb stairs.

CONCLUSIONS
Despite the ambulatory status allowed by AFO use, neuromuscular and vascular deficits persist in recovered lower
limbs in survivors of stroke. It is unclear whether AFO use
attenuated or augmented deficits related to stroke, considering that compensatory increases in the sound limb may
have occurred during recovery. Further research into the
physiological effects of orthotic interventions for survivors
of stroke is warranted.

ACKNOWLEDGMENTS
All authors contributed to the concept, design, and data
collection and analysis of this study. Additional technical
help was not used.
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REFERENCES
1. Hesse S, Werner C, Matthias K, Stephen K, Beteanu M. Non-velocity-related
effects of a rigid double-stopped ankle-foot orthosis on gait and lower limb
muscle activity on hemiparetic subjects with an equinovarus deformity.
Stroke. 1999;30(9):1855-1861.
2. Simons CDM, van Asseldonk EHF, van der Kooij H, Geurts ACH, Buurke JH.
Ankle-foot orthoses in stroke: effects on functional balance, weight-bearing
asymmetry and the contribution of each lower limb to balance control. Clin
Biomech. 2009;24(9):769-775.
3. White MJ, Davies CTM. The effect of immobilization, after lower leg
fracture, on the contractile properties of human tricep surae. Clin Sci.
1984;66(3):277-282.
4. Yasuda N, Glover EI, Phillips SM, Isfort RJ, Tarnopolsky MA. Sex-based
differences in skeletal muscle function and morphology with short-term limb
immobilization. J Appl Physiol. 2005;99(3):1085-1092.
5. Khalid M, Brannigan A, Burke T. Calf muscle wasting after tibial shaft
fracture. Br J Sports Med. 2006;40(6):552-553.
6. Hafer-Macko CE, Ryan AS, Ivey FM, Macko RF. Skeletal muscle changes
after hemiparetic stroke and potential beneficial effects of exercise
intervention strategies. J Rehab Res Dev. 2008;45(2):261-272.
7. Mulroy SJ, Eberly VJ, Gronely JK, Weiss W, Newsam CJ. Effect of AFO
design on walking after stroke: impact of ankle plantar felxion contracture.
Prosthet Orthot Int. 2010;34(3):277-292.
8. NINDS. Post-Stroke Rehabilitation Fact Sheet. 2008; http://www.ninds.nih
.gov/disorders/stroke/poststrokerehab.htm. Accessed January 3, 2014.
9. Takeyasu N, Sakai T, Yabuki S, Machu K. Hemodynamic alterations in
hemiplegic patients as a cause of edema in the lower extremities. Int Angiol.
1989;8(1):16-21.
10. Kroese AJ. The effect of inactivity on reactive hyperaemia in the human
calf: a study with strain gauge plethysmography. Scand J Clin Lab Invest.
1977;37(1):53-58.
11. Ivey FM, Gardner AW, Dobrovolny CL, Macko RF. Unilateral impairment
of leg blood flow in chronic stroke patients. Cerebrovasc Dis. 2004;18(4):
283-289.
12. Geboers JF, Drost MR, Spaans F, Kuipers H, Seelan HA. Immediate and
long-term effects of ankle-foot orthosis on muscle activity during walking:
a randomized study of patients with unilateral foot drop. Arch Phys Med
Rehabil. 2002;83(2):240-245.
13. Lairamore C, Garrison MK, Bandy W, Zabel R. Comparison o tibialis anterior
muscle electromyography, ankle angle, and velocity when individuals post
stroke walk with different orthoses. Prosthet Orthot Int. 2011;35(4):402-410.

14. Kim CM, Eng JJ. The relationship of lower-extremity muscle torque to
locomotor performance in people with stroke. Phys Ther. 2003;83(1):49-57.
15. Hislop HJ, Avers D, Brown M. Ankle plantar flexion. In: Daniels and
Worthinghams Muscle Testing: Techniques of Manual Examination and
Performance Testing. 9th ed. St Louis, MO: Helen J. Hislop; 2014:251-257.
16. Kendal FJ, McCreary EK, Provance PG. Ankle plantar flexors. In: Muscles
Testing and Function. 4th ed. Philadelphia, PA: John P. Butler; 1993:206.
17. Sherk VD, Karabulut M, Bemben MG, Bemben DA. Age comparisons of
bone density and geometry in men. J Musculoskelet Neuronal Interact.
2009;9(4):256-262.
18. Adams WC, Imms FJ. Resting blood flow in the paretic and nonparetic lower
legs of hemiplegic persons: relation to local skin temperature. Arch Phys
Med Rehabil. 1983;64(9):423-428.
19. Gardner AW, Killewich LA, Katzel LI, et al. Relationship between free-living
daily physical activity and peripheral circulation in patients with intermittent
claudication. Angiology. 1999;50(4):289-297.
20. Newham DJ, Hsiao S-F. Knee muscle isometric strength, voluntary activation
and antagonist co-contraction in the first six months after stroke. Disabil
Rehabil. 2001;23(9):379-386.
21. Miller M, Flansbjer U-B, Lexell J. Voluntary activation of the knee extensors in
chronic poststroke subjects. Am J Phys Med Rehabil. 2009;88(4):286-291.
22. Fimland MS, Moen PMR, Hill T, et al. Neuromuscular performance of
paretic versus non-paretic plantar flexors after stroke. Eur J Appl Physiol.
2011;111(12):3041-3049.
23. Carin-Levy G, Greig C, Young A, Lewis S, Hannan J, Mead G. Longitudinal
changes in muscle strength and mass after acute stroke. Cerebrovasc Dis.
2006;21(3):201-207.
24. Metoki N, Sato Y, Satoh K, Okumura K, Iwamoto J. Muscular atrophy in
the hemiplegic thigh in patients after stroke. Am J Phys Med Rehabil.
2003;82(11):862-865.
25. Bohannon RW. Measuring knee extensor muscle strength. Am J Phys Med
Rehabil. 2001;80(1):13-18.
26. Jan MH, Chai HM, Lin YF, et al. Effects of age and sex on the results of an
ankle plantar-flexor manual muscle test. Phys Ther. 2005;85(10):1078-1084.
27. Ryan AS, Dobrovolny CL, Smith GV, Silver KH, Macko RF. Hemiparetic
muscle atrophy and increased intramuscular fat in stroke patients. Arch
Phys Med Rehabil. 2002;83(12):1703-1707.
28. Klein CS, Brooks D, Richardson D, McIlory WE, Bayley MT. Voluntary
activation failure contributes more to plantar flexor weakness than antagonist
coactivation and muscle atrophy in chronic stroke survivors. J Appl Physiol.
2010;109(5):1337-1346.

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