QUANTITATIVE
CLINICAL MEASUREMENT
OF SPASTICITY
by
ALFRED CHAO
S.B.,
Massachusetts Institute
of Technology
(1973)
SUBMITTED
OF THE
IN PARTIAL FULFILLMENT
REQUIREMENTS
DEGREE OF MASTER
FOR THE
OF SCIENCE
at the
MASSACHUSETTS
INSTITUTE
OF TECHNOLOGY
February, 1976
Signature
of Author
DepartiTnintf
to
ronaut i,'s
annd-As trIonautcs
January 28,
1976
Certified by
Thesis Supervisor
Accepted by
Chairman,
Dc'-artme0nta1 Graduatu
Committee
Room 14-0551
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2
QUANTITATIVE CLINICAL MEASUREMENT
OF SPASTICITY
.by
Alfred Chao
Submitted to the Department of Aeronautics and
fulfillment
Astronautics on January 28, 1976, in partial
of the requirements for the degree of Master of Science.
ABSTRACT
Present clinical methods of evaluating spasticity
is based mostly on subjective assessment. An existing
arm manipulator was modified into a device for applying
controlled rotation of the forearm- and strain gauges
and surface EMG electrodes were used for obtaining quantitative
and objective measurements of muscular activities.
device, studies were made of th.e abnormal
Using this
muscular reactions of spastic patients. Stretch reflex
in normal subjects, induced by isometric contraction was
also studied. These results were compared with data from
the spastic patient.
Thesis Supervisor:
Laurence R.
Young
Title: Professor of Aeronautics and
Astronautics
3
ACKNOWLEDGEMENT
I wish to express my sincere appreciation for
the patient
guidance of Professor Laurence R.. Young
throughout this research, and for his suggestions
encouragements..
and
I am particularly grateful to Mr. Bill
Morrison for his invaluable technical
expertise and
constant assistance.
This project was supported in part by a grant
from the Rehabilitation Services Administration,
HEW 23-P-55854/l.
-4-
TABLE OF CONTENTS
Chapter
1
Page No.
INTRODUCTION
5
1.1
Scope and Objective of Research
'
1.2
Review of the Neuromuscular Control
System
8
1.3
2
3
4
11
EXPERIMENTAL DESIGN
13
2.1
General Description
13
2.2
Motor Servocontrol
14
2.3
Measurement Devices
16
2.4
Safety Precautions
17
EXPERIMENTS ON NORMAL SUBJECTS
31
3.1
Experimental Protocol
31
3.2
Experimental Results
33
3.3
Summary
35
EXPERIMENTS ON SPASTIC PATIENTS
51
4.1
Experimental Protocol
51
4.2
Experimental Results on Passive
Stretch
52
Experiments with Pre-stretch
Isometric Contraction
55
Summary
56
4.3
4.4
REFERENCES
Related Research
80
-5-
CHAPTER 1
INTRODUCTION
1.1
and Objective of Research
.Scope
Spasticity is a neuromuscular disorder due to upper motor unit damage
and afflicts victims of spinal cord trauma, stroke, and a number of congenital cerebrovascular diseases affecting the motor cortex, frontal lobe
region, the internal capsule, or other extrapyramidal projections at the
These patients present a clinical picture commonly
basal ganglia level.
attributable to a state of greatly increased activity in the motoneurones,
leading to the condition of muscular hypertonia and hyperreflexia.
these signs include:
Some of
uncontrolled spasms as in chronic paraplegia, uncon-
trolled continuous contraction as in Athetoid Dystonia, excessive sensitivity
and reaction to noxious or tactile stimuli, and widely spreading reactions
which tend to overwhelm local reflex signs.
As in decerebrate rigidity,
spastic patients exhibit hypertonia in antigravity muscles.
stiffly extended and resists flexion.
The leg is
The arm is held flexed and pronated
and resists extension.
A particularly crippling factor affecting coordinated movement is
exaggerated and often spreading contraction in response to passive stretch
of a muscle.
It interferes with reciprocal innervation and hence diminishes
the patient's strength and interferes with his volitional movements.
A considerable amount of effort is expended in the treatment of spasticity.
Highly touted drugs, such as the widely used central nervous system depressent
-6-
Valium, and the special neuromuscular blocking agent dentrolene sodium, surface perennially, generating much hope.
New physical therapy programs, which
can be very strenuous and exhausting to the patient, are continuously being
proposed and applied.
In view of all this, the present method for evaluating
patient progress and effectiveness of therapy is very ill-defined.
Usual
clinical assessments, as in the case of cerebral palsied patients, consist of
observing the patient's gait and strength and degree of self-interference in
volitional movements as in hand slapping motions.
Evaluation of the exaggerated
stretch reflex is accomplished by the physician holding the patients limb and
stretching a stiff muscle slowly.
tive and highly variable.
This type of method is necessarily subjec-
To the extent that the physician probably prescribed
the drug or physical therapy, and hence has a vested interest in obtaining
improvements, his observation and assessment is prone to be self-fulfilling or
at least tainted with the "placebo" effect.
Considering the energy involved,
both physical and mental, a more reliable and objective means of clinical
evaluation is needed.
This research attempts to study the feasibility of an objective and
meaningful method of measuring spasticity.
An existing arm movement device
has been modified and the necessary instrumentation built so that accurate
and controlled muscle stretches could be applied to patients and quantitative
measurement data could be obtained for assessment.
Repeatability and con-
sistency of the test protocol must first be established.
Emphasis will then
be on the identification and definition of meaningful measurement parameters.
An initial set of experiments was run on normal subjects to provide a data
base for comparison with spastic patients.
Thus the main objectives of the
study are:
1.
The construction of the experimental device.
-7-
2.
The evaluation of the device on normal subjects to provide comparative data.
3.
The evaluation of the device on patients in order to establish a
consistent and useful test protocol for clinical application.
The actual clinical testing of patients is not included in this study and
shall be
left to further research by physicians in a clinical environment.
The patients selected for the study were from a pool of cerebral palsied
patients at the Children's Hospital Medical Center, Harvard Medical School,
Boston.
plegics.
The group was primarily adolescents, and had been diagnosed as hemiThe reason for choosing hemiplegics lies in the availability of the
unaffected side for comparative study.
The muscle group selected for study are those involved in the rotation of
the forearm, namely the pronator teres and pronator quadratus for pronation,
and the supinator and biceps brachii for supination.
These muscles were picked
since they are easily accessible, being used frequently by physicians in subjective tests, and because they are less commonly altered through the need for
corrective surgery than is the case for the ankle joint where bone fusion is
often administered to compensate for spasticity in the antigravity muscles.
1.2
Review of the Neuromuscular System
Most muscles are composed of three types of extrafusal fibres.
The large
pale A fibres have few mitochondria ATPase and receive few blood vessels. The
small C fibres are loaded with mitochondria and have the richest blood supply,
hence the dark color.
B fibres are intermediate in structure.
Most pale muscles contain varying ratios of the three types of fibres,
hence the pale color.
Red muscles such as the cat's soleus muscle consist solely
of type B fibres and appear homogeneous under the microscope.
-8-
A functional motor unit is defined as being composed of an a-motoneurone
and the muscle fibres innervated by its many axon collaterals.
Evidence sug-
gests that a-motoneurones innervate only a single type of muscle fibre, so
that there are essentially three types of motor units.
Large type A units have more fibres per unit than type B and C units and
are innervated by larger and faster conducting neurones.
tracting and develop higher maximal tension.
There are more slower and smaller
units since the number of fibres per unit is less.
tension and allow for finer control.
due to their abundant blood supply.
They are fast con-
Hence they develop less
They are also less susceptible to fatigue
The order of recruitment is organized and
determined at the spinal level by the size of the motoneurone.
Smaller moto-
neurones and hence smaller units are easily excitable and provide fine control
at low tension levels, and since they are activated more often, need to be
relatively unaffected by fatigue.
As tension increases, larger units are
recruited, providing larger increments of force.
There are two types of stretch receptors.
Muscle spindles are composed
of connective tissues containing two kinds of intrafusal fibres.
Nuclear bags
are larger and contain large nuclei in the central expanded region.- The smaller
nuclear chains are attached at the two ends to nuclear bag fibres.
Motor inner-
vation of these fibres are provided by two types
of small y-motoneurones.
y1
fibres terminate in discrete motor end plates and appear identical except in
size to extrafusal fibres.
y2 fibres end in complex ramifications.
mental evidence suggests a distinct scheme of innervation,
and
Some experi-
Y on nuclear bags,
y2 on nuclear chains.
Spindle afferents consist usually of one Group Ia fibre supplying primary
annulospiral endings on both bag and chain fibres, and several group II fibres
supplying secondary endings primarily on chain fibres.
With gamma support, the
-9-
primary endings respond to both velocity of stretch and static stretch, whereas
secondary endings are essentially tonic length sensitive devices.
Recent
experimental evidence (Bergman and Grillner, 1969) suggests differential control
of the two gamma cells.
Thus the phasic (velocity) sensitivity of the Ia affer-
ents derives from primary endings on the nuclear bags and hence is controlled by
Y1 fibres, while their static sensitivity originates in the primary endings on
nuclear chains and is adjusted via Y2 fibres.
Ia afferents are excitatory to their own motoneuronal pool and inhibitory
to
y-motoneurones of the antagonist muscle; whereas Group II afferents are
excitatory for flexors and inhibitory for extensors.
The mechanism of the so-called stretch reflex, and the role of the spindle
afferent loop, as elucidated by Sherrington, is reviewed below because of its
significance in the pathophysiology of spasticity.
Merton (1951) proposed the follow-up servo model, which features the spindle
afferent reflex loop as the principle mechanism for voluntary muscle contraction.
According to this theory, movements are initiated via y-motoneurones.
Efferent
volleys in the gamma fibres cause the intrafusal fibres to contract and thereby
elicit afferent discharge in Ia and II afferents.
the
This activity reflexly excites
ot-motoneuronal pool, causing the extrafusal fibres to contract, unloading
the spindles until a new steady state length is reached.
Eldred, Granit and Merton (1953) showed that reflexly evoked contraction of
the soleus muscle of the decerebrate cat, as by neck flexion, was accompanied by
accelerated spindle discharge, indicating fusimotor stimulation to compensate
for spindle unloading.
If the servo loop was opened by dorsal root section, no
contraction was observed, but increased spindle activity was again reported,
pointing to gamma activity.
However, voluntary movement can occur even in a
totally de-afferented limb (Eldred, 1960).
It is generally accepted that in
-10-
most centrally initiated movements, alpha and gamma coactivation is involved.
Alpha activity directly commands extrafusal contraction, while gamma firing
maintains the spindles in
their sensitive region and hence in a position to
correct for load disturbances.
Wilson's (1964) elegant analysis of the locust flight control system,
which consists of fewer than twenty motoneurones for each wing, showed that
the removal of the two sources of proprioceptive input, namely stretch and lift
transducers in the wings, caused no qualitative alteration in the motor pattern.
There was only a reduction in the wing beat frequency.
Thus the phasic affer-
ent information appears to provide no more than a tonic reinforcement to a
centrally patterned motor output.
Recent studies by Engberg and Lundberg (1969), correlating EMG activities
of the flexors and extensors of the cat's hindlimb in normal walking,
found that
the onset of extensor activity during placement of the paw actually precedes
contact with the floor.
Hence it could not have been produced by proprioceptive
feedback from spindle afferents.
trally programmed.
It was concluded that stepping motion is cen-
Peripheral feedback may augment and modify this activity,
but does not initiate or maintain it.
In contrast to the apparently supplementary and compensatory role it
serves in normal volitional movements, the afferent feedback loop appears to
exert a heavy influence upon the
a-motoneuronal pool in a spastic muscle.
The
hyperactive tonic stretch reflex reflects an abnormally heavy inflow in the
gamma system, leading to the high reflex gain.
It is also plausible that it
is the loss of descending presynaptic inhibitory influence, or a release of
descending, supraspinal, facilitory lines converging on the afferent pathways,
together with some degree of gamma support, that is responsible for the spastic
reaction to passive stretch.
-11-
This is plausible in the light of considerable experimental evidence
(Lundberg, 1962; 1967) which suggests that most segmental pathways between
primary afferents and motoneurones receive convergent inputs from descending
systems.
Thus, for instance, the interneurones that mediate Group Ia inhibi-
tory influence on an antagonist flexor muscle were shown to receive, monosynaptically, axons originating from the Deiter's nucleus and descending
in the vestibulospinal tract.
And Group Ia inhibitory interneurones projecting
to both flexor and extensor muscles are excited by fibres in the rubrospinal
tract (Hongo, 1969), and, in fact, with longer latency, by axons of the corticospinal tract (Lundberg, 1962).
According to these observations, the inter-
ruption of this type of descending supraspinal projections, as in spasticity,
would lead to a state of hyper-reflexia.
At the same time, it would explain
the concommitant deficiency in reciprocal inhibition in antagonist muscles.
1.3
Related Research
Bomze (1973) developed an elaborate hydraulic system for studying spasticity in the biceps.
His data, as well as Leavitt and Beasley's (1964)
suggests that patient data are highly variable, and depend on mood, cigarettes,
and inadvertent tactile stimulation during testing.
Measurements of resistance
in spasticity were complicated by voluntary non-reflex components of tension
in studies by Herman (1970), while tests utilizing EMG such as reported by
Burke et al (1971) with sinusoidal stretches of the hamstring and quadriceps
yielded valuable phase relationships, pointing to the dynamic and tonic components of the stretch reflex, but little quantitative force measurements.
Dmitrijevic and Nathan (1967) did extensive clinical observations of spastic patients with spinal cord injury.
However,
and only phasic tendon jerk stimuli were given.
ponses that spread to other muscles.
again only EMG were recorded
They reported exaggerated res-
-12-
Neilson (1972) worked with athetoid-spastic patients and used elaborate
statistical methods for data reduction.
Frequency response characteristics
of the tonic stretch reflex in both normal and spastic subjects were obtained
with the subjects sustaining various levels of voluntary contraction of the
biceps brachii.
Correlation techniques were used to get rid of the voluntary
components of reaction and the results indicated the gain of the tonic stretch
reflex increased with the level of voluntary contraction in normal subjects,
but remained at a high constant
level in spastic patients.
Also the gain
versus frequency curves for normal subjects contained sharply tuned resonant
peaks, pointing to rather complex long loop pathways in the reflex.
Patient
data did not show such peaks, suggesting the loss of complex supraspinal loops
as well as descending spinal influence in spastic patients.
Study of tonic vibration reflex by Hagbarth and Eklund (1968) and
Burke and Ashby (1971) also point to similar conclusions.
Vibrations were
found to suppress the monsynaptic reflex and the H reflex in normal subjects,
whereas the suppression is less in spastic patients, indicating a loss of
spinal presynaptic inhibitory mechanism.
Hyperactivity in the gamma system appears to be a necessary condition
for the exaggerated stretch reflex in spasticity.
Rushworth (1969) showed
that in the decerebrate cat, selective block of gamma fibres abolished the
rigidity and stretch reflex.
In man, he reported that 1% procaine applied
around the major nerve trunk abolished hyperactive stretch reflexes without
affecting voluntary motor power.
-13-
CHAPTER 2
EXPERIMENTAL DESIGN
General Description
2.1
The particular muscles selected for clinical evaluation were the
pronators of the forearm, the pronator teres and the pronator quadratus.
The choice was based on the fact that rotation of the forearm can be
easily performed and is often used by physicians in qualitative assessments of spastic patients.
The forearm is also less often interfered
with by prior corrective surgery as is often the case with the ankle
joint.
An existing arm movement (humeral rotation) device was modified into
a servo-controlled manipulator of the forearm.
A high torque motor is
mounted vertically in an aluminum block which also houses a 6:1 step down
gear train.
The stall torque at the output handle is approximately 350
lb-in (Allum, 1974).
A spade type handle (Figure 2.1) is attached to the output shaft.
Strain gauges on the integral torsion tube of the handle register the subject 's muscular reaction.
Separate feedback and measurement potentiometers are attached using
anti-backlash gears.
A separate measurement potentiometer was used to
reduce the effect of slack present in the gear train between the motor
output and the final geared down output shaft.
-14-
The motor is servo-controlled with the control circuits on an analog
computer (GPS 290T) and is driven by a pulse-width modulated power supply.
Microposition switches cut off the power to the motor in case the handle
exceeds about 800 of rotation in either the pronation or supination direction.
Mechanical stops also prevent such excessive excursions should the
electric stops fail.
This entire structure with the motor, gears, handle, strain gauge
electronics and two 60 Hz filters for the input and feedback signals is
mounted on a heavy metal stand.
A horizontal beam attached to the stand
has on its distal end a movable elbow cup which serves to support the
subject's elbow as well as align his ulna with the axis of rotation.
A modified dental chair is used which allows for the proper positioning
and posturing of the subject.
Shoulder harnesses are employed to provide
a certain amount of restraint and support for the subject and are especially
useful for some of the patients.
The surface electrodes used were buffer-amplified types (Jacobssen).
Grass P5-AC preamplifiers were used.
EMG signals were recorded from the
pronator teres, the powerful pronator of the forearm, and the biceps brachii,
which is employed in supination.
EMG signals were full-wave rectified and
filtered on the analog computer.
Arm angle, torque and two channels of EMG were recorded on a four
channel strip chart recorder (Brush) and the torque was plotted against arm
angle on an X-Y plotter (Moseley Model 135).
Figure 2.2
shows some of the
experimental set up and equipment.
2.2
Motor Servocontrol
The motor servomechanism consists of a positional feedback and a pulse
width modulated power supply (Figure 2.3).
If a simple unity feedback gain
-15-
is used without any series compensation, the system dynamics is very sluggish and the output impedance is too high for any reasonably heavy load.
Thus lead compensators were used in both the forward and feedback paths
and a high feedback gain is used so that the system now has a response time
of about 450 milliseconds.
It has
negligible overshoot and is fairly unFigure 2.4 shows the uncompensated
affected by disturbance in the output.
and compensated time responses.
Note that the dynamics are very accurate
for step and ramp inputs (Figure 2.5).
The reduced third order model for the motor system has the transfer
function:
E)(s)
=
I
)2
(
n
K -(S+
-S
( + a) S2 + 2Cw +W
n
where
w
n
=
= 25 rad/sec
a
= 0.7
2
fl
137 rad/sec
= 56.6 rad/sec
The motor control and compensation circuits are shown in Figure 2.6.
The
detailed derivation can be found in Allum's thesis (1974).
The error (control) signal modulates
nominal frequency of
1 kHz.
a ± 35 volt square wave with a
Since there is an inherent instability in the
flipflop stage of the modulator preamplifier which causes the square wave
to saturate to a constant 35 V level of the opposite sign, the input has to
be limited so that saturation never occurs.
This does not happen in any
case except at the edge of a step which has been lead compensated.
Both the control and feedback signals are filtered (first order filtered,
break frequency 40 Hz) to reduce the effect of 60 Hz noise.
-16-
Measurement Devices
2.3
The method for measuring the subject's muscular force was to use the
torsion in the tube part of the spade handle.
The design of a torsion tube
requires that it have sufficient sensitivity to torsional stress.
A hollow
tube of a high enough sensitivity would have a wall so thin that it would
be very susceptible to the bending mode.
Instead a slit tube of one inch
outer diameter and 1/32 inch thickness was bored into the integral part of
the handle that fits over the motor shaft.
The slit effectively interrupts
the shear flow and drastically reduces its torsional stiffness.
The derivation of the stress-strain characteristics of the tube is
quite involved due to the complex boundary conditions.
Figure 2.7 shows the
bridge and amplifier circuits.
Four BLH film gauges are attached to the center portion of the tube and
are arranged in a push-pull bridge configuration.
is 5 volts.
Thus
V
gauge
where R
Factor
=
=
120 ohm,
2.
The bridge input voltage
= V. AR/R
i
V. = 5 volts, AR/R = (Gauge Factor) x 6, and Gauge
Thus Vgauge = 10s, where
e is the strain carried by the gauges.
The bridge output is amplified 104 times and the calibration curve (Figure 2.8)
shows a slope of 0.21 V/lb-in with good linearity.
hanging weights.
5
Therefore, V
output
= 10 5,
Calibration was done with
and the actual strain per lb-in
is 2.1 x 10-6 which is approximately the theoretical value calculated.
Since
the maximum torque is not expected to be over 50 lb-in, the maximum strain will
be less than
aluminum.
10
4, which is within the elastic strain limit of 10 3 for
-17-
The measurement potentiometer is a Helipot (3 turn, 20K).
The calib-
ration curve is shown in Figure 2.9 and has a slope of 90 mV/deg.
The
Jacobssen electrodes require a ± 5 volt supply and have a mid-frequency gain
of 350.
They have a built-in low frequency roll off (20 dB/decade) with
break frequency at 50 Hz and a high frequency first order roll-off breaking
at 5 kHz.
The integral FET buffer amplifier produces a better signal to
noise ratio.
The Grass P5-AC preamplifiers have gain of about 20 and have
first order roll-offs at 35 Hz and 2 kHz.
Raw EMG signals are full-wave rectified and first order filtered to
The processor circuit is shown in Figure 2.10.
simulate peak-followers.
Figure 2.11 shows some typical raw and filtered EMG.
The filter time con-
stant was about 100 msec.
The pronator quadratus and the supinator are the primary muscles
involved in the rotation of the forearm, however they are imbedded among
other forearm muscles.
Thus the pronator teres and the biceps brachii are
used.
2.4
Safety Precautions
The safety shutoff mechanism consists of a relay box and a bell which
is excited when the motor power is cut off.
This is important since the motor
has more than enough torque to overpower the forearm.
Four switches can trip the relay:
the two microposition switches on the
motor chassis, a switch on the analog computer, and a hand-held panic button.
The microswitches are mounted on aluminum brackets and a one-inch steel rod
attached radially to the handle shaft will contact the switches should the
-18-
rotation exceed approximately 800 from the vertical in either direction.
In the unlikely case that these switches fail, the steel rod will hit the
brackets and the handle will be stopped mechanically.
A further safety device is used on patients who exhibit a continuously
contracted fist.
Since these patients may not be able to let go of the
handle in case the movement is in fact causing pain, an electronic circuit
on the analog computer is used to monitor force level.
This will switch
off the power should the force exceed a certain preset level.
The torque output from the gauges is summed with the reference level
and feeds a comparator.
When the torque becomes larger than the reference,
the comparator output becomes 0 V so that the Set input of the SR flipflop
is grounded, setting the ONE output to -3 V.
The output converter converts
the -3 V to 6 V which feeds an electronic switch and open-circuits the 10 V
power supply voltage to the relay, thereby cutting the power to the motor.
The flipflop output will remain at -3 V and the power remain cutoff until
the reset input is grounded via a Clear switch.
With the flipflop in the
low state, as long as the torque is less than the safety level, the comparator output will be at 6 V and the Set input of the flipflop will be at -3 V.
The flipflop output will thus be at 0 V so that the electronic switch will
remain closed and power will be delivered to the motor.
in Figure 2.12.
The circuit is shown
-19-
steel r od for
triggering s afety
switch
L5
V94V~e
FIG.2.1,-
Diagram showing. dimensions for the instrumented
spade handle and strain-gauge bridge circuit.
-20-
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FIGURE
2.2-
Pictures showing experimental
cquipment.
Compens ator
Motor
INPUT
Error-signal
Limiter
Pulse-width
Modulated
Power-Supply
Safety
Cutoff
Feedback
FIGURE 2.3
- Block Diagram of Servo-controlled Manipulator Drive System.
motor
angle
-22-
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t-4
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-
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-- -
~
System time response. Top traces with unity
feedback and no compensation. Lower traces
with input and feedback compensators.
.
i -I
..I I
-23-
LilI-
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I
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I
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I
I
-
f
I
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1I
- 20'
- I- -
-I - -I-
pron
I
I
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I
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-100
msec
I
L-
- -- I.--A --- I -- -I--
I i
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I -I I- 1 -1
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I
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TI
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--I----I* III:- ~~~~1~~~~
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1~~
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--
isec
-
-
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"I
-
----
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-
I---I-I
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i-ti-i--if-I~I1iIii~i~
I
I
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71
7?
~4
__-K1----~
-
71
__
//
.0
I
/
C6' VI,,P
K1irLLj~~
FIG. 2.5
-
Compensated systens dynamics.
I ~
___
Top traces show
step response; bottom traces response to
triangular wave.
Bias
-10.0
Input
Waveform
1/s1
1To
B Las
Error
Limiter
1.0
~11
An
Fe Edback
137
FIGURE
2.6
- Circuit Diagram for Input (Top) and Feedback (Bottom) Compensatorso
Battery switch
1M
Strain gauge
56K
50K
-15
Wheatstone bridge
Gauge switch
V.
6 v0
5. 11K
56K
25K
LO
CN
'
3
R vR
2
2
4
.
--
K
Output
-103 (v
2
50K
Bridge
Excitation
adjustment
Trimpot
balance
S+15 v
1K
FIG.
2.7 - Circuit for strain gauge bridge and amplifier.
-
rrrP
Volts
------- -- -- -
.......
_ _---_
-6-..
S--.
I
- 5
4.
-
.
.
.~
-
I
____
____
tI
____
1
20
1
4_____
.4
I_15
-IL
.... .. .
.
---
I S4
41
10
Lope
I
0,
-21--Yol 1 s/lb
UPinat ion
~~~~1~*~~
f
1:
51
2025
L
I
II
-3
.1
.4
1
3~0
-j-orq e- (l-in-
-2
I
I
15
4:1
-
25
-I
I
jI
__
1
Pronation
.1.
II.:;..
I
-__
_____
-
.*i*<y.KIY~<.I11
K:
I..fjl
.1
.1
_
____
-~-
I
__
....
I'
:1::
'7-
:.
TiI
-7 :_-7 -7
-.
* IG, 2. 8
-
Calibration Curve --f'or-S train. Gauge -Amplifier Output-----
I
____
I
T~4-
1
iI.....i I
-
... ._._....
_ .. .
sOJ ts/degrel
------------_
_
_
_
_
_
_
_77-
__
I
__
__
__
__
K***i
-----------
-L
75
-- 7
dl~e
is1,5
0.
i
7;~-
7~7i7IiI
0
-300
77-i
_
7_11A1Mr
___
-4I
i t
1
4-
7-747
1
14
FIG
2 9
----
Clbaoncurve---for -the -Arm-angle: me asurem enL -potenti.oieter
K-v-4
t
-. 7
--1ComparRaw
nc
Fator
no
E MG
10/s
Electronic
Switch
00
0.1
Full-Wave Rectifier
FIG.
2.10
-
Filter
Circuit for EMG Processor with Full-wave Rectification and
First-order Filter.
--
-29-
W71.
111 I
I I I
iji jIA
1
fr~ L
-1
11..
I -+-------1----I--I -I-f-I
I
I
I
111
I
~I ___ I ___ ~
I_
, [-I
1 1
*.
ba
,ws
-1-----I--f-'I-- I
I
I
Th~
-
I
-.
Fill- -F-i-_
44-{ 4+
-
-
-
.- I
I I 'liii
2V-
.A.
1
E
G
11 2. I - Raw EMG and
filtered
EMG. Top
two
traces
from
Pronator
from
traces
two
Biceps Brachii. Lower
Terres.
Records taken together to show action
of reciprocal innervation.
RELAY
POWER
-
MOTOR
nc
>O
+10V>c
Motor Power
no
Switch
Electronic
Switch
FlipFlop
TorqueSR
Comparator
Re
--
Input
Convert,---6V->;o - 3V
1
S
R
0
Output
Convert.-3V -+ 6V
.
Reset Switch
FIG. 2.12
- Circuit diagram for force-level safety monitor and motor cutoff
- ---1lr't 11'
,
I 1 -1
_f,
-31-
CHAPTER 3
EXPERIMENTS ON NORMAL SUBJECTS
3.1
Experimental Protocol
The following experiments were designed to study the tonic stretch
reflex in the forearm of normal subjects.
These results shall thus pro-
vide a valuable basis for comparison with those of spastically afflicted
patients.
The tonic stretch reflex, which is hyperactive in spasticitiy and more
easily demonstrable in decerebrate
animal preparations, is usually absent
or very small in the relaxed muscle of normals.
Monosynaptic reflexes to
highly phasic stimuli such as tendon tap may be elicitable in the normal
relaxed muscle, but reflexes with longer and more complex pathways appear to
be under conscious control and can be voluntarily modified and suppressed.
Thus it is difficult to
patients.
obtain results comparable to that from spastic
Even with methods that produce muscular responses resembling
stretch reflexes, it is still difficult to evaluate and interpret the experimental results.
They do however provide a qualitative basis for comparison.
The experiments involved the controlled pronation or the supination of
the forearm.
Movement waveforms included steps and terminated ramps.
sions were usually 45 degrees from the vertical.
Excur-
The subject was asked to
-32-
maintain prestretch isometric contraction in the muscles to be tested, that
is, the pronators or supinators.
The timing of the movement cycles was
randomized to minimize prediction on the part of the subject.
The subject was seated upright on the adjustable dental chair, with
the humerus abducted about 150 from the vertical.
The movable elbow cup
aligned his ulna with the axis of rotation and the height of the chair was
adjusted so that his elbow joint roughly subtended an angle of 1100.
EMG
electrodes were attached to the biceps brachii or the pronator teres and
the subject was told to hold the spade handle.
The experimental variables included:
1.
Velocity of stretch which varied from about 850 /sec (the
approximately linear response to a step input) to terminated
ramps of approximately 450 /sec and 200 /sec.
2.
Initial prestretch condition.
Subjects were required to
maintain different levels of isometric contraction before
stretch of 5, 10, 15 and 20 lb-in of torque.
The torque
was displayed to the subject on a small calibrated meter.
A few experiments were performed where the prestretch bias force was
maintained,
but with the forearm undergoing a slow movement in the direction
of the bias force, before the forearm was stretched in the opposite direction.
Results do not indicate any significant differences.
angles were also tried.
Different initial arm
The effects, if any, were small.
The recorded measurements were:
1.
Arm angle
2.
Torque supplied by the forearm
3.
Raw EMG from the biceps brachii (a supinator) and pronator teres
4.
Filtered EMG signals
-33-
These were displayed on a four-channel strip chart and force versus arm angle
diagrams were obtained on an X-Y plotter.
3.2
Experimental Results
The activated muscle
Precise instructions to the subject were difficult.
with increased alpha and gamma activity is known to facilitate the stretch
reflex in normals.
This can be achieved by isometric contraction.
The muscu-
lar response, however, is still dependent on the instructions given to the
subject so that some reflex components are not consistently present and are
not readily distinguishable from voluntary contraction.
Initially, experiments were run with the subject being told to-relax the
forearm, but not let go of the handle, as fast as possible after the stretch
was administered.
In this way, the voluntary component of resistance was
thought to be minimized or eliminated.
Figures 3.1 and 3.2 show the typical time history of response.
stretch EMG activity was due to isometric contraction.
As can be seen, a
short latency EMG burst of about 40 msec is usually present.
to a monosynaptic reflex pathway.
The pre-
This may be due
EMG activity decreases after about 70 msec,
indicating relaxation in accordance with the instructions.
A burst of renewed
ENG activity often occurs at about 120 msec, concomittant with or slightly
trailing the peak of the reaction force.
The force increases instantaneously
with the start of the stretch, before any change in the EMG.
to the visco-elastic property of the activated muscle.
This must be due
The reaction force is
very smooth and does not shown any "humps" in response to the EMG bursts.
Figures 3.3, 3.4 and 3.5 show typical force angle hysteresis loops for
these experiments.
The smooth linear rise in force is due to the elastic
-34-
property of the contracted muscle.
These plots were obtained real-time,
where usually the second applied stretch was recorded, and thereafter,
alternate cycles were selected for display.
Invariably, the first cycle
shows a longer relaxation time and hence reached a higher force level.
The spring constant for the activated muscle, as reflected in the
slope of the force-angle diagrams, increases with the level of isometric
contraction.
Figures 3.3 and 3.4 show the hysteresis loops for two stretch
speeds for the same subject.
dependent on stretch speed.
As expected, the spring constants are not
Figure 3.6 shows the spring constant as a func-
tion of isometric pre-stretch force level for three subjects.
The stretch
in these cases was &510/sec ramps in response to. step inputs.
Control experiments were performed with the subject's forearm relaxed
and the subject instructed to resist the movement as fast as possible. Figure
3.7 shows two representative time courses of response.
Response time, as
indicated by the onset of EMG activity is about 120 msec with very small
variance from subject to subject.
This figure is substantially smaller than
Allum's (1974) results with humeral rotation where voluntary response was
interpreted to have a latency of about 225 msec.
Evarts (personal communica-
tion) however found a voluntary component in pronation and supination as fast
as 70 msec.
As reported in the first set of experiments, there is usually a 120 msec
EMG burst which appears to be involuntary and comes after EMG activity has in
fact decreased to a very low level.
Thus this 120 msec latency response may
in fact represent a long supra-spinal reflex
loop which
is biased on during
the voluntary resistance task and which is also activated by pre-stretch isometric contraction.
In the latter case, its reflex action to stretch appar-
ently occurs even after conscious relaxation of the muscle.
-35-
Two other experimental conditions were tried.
contraction was again required of the subject.
Pre-stretch isometric
Post-stretch instructions
were changed in one case to voluntary resistance to stretch.
shows some typical results.
Figure 3.8
The fastest component of response is again
about 40 msec which is probably monsynaptic, and a long latency component
at approximately 120 msec.
In a few cases, an intermediate latency response
(about 80 msec) can be discerned.
The peak force reached was much higher.
However, the force increase was again very smooth in most cases.
Another set of experiments was run where the instruction was not to
relax, but also not to consciously resist movement.
The instruction is
somewhat ambiguous, but results again revealed a 40 msec reflex and a 120
msec main burst.
The peak force is lower than in the case of voluntary
resistance, but is sustained longer than in the case of conscious relaxation.
Figures 3.9, 3.10, and 3.11 contain typical time history and force-displacement
loops for this test condition.
Figures 3.12, 3.13, and 3.14 contain force displacement hysteresis loop
diagrams from three different subjects comparing the response to the three
test instructions.
As expected, the spring constants, which are the initial
slopes of the loops, are essentially
identical in the three cases.
The
reaction force is higher in the case of conscious resistance, however the
force increase in all cases was smooth.
3.3
Summary
Results on the tonic stretch reflex in normals were obtained.
Precise
instructions were difficult and the subject's response varies accordingly.
-36-
In all three cases, pre-stretch isometric contraction was needed to elicit
a stretch reflex.
With higher velocities of stretch, namely 850 /sec and
45 /sec, there is present in most cases a 40 msec monosynaptic reflex and a
120 msec delayed main component of EMG activity.
This is true under all
three test instructions, although in the case of conscious relaxation, the
120 msec burst occurs after EMG activity has actually declined in accordance
with the instruction to relax.
Thus it appears that the 120 msec EMG activity
is probably reflex in nature and is biased on even in the case of voluntary
resistance without prestretch isometric contraction.
It is unlikely that
this burst represents a conscious maneuver, say to regain grip on the handle,
since if that were the case, the burst will have a minimum delay of 120 msec
after relaxation began.
The spring constant of the activated muscle is not dependent on velocity
of stretch or instructions to the subject.
It increases however with the
level of prestretch isometric contraction.
The force-angle hysteresis loop diagrams are of different shape according
to test instructions.
However, they all exhibit smooth and even slopes.
They
do not contain segments of noticeably different slopes in the region of increasing force.
This feature is not expected to be found in measurements
of spastic patients.
-37-
i-1t~Fii1I'~H'~
_I
_______
'1
7~I~7'F
-~
- ---
-
-1
-
_-
1O-Ilb-inn
-
--
I I I~I I ~
-
- -
-
-
-
-
-
I~LILLi
-
~1~
I
-h+-'
FE -I-i~tiIijij
-
Li2__(1)(Z)
~4
(13Y
I
I
-
t
I
I----
I
S ms1~
1 1T1.I
11
-
j
j.-
If
Pronator
Teres
-T-1
-4L
FIG.
I111I
I I I
T~1~~~f.Ti _J1
!......
0 0 -ms
-
-
iII7
711
-1
-
--
3.1 - Response to 85 /sec stretch with instruction
to relax as fast as possible. Trace 1, angle;
trace 2,
torque;
trace 3,
raw EMG; trace 4,
integrated EMG.
Arrow l indicate timing of start
of stretch,
indicates short latency burst
(2)
and (3) shows long latency (120mscc) burst.
Irregularity in angle trace is due to pot noise.
-38-
YORK
:1
II
I
I
iii:
'FFF
ZJIlIiIIIII1IiTVPTh
1 1 1 1~
1'
_
_
I I
1
I
hi PHi
fi
114
I I
ZiI'I~K
-
-
-
.
-
71]itIT
-~
5...sUp~.
I
Iii'
I
-I----I--I-----I-----1---]-I-- -I.--- I--- -I
I -- I---I----4--I----t--- ---I -4----]
-
___
-
i
4b
.7
-
I~
~
-
r
1}iiLj iyhih
___________j
1' 1
3Fd~.L~
-
-
11
-
-
zHizi.L1 .Jzz1
__
-----I--]-----I--I-
-
ms
0-0Teres
FIG.3.2
-
Pronator
-
-
-
Response to 85 0 /sec stretch with instruction
to relax as fast as possible.
4
,p.
i
:.
_ _
p_
I
20
Im
t:
7
-7
7T
77____
-. '-'
7~"i
-4
nhaedretoo
ws t aspossbl0
relx a soo
Instucton
/sec.~
stec.Arw ~~
1
.1
rvlo
op
-
...
7
.......
-f
7
7-
I.
I
+
1;
I-
-
7
-7:',-
-
-
;
-
--
-
-
I
_
-
--
-
-
-7
-
-
10-
1'
;
-
in
0FIG.
3.4
Response to 20 /sec. stretch. Instruction was to relax consciously.
as fast as possible after stretch.
.
.........
..........
..........
77
.....
.. ............
...
...
.... ...
.....
..
...
...
-
-Arm
rl
Ow
V
rt
%A\-
7N
..........
......
..
. ... ...
.............
LAI
XX
WR
-
.... ...
V:
Al
V
Lo
4J
- ---------
-4J
4-)
Ln
4J
o
444
Ln
........0 1 H
Ln'
...........
K
--
sprin'g-constatt:
in/deg
__
*' .i**...
-- -----
------ -----__-lb
_
H
___
~
I-
7.I.'7-I7
~~IiI~
. ~ I.
-----. I......
.1
__
_
___
_-7
-:0-1-__2-
7K
-- --
*1
---_-
- --
- ---
-
----
-- 45
---
_______
__
___
-1 ___i7tT~
1
_--__1
I
_5_--
I
-4 ''
Lw-
,
L
-1
*
-1
_2d
F ismetrc cotracionievei
lbin,
7 Muscle spring constant~ as a
0uc b fpre-seretch :.
I..
i
i
I
.1
t
~
it!
mti
'--contraction .. level .?-oints ~&averages: of....atlea-st__ foturyc.1e.4
- --Data f or th ree subj cts,
.
1
VHfl7i7~
i
FG:3.6
,.
* j.777
and' stretch' speed wa5 85 /se6,
I
?
-43-
FT
7
45profl'p_
-f
-~
*1II *j}
~.41II. jiff
I
-~-1 ~[ 1 1 1 1 I 1
I
1 1 ~II
I --1---1-[-f---I----4-----I------I
I
I
I
I
5-
-
h{-
-~y±
I
-
I -I---I----4--I-----f----1----f---I----I
~rach"i-7
---1-
00
-
I
-
1I
I
[JfI
--
~
I
I
-1L4
___
-I---I----f----f
- --
I
-[
I
I
I
II
t
--
-.-.
-
Ill-
-
3
FIG. 3.7
~~1~~
I----1---i---1-I---I.-.-I --I
--
-
I
~iI II 'I I II
-
b n
t* -4.
I
'I'l-~ -i-~i-i7I--1--I-~ I I Fv-i-I-i-K 0
I
.
l~
-
Response to 85 0 /sec stretch, voluntary
resistance to stretch with no prestretch
isometric activity.
-44-
F 11111
JZLLLLLL
11 ~II17~~
7
F I ~ I 'I I
-7
Ff
-P1
30
------
5.
n...I
----
- -------- I--- ----- --ps- I -
-----
i
-I--I ----
LJJ~~~]
~TT7.
L1~
ET
;I-L
Hi-,,
~
__________________-I
(x)
--
i---'
H a)
Ci)t~.)
I
1
~
I
*
3.8
- Response to 85 0 /sec.
I-
11.11
~
-*--.
I
FIG.
I
--I------I- I-
-
V.F-
1
I I'i 'j ~
____________
Cl)2)
'-
I -I-I
I
I
I
stretch; instruction was
to resist consciously.
5 lb-in prestretch
isometric contraction. Arrows (1)
for start of
for short latency ; (3) for long
latency bursts. (x) indicates intermediate burst.
stretch; (2)
-45-
I~
i~~ILrr
--
o.p
-
--
-.-
1
-4
F-
---
lbV-in
mI*I--[--{-*-*---II--
I
--
I-
Me,1-- I
F
I
i00ms-
rr
Biceps
I
Brachii
-4.0
li-I I
+3142
i 4
FIG. 3.9
I
I
I
I
I
I
I
~'T'"T
Response to 85 /sec. stretch. Instruction to
not relax or resist consciously. Arrows 1
show start of stretch, 2 show short latency
burst, 3 indicate long lantency burst.
-f-77--
. .....
..... ..........
--J
.
.....
....
T A
..... . .... ....
...
7T
.. .... ...
... ..
. . ..
. .. .
. . . .
a
...... .... ..I . .... ....
TI.... ..
........ .....
.... .... ...
.. .... .
.... .... .. . .... .... ...I .... ...
.... .........
.. .... ....
............
1-7
;iZ
.... .. . .... .
.... .... ....
'77
.
.. ...
....
... .... .... ....
.... ....
.. .... ....
I
a
. .... .... ...
T
PI/,
L------
7: - 7 .
.
...
.... .... .... ..
... ...... ... .... .... ....
. ... .... ....
... ...
--------77
45 sup
'r0
m%4-
1%
T
17
k"
e-. 4-! 4-rk
v-k%
----- [777 7-
....
%F in V,
0
rga a
t-
TI
eq.A e%
a
T
.
.
t
ir
-7
7
~-
L
1 T.
..
7_
S7P
145
FI
4FI.374
-7---77-
i
3
s u
dc
teeSbetwa
0t
-0-
- odntt
ea
rrss
-
-- -
-
--
--
-
.... ..
...
4 ..........
. . . ..
. . .
1
.......
~
.....
I
-----------
Co
__
__71{i7
-.-
.
7....
.~.. .
-
I
. . .. . . . . . . . . .. .
0
FIG. 3.12- 45 /sec. stretch. Top three traces voluntary resistanceA-middle two,
traces not consciously resisting or relaxing; lower traces relaxation,
.
* ~. .. . .
.....
1
.......
7
7-
7.
.....
--------
-- 7-7-
7
..
.
7-
J -
II
45.
s.
0
F'IG.
3. 13
8 5 /sec.
stretch.I
I
7
7-
.~ ..
...
0
. .
. .. .........
- ------------
....... ....
...
. .. . . . .
-7
. . . .. . .
. . . .. . .
- -- - - - - - - -
. .. . . .
7
. . . .. .
. . . . . .. .
. . . . . .
It
-- - - - - -- -- -
.
.......
..
A
m
:A
... ... ..
7
w.
7
....
. ....... ....... .. ...
7.
.7
..
......
---------
a
I
:7-7-T---7-
t-n
0
I
-7
7-
r
L
1-4 -r'i RES IS,T
01
,E/A)(
7
.77
I
r
'00;.
-7
.. .... ...
....
-PEtAX
A:
--- f7-7
.177-7 -7
... ...
77 '77
------------
.... ....
16
......
Aa".41
-
.450
FIG.
3 14
0
-85:,./sec.-.stre ch%---
FJA
-51-
CHAPTER 4
EXPERIMENTS ON SPASTIC PATIENTS
Experimental Protocol
4.1
Special precautions were observed in experiments with patients.
It
was observed that patients will often shift the position of their torso to
accomodate the stretching of the forearm.
Thus shoulder harnesses were used
to somewhat restrain this motion, but without causing undue discomfort.
Also,
the force level monitor and cutoff switch (Chapter 2) was used to prevent
excessive force from developing.
Trapezoidal stretches with speeds of approximately 20, 45, 90, and 135
degrees/second were given.
The range of motion was determined before the
actual experiments by manually controlling the voltage from a motor position
bias potentiometer.
In this way, a slow and smooth rotation of the forearm
can be achieved; and the patient was asked to report any excessive stiffness
or pain that was induced.
obtained.
An initial estimate of motion range was thus
Faster movements were then given to make sure that the range
was not excessive for higher speeds.
The measurements taken were again arm angle, reaction torque, EMG from
the pronator teres, and EMG from the biceps brachii.
recorded on tape as well as on a strip-chart.
Measurements were
Torque versus angle hsyter-
esis loops were again obtained on an XY-plotter.
-52-
the patient was told to relax as much as possible and allow his forearm to be
passively rotated.
speeds.
About 12 to 15 cycles were used for each of the four
Stretches were given first in order of increasing speeds, with a
About 5 cycles per
rest period of about 5 minutes in between these groups.
group were then applied in reverse order of speed in order to observe any
correlated or adaptation effects.
Experimental Results on Passive Stretch
4.2
Patient J.K., male, age 33, had been diagnosed as left hemiplegic.
The
results showed spasticity of the supinator muscles, and to a milder degree, of
the pronators.
The preoators, in particular, showed spastic reactions that
were more pronounced when stretched at higher speeds.
For both pronators and
supinators, muscular responses were highly variable from cycle to cycle, but
did not show any
trend toward adaptation.
EMGs were taken from the pronator teres, which is more superficial, even
though the pronator quadratus is usually more active.
However, the signal
suffers- from contaminating discharges from other flexor muscles of the hand.
This is particularly a problem in spastic patients whose reactions more often
than not, involve several muscles at the same time.
Figure 4.1 defines some of the quantities and variables that appear in
subsequent time records.
Figures 4.2 through 4.5 show typical responses for
stretches of 20 deg/sec.
At this speed,
stiffness.
the pronators exhibit very little
With the forearm in the maximally pronated position, there is
usually a rapid decline in the biceps EMG, along with a similar drop in force,
indicating relaxation of the biceps immediately following stretch.
With the
start of linear stretch in the supination direction (Phase 1, Figure 4.1), the
force records invariably show a small reaction force with no increase in pronator EMG (Figures 4a, 5a, these designations refer to events marked in the
-53-
respective figures).
This probably represents a combination of the static
weight of the forearm and the stiffness in the flexor muscles of the hand.
The force reduces to zero as the arm appraoches the vertical position (see
Figure 4b, 5b).
The pronator EMG, meanwhile, remains at the same level, or
in the region about the
in some cycles actually decreases to a lower level,
vertical.
The EMG starts to increaseas, or shortly after (Figures 2a, 3a, 4c
and 5c) the arm goes into supination (Phase 2).
around maximum supination (Figure 4d).
It peaks with the force
The pronator EMG and force drop only
slightly during static extension.
The pronator EMG (Figures 2b, 3b) continues to decay as the arm moves
toward pronation (Phase 3), but does not reach a low level until the arm is
nearly vertical (Figures 2c, 4e).
Biceps EMG and supinator force usually
show no immediate rise (Figures 3c, 4f) as the arm moves from the maximal
supinated position (Phase 3).
They then undergo a big increase (Figures 2d,
4g) as the arm goes through the vertical into pronation (Phase 4).
This in-
crease is usually accompanied by either a rise in the slope of the torque
record, or in some cases, by almost a step change in the supinator force. The
biceps EMG peaks, with the resultant force, slightly before maximum pronation
and decays rapidly in the stationary flexed position.
The pronator EMG activity decreases as the forearm was moved from the
maximum pronated toward the vertical position (Phase 1).
This occurred even
though the pronators are being stretched during this phase.
As the arm goes
into supination (Phase 2), the pronators begin to resist and the resistance is
maintained during the period of static-extension.
In fact, it continues even
when the supinated arm begins to pronate towards the vertical position.
This
happens despite the fact that the pronators are now in fact in the shortening
phase.
Thus the pronators appear to be activated when the forearm is in any
supinated position.
-54-
EMG
The biceps, on the other hand, appears to behave quite differently.
activity and supination force rise as soon as the arm moves in the direction
This is true even when the arm is in a supinated position as
of pronation.
during Phase 3.
The EMG and force shows an increase as the forearm goes into
pronation (Phase 4).
They then decay rapidly during static pronation, and
remain at a low level as the arm rotates towards supination (Phase 1).
During
this phase, the biceps is shortening even though it is still in stretch.
Hence,
it appears to be primarily sensitive to velocity of stretch; and when that condition is met, as during Phase 4, it receives reinforcement from a static stretch
sensitive component of resistance.
Thus, at this slow speed, at least, the pronators appear to be sensitive
to position of stretch and hence their EMG are in phase with the angle record.
The supinators, or at least the biceps, appear to be most sensitive if stretched
in the pronated region.
Thus their EMG usually leads the arm angle by 900.
Figures 4.6 through 4.10 show typical records of response for higher stretch
velocities.
tests.
Both the pronators and the supinators become more spastic in these
This is revealed in the average level of reaction force, although the
stiffness still varied significantly from cycle to cycle.
The phase relationships described above still obtain for the biceps.
is shown inFigures 6a, 7a, 8a, 10a, and 10b.
This
In several cycles, the biceps
develop some level of excitation during rotation towards supination (Phase 2),
as seen in Figures 6d and 8c.
This is however almost certainly due to coacti-
vation with the large pronator activity at those instants.
The pure positional dependence of the pronator EMG, however, is observed
only at Figures 6b and 6c.
At Figures 8b, 9a and 10c for instance,
the
pronator exhibited velocity sensitivity similar to that observed in the
-55-
biceps: EMG activity increases simultaneously with the start of movement
towards supination (Phase 1), and undergoes another increase as the arm is
led into supination (Phase 2).
In Fig. 8[b],
the early EMG signals (during
Phase 1) may be attributable to the activity in the biceps.
However, this
is not the case in Fig. 9[a] or 10[c], where biceps activity was in fact
constant and low.
Thus a velocity sensitive component is present in the
pronator reaction to fast stretches.
Fig. 4.11 shows a stretch cycle at 135*/sec. with an expanded time scale.
In this cycle at least, the pattern of the pronator's positional and the
biceps' velocity sensitivity appears to be similar to that observed under
slower stretches.
Fig. 4.12-18 are typical torque-arm angle hysteresis loops
obtained from the patient.
The four stretch phases (ref. Fig. 4.1) are
marked on Fig. 4.12.
The pronator force is very small during Phase
1 of the cycle.
In some
of these loops, an almost linear rise in pronator torque is observed,
starting early in Phase 2 when the arm goes into supination.
13[a), 14[a] and 17[a]).
(Fig. 12[a],
The higher supinator force increases quite linearly
from the maximal supinated position, especially in faster stretches.
In
some cases (Fig. 13[b] and 15[a]), an increase in slope can be seen as the
stretch
enters into the pronated region.
biceps EMG activity described earlier.
This reflects the increase in
Except for Fig. 4.18, all these
superimposed hysteresis loops indicated considerable variation in the
patient's response between cycles.
4.3
Experiments with Pre-Stretch Isometric Contraction
Experimental conditions similar to that used for testing normal subjects
were also tried on patient J.K.
-56-
Tests involved the supination of the spastic arm.
As reported before,
the pronators of this patient were mildly spastic, and pre-stretch isometric
contraction was easily achieved.
on a meter for the subject.
The level of contraction was again displayed
Stretches were 45* supination from the vertical;
and the instructions were, as before, to relax or resist as fast as possible.
Selected results from both test conditions are shown in Fig. 4.19 and
4.20.
They reveal results quite similar to those from normals.
There is
a monosynaptic burst with about 40 msec. delay, and a bigger, longer burst
at 120 msgc.
The patient takes much longer to relax, and his biceps EMG
shows some coactivation.
Fig. 4.21, which shows the hysteresis loops for
the relaxation condition, in fact bears a strong resemblance to those obtained from normals with the instruction to not consciously resist or relax.
Fig. 4.22, showing the plots for voluntary resistance, are similar to those
from normals.
Summary
4.4
The results obtained agree with reports from other researchers (Bomze,
1973) and (Leavitt, 1964), namely, that spastic reactions are highly variable even for the same patient.
Muscular reactions can vary considerably
from cycle to cycle, but they do appear to increase with speed of stretch.
The phase characteristics for the biceps and the pronators are quite
distinct at slow speeds.
The biceps is primarily sensitive to velocity of
stretch, while the pronators react mostly according to the position of
stretch.
At higher stretch velocities, a velocity sensitive component of
pronator activity can sometimes be discerned.
The patient's pronators are capable of quite powerful voluntary contractions.
With prestretch isometric contraction, the instructions to either
relax or resist supination, it was found that the mildly spastic pronator
appears to have the same reflex activity as a normal muscle.
The EMG
bursts do not appear to be stronger.
However, in the patient, conscious
relaxation takes considerably longer, and the muscle remains active when
in the case of normals, such acitivity would have been suppressed.
-58-
.
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FIG. 4.1 - Typical results to illustrate and define
parameters and variables. Top trace: arm
angle is divided into 4 phases, numbered
accordingly.
-59-
GRAPHIC CON
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FIG, 4.2 - Typical patient results. Stretch speed : 20 /sec.
Arrows and letters mark events referred to in the
text.
-60-
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-63-
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Patient data. Stretch speed:45 /seCo
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-64-
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-66-
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Torque-Arm angle hysteresis loops. Arrow indicates
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Response with isometric contraction and instruction
to relax as fast as possible after stretch starts.
Arrows (l)- onset of stretch; (2)-first EMG burst;
(3)-Second EMG burst.
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Isometric contraction L.Instruction. to
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-80-
REFERENCES
1.
Allum, J.H.J. [1974], "The Dynamic Response of the Human Neuromuscular
System for Internal-External Rotation of the Humerus," Sc.D. Thesis, M.I.T.
2.
Bergmans, J. and Grillner, S. [1969], "Reciprocal Control of Spontaneous
Activity and Reflex Effects in Static and Dynamic Flexor Gamma-motoneurons
Revealed by an Injection of DOPA," Acta. Physiol. Scand., 74:629-636.
3.
Bomze, H.A. [1973], "The Devlopment of an Automated System for the Measurement of Spasticity," D.Sc. Thesis, Washington Univ., St. Louis.
4.
Burke, D., Andrews, C.J., Gillies, J. [1971], "The Reflex Response to Sinusiodal Stretching in Spastic Man," Brain, 94:455-470.
5.
Burke, D., and Ashby, P. [1972], "Are Spinal 'Presynaptic' Inhibitory Mechanisms Suppressed in Spasticity?" J. Neurol. Sci. 15:321-326.
6.
Dimitrijevic, Nathin [1967], "Spasticity in Man: Analysis of Stretch Reflex,"
Brain 90:333-358.
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