Beruflich Dokumente
Kultur Dokumente
ORIGINAL ARTICLE
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.
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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)
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
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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-
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.
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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
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.
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