1636

ORIGINAL ARTICLE

Evaluation of Spastic Muscle in Stroke Survivors Using

Magnetic Resonance Imaging and Resistance to Passive Motion
Lori L. Ploutz-Snyder, PhD, Brian C. Clark, PhD, Lynne Logan, PT, Margaret Turk, MD
ABSTRACT. Ploutz-Snyder LL, Clark BC, Logan L, Turk
M. Evaluation of spastic muscle in stroke survivors using
magnetic resonance imaging and resistance to passive motion.
Arch Phys Med Rehabil 2006;87:1636-42.

2006 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and
Rehabilitation

Objective: To assess the feasibility of using magnetic resonance imaging (MRI) and resistance to passive movement to
evaluate spastic muscle.
Design: T2-weighted MRI scans of the upper arm were
obtained at rest and after the performance of upper-arm exercise. In addition, resistance to passive movement was measured
subjectively (Modified Ashworth Scale [MAS]) and objectively by an isokinetic device while the arm was moved at
varying speeds (stretch reflex torque).
Setting: Research laboratory.
Participants: Six hemiplegic stroke survivors (single group)
with spasticity in the elbow flexors and extensors.
Interventions: Not applicable.
Main Outcome Measures: Strength, stretch reflex torque,
MAS, MRI-derived muscle cross-sectional area (CSA), and
transverse relaxation time (T2).
Results: The affected sides exhibited spasticity (as assessed through MAS), with the extensors displaying a range
of 0 to 3, and the flexors between 1 and 1. The affected
muscle groups were significantly weaker than the unaffected
muscle groups (extensors: 61% less, flexors: 65% less;
P.05). The affected CSA of the triceps was 25% smaller
than that of the unaffected side (P.01), but the biceps
muscle group was similar (5% less on the affected side,
P.05). There was a tendency (P.07; effect size, .48) for
the resting T2 to be higher in affected versus unaffected
biceps, but triceps values were similar (P.05). Both muscle groups showed an increase in T2 after exercise (30%,
P.05); however, the affected sides did not show an increase (P.05). For both muscle groups, the affected side
had a greater stretch reflex torque, with the range of torque
values being greater than the range of MAS scores.
Conclusions: MRI and quantitative resistance to passive
movement may be useful in the evaluation of spasticity. This is
clinically relevant for the development and evaluation of antispasticity treatments.
Key Words: Atrophy, muscle; Magnetic resonance imaging,
functional; Reflex; Rehabilitation; Torque.

PPER MOTONEURON DAMAGE, such as that which

U
occurs with stroke, is often associated with muscle weakness, loss of function, andthereforereduced quality of life.

From the Department of Exercise Science, Syracuse University, Syracuse, NY

(Ploutz-Snyder, Clark); and Physical Medicine and Rehabilitation, SUNY Upstate
Medical University, Syracuse, NY (Ploutz-Snyder, Logan, Turk).
Presented in part to the American College of Sports Medicine, June 2004, Indianapolis, IN.
No commercial party having a direct financial interest in the results of the research
supporting this article has or will confer a benefit upon the author(s) or upon any
organization with which the author(s) is/are associated.
Reprint requests to Lori L. Ploutz-Snyder, PhD, Dept of Exercise Science,
Syracuse University, 820 Comstock Ave, Rm 201, Syracuse, NY 13244, e-mail:
llploutz@syr.edu.
0003-9993/06/8712-10827$32.00/0
doi:10.1016/j.apmr.2006.09.013

Arch Phys Med Rehabil Vol 87, December 2006

Spasticity is often secondary to upper motoneuron lesion, and

considerable clinical efforts are made to treat spasticity in an
attempt to restore function to affected people. Because the
original injury is neural in origin most efforts to quantify
spasticity or study stroke rehabilitation have focused on the
nervous system. For example, brain magnetic resonance imaging (MRI) scanning is used to identify the central lesion site,
and evaluation of the peripheral electromyographic signal from
spastic muscle has been used in attempt to quantify spasticity.1
Given the fact that skeletal muscle adapts very quickly and
dramatically to altered neural recruitment patterns and to the
amount and type of loading and activity that is placed on it, it
is also logical to study the skeletal muscle properties that result
from a neural lesion. In fact, the muscle itself may provide a
proxy view of the nervous systems adaptations to damage and
certainly is expected to be highly related to a persons ability to
function in the environment. Although it is commonly known
that muscle strength is reduced in affected muscles after stroke,
there is sparse and controversial information regarding other
muscle properties.2 For example, there is considerable controversy regarding the influence of stroke and spasticity on affected muscle cross-sectional area (CSA), and even spasticity
itself cannot be accurately measured. The clinical evaluations
such as the Modified Ashworth Scale (MAS) for spasticity or
handheld dynamometry for estimating strength lack the sensitivity and reliability typically required for research testing.
The notion of evaluating the muscle itself (as opposed to the
nervous system) in an attempt to quantify upper motoneuron
lesionaffected muscle has been previously recognized but
only superficially studied. A few laboratories3-7 have successfully evaluated muscle spasticity by measuring the resistance
(torque) to passive motion with specially built dynamometers
that passively move a limb at set velocities while simultaneously measuring torque through all or part of the range of
motion (ROM). Such dynamometers could also be used for
careful evaluation of muscle strength.
MRI of skeletal muscle has not previously been used with
stroke survivors but may hold promise both for evaluation of
muscle CSA or volume and for evaluation of muscle function.
MRI offers unparalleled spatial resolution and is ideally suited
for detailed and accurate measures of muscle size. Muscle
functional MRI (fMRI) has been used extensively in the exercise physiology literature to evaluate muscle involvement in
exercise.8,9 The signal intensity in T2-weighted images obtained immediately after exercise is elevated, and the extent of
elevation is quantitatively related to load and electromyographic activity (correlation, .95).

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EVALUATION OF SPASTIC MUSCLE, Ploutz-Snyder

Table 1: Subject Demographic Data
Subject

1
2
3
4
5
6
Mean
SD

Weight (kg)

69.09
93.18
90.91
71.82
80.00
90.91
82.65
10.54

Site of Lesion

L MCA
R thal
R MCA
R MCA
R MCA
R MCA

MAS Biceps

MAS Triceps

Age (y)

Months Since Stroke

2
1
1
1
1
1

1
2
2
0
2
3

51.2
55.8
62.6
57.4
52.9
55.7
55.93
3.96

72
125
10
35
115
33
65
47.11

Abbreviations: L, left; MCA, middle cerebral artery; R, right; thal, thalamus; SD, standard deviation.

Very few studies have evaluated the muscle of stroke survivors; to our knowledge none of these has included either
anatomic or fMRI measurements. Therefore, the purpose of
this study was to assess the feasibility of using both MRI and
dynamometry to evaluate spastic muscle in stroke survivors.
Given that MRI requires patients to remain very still in a fixed
and sometimes awkward position for an extended time and that
dynamometer measurements require subjects to grip a handle,
move through a wide ROM, and maintain fixed positions, we
believed it was important to document the feasibility of such
measurements before embarking on a large-scale study.
We hypothesized that subjects with moderate levels of spasticity would be able to tolerate all testing. Furthermore, we
hypothesized that the muscle CSA and strength would be
reduced in the affected compared with the unaffected sides,
that resting transverse relaxation time (T2) would be slightly
elevated in spastic muscle (when compared with the nonaffected side), and that the exercise-induced T2 change would be
attenuated in spastic muscle.
METHODS
Participants
Six hemiplegic stroke survivors (5 men, 1 woman) were
recruited from the outpatient Tone Management Program at
University Hospital (Upstate Medical University) to participate
in this study (table 1). None of the subjects was currently
receiving pharmacologic or other forms of management therapy for the hemiplegia. The Syracuse University and Upstate
Medical University institutional review boards approved the
experimental protocol, and all subjects provided written informed consent before testing.
General Overview of the Experimental Design
When subjects reported to the laboratory, T2-weighted magnetic resonance images were obtained from the upper arm of
both the affected and unaffected sides. Next, each subjects
affected arm was passively moved through elbow extension
and flexion at varying speeds via a motor-driven dynamometer,
and the generated torque was recorded. The velocity-associated
torque increase from the slowest speed (.087 radian/s) was
calculated to quantify spasticity. In addition, subjects spasticity was assessed as the passive resistance to manual movement,
and a score was assigned according to the MAS.10 After these
tests were completed, the maximal voluntary contraction
(MVC) strength for both elbow flexion and extension were
determined, and subjects performed 3 sets of 10 repetitions of
concentric-action elbow flexion and extension exercise at 33%
of their MVC. Immediately (5min from end of exercise to
beginning of scan) on completion of the exercise bouts subjects
returned to the MRI scanner, and T2-weighted images of the

upper arm were again obtained. Subsequently, this protocol

was repeated for the unaffected side. Detailed information on
all procedures is described below.
Magnetic Resonance Imaging
Standard spin-echo magnetic resonance images of the right
and left upper arms were obtained using a 1.5-T superconducting magnet.a These procedures were similar to those previously
described.11-14 Briefly, 10-mmthick transaxial images (repetition time, 2000ms; echo time, 30ms; slice-to-slice interval,
12mm) were obtained along the entire length of the upper arm.
During acquisition, subjects lay on the contralateral side so that
the arm of interest was positioned along the midline of the
body. After data collection the magnetic resonance images
were saved to a disk for postprocessing (see Data Analysis).
Resistance to Passive Movement
Resistance to passive movement was assessed in 2 ways:
mechanically recorded torque response to motor-driven
movements at various specific velocities6 and the more
clinically used subjective grading based on an experienced
investigator manually moving the arm at a rapid velocity
(MAS) (see table 1).10
The generated torque of motor-driven movements was measured in a similar fashion to that previously described.6 Briefly,
subjects were seated in a Biodex System 3 dynamometer.b The
arm was positioned in a wrist-hand orthosis,c which was securely attached to a lever arm connected to the motor axis that
housed a torque transducer, optical encoder, and potentiometer.
The elbow axis of rotation was positioned directly over the
motor axis, with a shoulder abduction angle of about 80 and
shoulder flexion of 0. Subjects arms were moved through a
comfortable ROM via a direct-current servomotor at velocities
of 0.087, 1.047, 1.571, and 2.094 radians/s (5, 60, 90, and
120/s, respectively). The slowest velocity was always tested
first; if a subject tolerated the velocity, the next faster velocity
was attempted. If a subject had not tolerated a given velocity,
the testing would have been terminated at that speed; fortunately, all subjects tolerated even the fastest velocities. The
average comfortable ROM was 9214. Three trials at each
speed were conducted for both the elbow flexors and extensors.
Specifically, 3 trials of elbow extension and flexion were
initially made at .087 radian/s, then 3 trials were assessed for
elbow extension at 1.047 radians/s, during which the return
flexion movement was at 0.087 radian/s. The extension velocity continually increased to 1.571 and 2.094 radians/s while the
returning flexion movement was still maintained at the slow
velocity (.087 radian/s). After the extension movements were
completed, the various movement velocities were repeated,
except with the faster velocities occurring during flexion, while
the extension movements were kept slow (.087 radian/s) and
Arch Phys Med Rehabil Vol 87, December 2006

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EVALUATION OF SPASTIC MUSCLE, Ploutz-Snyder

constant. Torque, position, and velocity were amplified 500

times and sampled at 100Hz. These signals were subsequently
averaged over 8 weighted epoch samples of a sliding window
and saved on a disk for subsequent analysis (see Data Analysis).
The MAS assessment was conducted by an experienced
physical therapist who conducts spasticity assessments on a
regular basis. The grades of the MAS range from 0 to 4
(includes 1), with 0 indicating no increase in muscle tone and
4 indicating that the limb is rigid in flexion or extension. For
both measures of resistance to passive movement the unaffected and affected sides for the extensors and flexors were
assessed.
MVC and Resistance Exercise
During the voluntary exertions subjects were seated in a
Biodex System 3 dynamometer arranged to assess elbow flexion and extension forces. The forearms were positioned neutrally (half-way between pronation and supination), and the
lower portion of the upper arm was rested on an arm rest at an
angle of approximately 45 lateral from and vertical to the
torso. Straps were used across the pelvis and torso regions to
minimize movement and synergistic contributions. One subject
was unable to comfortably perform the exercise in this anatomic position because of shoulder pain; thus this person was
positioned with a lesser angle from the torso for both the
affected and unaffected sides. If subjects were unable to effectively grasp the handle their arm was rigidly attached to the
lever arm via the orthosis.
To assess MVC strength, each subjects arm was maintained
at an elbow flexion angle of 90, and a minimum of 3 trials
were provided for both flexion and extension. During the
strength assessments subjects were asked to gradually increase
torque and perform a maximal contraction for 5 seconds.
During testing, strong verbal encouragement was provided by
the investigators. The highest torques recorded for flexion and
extension were considered the MVCs. The torque signal was
amplified 500 times, sampled at 100Hz, and averaged over 8
weighted epoch samples of a sliding window.
Resistance exercise was performed using the isotonic mode
of the Biodex System 3 dynamometer. This allows for repetitive movements of the concentric action only (concentric elbow
flexion, then extension). Subjects performed 3 sets of 10 repetitions at an intensity set at 33% of the MVC. A 2-minute rest
was provided between the sets.
Data Analysis
The magnetic resonance images were transferred to a computer and analyzed with ImageJ software.d From the magnetic
resonance images 2 variables were calculated: (1) muscle CSA
and (2) T2. Muscle CSA was calculated from the pre-exercise
(resting) images for the biceps and triceps brachii. This calculation was based on an average CSA over 5 slices on both the
affected and unaffected sides, which were matched based on
anatomic markers. Muscle T2 was calculated on a pixel-bypixel basis and averaged over the entire muscle using the same
5 slices in the biceps brachii and triceps brachii for each
respective side from the pre-exercise and postexercise magnetic resonance images.
Spastic hypertonia was quantified by calculating the reflex
torque in a similar manner as previously described.6 Briefly,
the reflex torque was considered the peak torque recorded at
1.571 radians/s between a constant-velocity segment of movement (elbow flexors, 100120; elbow extensors, 8090)
after subtracting the passive torque recorded at the slowest
Arch Phys Med Rehabil Vol 87, December 2006

velocity (.087 radian/s). The movement velocity speed of 1.571

radians/s was chosen for this analysis because it evoked the
largest reflex torque responses, and an average of the 3 trials
was used in the calculation. We calculated the torque in this
fashion because by subtracting the torque generated during a
slow movement, the passive tension generated from noncontractile elements (ie, tendon) is removed; thus the calculated
outcome (reflex torque) should primarily be due to the evoked
stretch reflex response and represent hypertonicity. Data analysis was performed with the System 3 Advantage Software
(version 3.29).a
Statistical Analysis
Mixed-model analysis-of-variance techniques with least significant differences post hoc tests were conducted to evaluate
the differences in the dependent variables (passive resistance
torque, reflex torque, CSA, T2, strength) with respect to the
independent variables (ie, side [affected, unaffected], movement velocity [0.087, 1.047, 1.571, 2.094 radians/s], exercise
state [pre-exercise, postexercise]). The SPSS statistical softwaree was used for all analyses. A preset level of significance
was established at .05.
RESULTS
Passive Resistance to Movement
MAS scores for the elbow extensors ranged from 0 to 3 and
for the flexors ranged from 1 to 1. On the Biodex dynamometer test both the elbow extensors and flexors had a velocityrelated increase in torque as movement velocity increased
when compared with the unaffected side (P.05) (figs 1A,
1B). Overall, the extensors had a greater degree of spastic
hypertonia compared with the flexors (reflex torque,
5.891.65Nm vs 0.840.44Nm; P.04). Interestingly, in
comparing the measured values of spastic hypertonia obtained
via mechanical recordings (reflex torque) versus manual assessment (MAS), it appears that the mechanical recordings
provide a considerably wider range of values for the reflex
torque compared with MAS (figs 2A, 2B).
Muscle Strength and Size
Muscle strength was drastically lower on the affected side
compared with the unaffected side, with a 65% and 61% lower
strength observed for the flexors and extensors, respectively
(P.05) (fig 3A). Muscle CSA was 25% less in the extensors
(P.05) and only 5% lower in the flexors (P.05) (fig 3B).
Resting and Postexercise T2
The T2 of the resting elbow flexor muscles (pre-exercise)
had a tendency to be slightly higher on the affected side
(30.710.79ms vs 29.940.47ms, P.07; 2 effect size, .48)
(figs 4, 5). However, the extensors did not show a trend toward
having a higher resting T2 value on the affected side
(30.571.88ms vs 30.40.72ms, P.95) (see fig 5). For both
the extensors and flexors the contraction-induced increases in
signal intensity were significantly blunted for the affected
sides: the exercise-induced change in T2 was 1.9 and 2.9ms
less for the flexors and extensors, respectively (P.05).
DISCUSSION
This was a pilot study designed to suggest future directions
in the quantification of spasticity. The major findings of this
study were (1) stroke survivors with mild spasticity are indeed
able to tolerate the testing itself and the positioning required for
exercise testing, the resistance to passive motion even at the

EVALUATION OF SPASTIC MUSCLE, Ploutz-Snyder

1639

Fig 1. Generated torque in response to passive movement of spastic (affected side) and nonspastic (unaffected side) arm movements at
varying velocities for the (A) elbow extensors and (B) flexors in 6 hemiplegic stroke survivors. *Affected greater than unaffected at respective
velocity. Affected extensors: 1.571>0.087 radians/s, affected flexors: 1.571>1.047>0.087 radians/s.

fastest speeds, and the MRI; (2) muscle strength was dramatically lower in affected muscles (65% and 61% lower in the
flexors and extensors, respectively), whereas CSA was better
maintained (25% and 5% lower in the flexors and extensors,
respectively) but still markedly reduced in the extensors; (3)
reflex torque seems to provide a wider range of values compared with MAS; and (4) spastic muscle shows altered restingand postexercise-induced responses in its muscle fMRI response.
Feasibility of Testing
Initially we had several concerns about the feasibility of the
study, mostly relating to the positioning and ROM of subjects.
For example, the MRI scanning required subjects to remain
still with the arm outstretched above the head for about 10
minutes. Subjects had trouble with this on the affected side, and
there was not a standard positioning that worked for all sub-

jects. We were required to use pads inside the MRI device to

position the upper arm appropriately in a manner that could be
held for the duration of the scan. Typically it took about 30
minutes to find a suitable positioning for each subject. We were
also concerned about how quickly we could transport subjects
from the exercise facility to the MRI scanner in the next room.
Subjects were able to be unstrapped from the Biodex and
moved quickly into the scanner; it was critical, however, that
we could rapidly position them in the scanner. On average it
took about 5 minutes from the end of exercise to the start of the
scan. It was important that we not disrupt the arrangement of
the pads set up on the initial scan. We also had a concern about
the ROM and the velocity of testing on the passive motion
dynamometer tests. We were careful to use a comfortable
ROM, which inherently varied among subjects. This comfortable zone ranged from 71 to 115 and averaged 91. Accordingly, we were concerned about what velocities of movement

Fig 2. Variation in reflex torque with respect to subjective scoring based on the MAS. Note the more sensitive detection of spastic hypertonia
(reflex torque) via mechanically detected force to passive movement in (A) the elbow extensors of subjects with varying degrees of MAS
scores and the variation in reflex torque in (B) the elbow flexors despite all subjects having an MAS score of 1 or 1.

Arch Phys Med Rehabil Vol 87, December 2006

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EVALUATION OF SPASTIC MUSCLE, Ploutz-Snyder

Muscle Streng

70
*

60

Affected side
Unaffected side

CSA (cm2)

Strength (Nm)

50
40
30

5
4
3

20

10

1
0

0
Flexors

Extensors

Flexors

Extensors

Fig 3. (A) Muscle strength and (B) CSA of the affected and unaffected sides. *Unaffected greater than affected.

should be used. The faster the velocity the higher the likelihood
of detecting resistance, but higher velocities also have the
potential to exacerbate the spasticity and be uncomfortable for
subjects. For the upper arm we found that velocities ranging
from 5 to 120/s were well tolerated. The fact that we observed a wide range of reflex torque scores suggests that this
velocity range would be suitable for further study. A faster
velocity could probably be included as well.
Muscle Size and Strength
In terms of muscle size and strength, it is not surprising that
we observed lower maximal voluntary strength in the affected
biceps and triceps (60%65%). What is more surprising is
the 25% lower muscle CSA in the triceps on the affected side
compared with the unaffected side. This disproportionately
large decrease in strength is probably due to the ability (or lack
thereof) to centrally activate the muscle.
It has widely been reported that upper motoneuron lesions
such as those occurring with stroke result in minimal or no
muscle atrophy.15 This notion has been supported by the observation that in people with spinal cord injury muscle spasticity actually plays a protective role in the preservation of

Fig 4. A representative example of an MRI scan of the unaffected

and affected upper arm. Note the reduced muscle size in the elbow
extensors and the increased signal intensity of the elbow flexors on
the affected side.

Arch Phys Med Rehabil Vol 87, December 2006

muscle mass.16 However, there are also reports showing atrophy after stroke. For example, a 3% to 4% difference in thigh
mass between the affected and unaffected sides after stroke has
previously been reported,17 which is similar to what we observed in the less-affected biceps muscles. Others, however,
have shown much greater atrophy: Metoki et al18 reported a
25% difference in thigh muscle volume between sides. In our
subject population, the triceps were more severely affected, and
we too report a 25% difference in muscle CSA between sides.
Therefore, it seems plausible that the extent of atrophy might
be related to the severity of spasticity, although we did not
observe significant correlations between muscle CSA and MAS
score or CSA and reflex torque.
However, only 1 longitudinal study19 has actually investigated the atrophy process in hemiplegic stroke survivors; it
found about a 22% side difference in thigh muscle CSA on
admission to a rehabilitation program. Both sides increased
thigh CSA about 10% during the rehabilitation program, and
thus the side differences remained the same after the program

Fig 5. MRI T2 values of spastic (affected) and nonspastic (unaffected) skeletal muscle at rest and after resistance exercise. *Significant increase from postexercise value. Affected postexercise
greater than unaffected postexercise.

EVALUATION OF SPASTIC MUSCLE, Ploutz-Snyder

(mean rehabilitation length of stay, 104d).19 Studies of muscle

CSA using muscle biopsies to evaluate the CSA of individual
fibers also show mixed results, with some showing normalsized fibers,20 others showing selective type II atrophy,21-23 and
yet others showing type I and type II atrophy in hemiparetic
stroke patients.24 Regardless of how atrophy is measured (muscle biopsy of individual fibers vs whole muscle volumes), there
are dramatic differences among studies showing anywhere
from no atrophy to large (25%) differences between sides in
hemiparetic subjects. Our study used MRI to evaluate the CSA
of individual muscles, whereas other studies have used computed tomography, which has lower spatial resolution and is
used to identify whole muscle groups.19 This may explain some
discrepancy, but more likely individual stroke survivors vary
considerably in the extent of atrophy. This is an area that
deserves further study, because it seems there are wide disparities among the extent of motor loss and strength compared
with the amount of atrophy. There is clearly not a straightforward relation between muscle strength and size in stroke survivors, and it would be clinically useful to understand what
factors influence or how to predict the extent of atrophy in a
given patient, especially for the more severe cases of atrophy.
Resistance to Passive Movement and MRI to Assess
Spasticity
A number of laboratories have introduced the concept of
measuring the resistance of spastic muscle to passive motion at
varying speeds essentially mechanically automating the
MAS.3-7 Although previous reports indicate that this technique
has promise,4,6,7 it has not been sufficiently studied to know
what velocities to use for various muscle groups, if normative
values can be obtained, or whether it is reliable. We confirm
that resistance to passive motion can be detected with a commercially available device and that it yields values with a wider
range than the MAS. We observed that the flexor reflex torque
measurements showed a 3-fold difference among subjects who
all received an MAS score of 1. Given our small sample size
and relatively homogeneous subject pool, we are not able to
identify correlations among the various methods of assessing
spasticity, but this is suggested for future research.
Our MRI data are novel, because this is the first study to
report on the MRI characteristics of spastic muscle. Muscle
fMRI is widely used to evaluate muscle activation9,13 and is
known to correlate highly (.99) with muscle electromyographic activity and load lifted.25 Resting T2 is 283ms in
normal resting muscle.11-14 We hypothesized that resting T2
would be elevated in spastic muscle given its constant state
of slight activation, and although not statistically significant
(P.07), we observed a large effect size (2.48) for the
flexors, suggesting a trend toward higher resting T2 values
(P.07). However, a similar finding was not observed for
the extensor muscles, which actually had higher spasticity
than the flexors (as assessed from the higher MAS and reflex
torque values); therefore, it is difficult to fully interpret
these results, and future research is warranted to explore this
issue.
The postexercise T2 is reflective of muscle activity during
the prior exercise bout. We observed a failure of the spastic
muscle to increase T2 in response to exercise, especially in the
extensor muscle group, which was more spastic. Based on
these data it is not possible to know why the spastic muscle
displays an attenuated exercise-induced T2 response, although
there are several plausible explanations. It could be as simple
as the fact that spastic muscle cannot lift a heavy enough
absolute load to cause the metabolic changes required for T2 to
increase or that the spastic muscle is not able to be fully

1641

activated during the MVC (central activation failure) and,

therefore, the relative loading is not a true relative for the
spastic muscle. Alternatively, it could be more complex, such
as an altered metabolic capacity of spastic muscle, either as a
direct result of the neural lesion or, more likely, as a secondary
adaptation. In any event, these MRI techniques indicate disparate adaptations between spastic and nonspastic muscle, and
it is recommended that further experiments using these and
similar MRI techniques such as the evaluation of the heterogeneity of T2-pixel values in higher resolution images be
performed. It seems quite likely that muscle fMRI techniques
hold promise for more precise spatial information regarding
muscle spasticity.
Study Limitations
Given that this is a pilot study, there were several limitations.
There were a small number of subjects, mostly men, with a narrow
age range and mild spasticity. This study is not meant to be
generalized to a wide variety of clinical populations but rather to
show that the exercise, resistance to passive motion, and MRI
measurements can be performed on spastic arm muscle. The study
is also intended to encourage other researchers to study spastic
muscle itself and not just the nervous system.
CONCLUSIONS
This pilot work supports the notion and shows the feasibility
of developing both reflex torque and muscle fMRI for the
quantification and localization of muscle spasticity secondary
to a variety of neuromuscular conditions, because the implications for clinical research could be immense. For example, the
precise quantification of spasticity would allow for better evaluation of antispasticity treatments, especially in the ability to
detect small or early changes. The ability to better localize
spasticity with imaging could guide treatments based on sitespecific injections. Future studies should include more subjects
with a wider range of spasticity and attempt to develop standardized protocols for muscle fMRI and reflex torque.
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