Strategies Underlying the Control of Disordered

Movement
Daniel M Corcos
PHYS THER. 1991; 71:25-38.

The online version of this article, along with updated information and services, can be found
online at: http://ptjournal.apta.org/content/71/1/25

Collections This article, along with others on similar topics, appears

in the following collection(s):
Kinesiology/Biomechanics
Motor Control and Motor Learning
Neurology/Neuromuscular System: Other
e-Letters To submit an e-Letter on this article, click here or click on
"Submit a response" in the right-hand menu under
"Responses" in the online version of this article.
E-mail alerts Sign up here to receive free e-mail alerts

Downloaded from http://ptjournal.apta.org/ by guest on November 8, 2013

 Strategies Underlying the Control of Disordered
Movement
Daniel M Corcos
PHYS THER. 1991; 71:25-38.

Cited by This article has been cited by 1 HighWire-hosted articles:

http://ptjournal.apta.org/content/71/1/25#otherarticles
Subscription http://ptjournal.apta.org/subscriptions/
Information
Permissions and Reprints http://ptjournal.apta.org/site/misc/terms.xhtml
Information for Authors http://ptjournal.apta.org/site/misc/ifora.xhtml

Downloaded from http://ptjournal.apta.org/ by guest on November 8, 2013

Movement Science Series

Strategies Underlying the Control of

Disordered Movement

The purpose o f this article isfou~fold.First, a theory o f motor control-the dual- Daniel M Corcos
stratem hypothesis-is outlined. Second, the methodologies and theoretica1,franze-
work that are used to develop this theory are examined. Third, molor d11Sfunction
is discussed in the context of this theory. In particular, Down ~ n d r o m eParkin-
,
son S disease, cardiovascular accidents, and spasticily are discussed. Finally, poten-
tial applications of the theory to physical therapy are considered [Corcos IIM.
Strategies underlying the control of disordered movement. Phjs Ther.
2992;72:25--38.1

Key Words: Electromyography; Kinesiology/biomechanics,general; Molor activily;

Motor control theories: Motor dysfunction; Moz~ement.

The field of motor behavior is con-
cerned with understanding how
movements are controlled and how
they are learned. A subset of the field
of motor behavior is concerned with
motor dysfunction in which questions
are asked concerning the characteris-
tics and underlying causes of particu-
lar motor deficits in individuals with
movement impairment. This article
presents ideas primarily from one
theory of motor control to suggest
how they can be used to develop a
rational basis for therapeutic interven-
tion in motor dysfunction. One major
assumption that underlies this ap-
proach is that theories of motor con-
trol developed from studies per-
formed on healthy individuals can be
used to form a basis for treating
movement impairment. This article
will suggest that this may be the case
for several disorders of movement,
but may not always be true. Certain
disorders of movement, specifically
D Corcos, PhD, is kssistant Professor, College of Kinesiology (MIC-194), University of Illinois a[
Chicago, PO Box 4348, Chicago. IL 60680 (USA).
This work was partially supported by NIH FIRST Grant R29 NS23593 and [he Down Syndrome
Research Fund.
those in which unwanted involuntary
movements interact with voluntary
movements, will be considered be-
cause it may well be that, in such dis-
orders, the principles that underlie
treatment should be determined func-
tionally and not from models of mo-
tor control. This point can b e illus-
trated by considering different
possible treatments of cerebral palsy.
If the primary cause of motor dys-
function is coactivation, then one can
either teach an individual with ccre-
bra1 palsy how to move despite the
coactivation o r try to first reduce the
coactivation and then teach "normal"
movements. The first approach will
not lead to generating movements in
a normal fashion, but will allow cer-
tain types of movement tasks to be
accomplished. The second approach
may ultimately prove to be preferable
because performance in the presence
of pathological coactivation will prob-
ably never reach the same levels as
without this coactivation.
Theories of Motor Control
One central question of interest in
the study of motor behavior is: How
are movements controlled? In order
for movement to take place, neural
commantis must activate muscle. Sev-
eral theories have been advanced
concerning the representation of
these commands. These theories dif-
fer in terms of what is being con-
trolled to generate a movement. The
dual-stratem hypolhesis of motor con-
trol, the principle theory to be devel-
oped in this article, suggests that
movements are controlled by two
different sets of rules for activating
muscle.' The first set of rules applies
to tasks in which movements can be
successfully made at any speed. For
example, if an individual is asked to
move from point A to point B, the
movement is correct if the individual
moves to point B. The time it takes to
make this movement is unimportant
for successfully completing the task.
Contrast this type of movement with

36/25 Physical Therapy /Volume 71, Number 1/January 1991

the task of catching a ball. If an indi-
vidual does not get his o r her hand to
the right place at the right time, the
movement will be unsuccessful.
Movements of the first kind are re-
ferred to as "speed-insensitive,"
whereas movements of the second
kind are referred to as "speed-
sensitive." These two types of move-
ments are controlled differently. In
the case of speed-insensitive move-
ments, the duration of excitation to
motoneulron pools is prolonged and
the muscles are activated later for
longer niovements o r movements
made against larger loads.' These fac-
tors lead to predictable changes in
both e1el:tromyographic (EMG) activ-
ity and n~ovementkinematics, which
will be discussed in the section o n
methodological issues. Movements
that are made at different required
speeds are termed speed-sensitive
and are controlled by changing the
intensity of activation to motoneuron
pools ra~therthan by changing the
duration of activation.3 In the case of
speed-sensitive movements, the antag-
onist muscle is activated earlier as
movement speed increases.
Another theory of motor control is
the equilibrium-point hypothesis. Ac-
cording to one version of this theory,
movements are made by regulating
the threshold of a length-sensitive
reflex. In this theory, a movement
occurs when there is a shift in the
equilibrium point from the current
limb position to a new position.
Movement control can then be de-
scribed in terms of two parameters:
the final value of the threshold of the
reflex (A) and the speed at which the
threshold moves (o). For isotonic
movements, the final value of the re-
flex threshold is related to final posi-
tion, and the speed at which the
threshold moves is related to move-
ment speed (ML Latash, GL Gottlieb;
unpublished research).4 This theory is
entirely compatible with the dual-
strategy hypothesis (see Gottlieb et
a15 for a discussion of this point)
and is mentioned here because
some articles o n disorders of move-
ment have been written based o n
this hypothesis (ML Latash, DM Cor-
cos; unpublished research).
Physical Therapy /Volume 71, Number 1 I'January 1991
Another class of models suggests that
movements are controlled by sets of
commands to muscle.- One com-
mand is to the agonist muscle and is
associated with a relatively constant
EMG duration for movements that are
less than 30 to 40 degrees.9Jo A sec-
ond command is to the antagonist
muscle and is sometimes followed by
a second command to the agonist.
These three commands are often re-
ferred to as the "triphasic EMG pat-
tern." According to this model, move-
ments are primarily controlled by
increasing the number of motor units
recruited, not the duration over
which they are recruited. This model
has formed the basis of a large num-
ber of studies on movement dysfunc-
tion. However, it is important to note
that this pattern is mainly observed
during very rapid movements and has
not been observed over a wide vari-
ety of movement tasks.'
Methodology In Motor Control
The study of motor behavior involves
integrating findings from behavioral
work, physiology, and biomechanics."
In order to fully understand the na-
ture of a movement deficit, it is im-
portant to understand (1) which
movement tasks can and cannot be
performed, (2) the physiological
mechanisms (both normal and abnor-
mal) underlying the performance of
the task, and (3) the type of move-
ment trajectory that is generated.
Task Analysis
Any time a person performs a move-
ment, he o r she requires two sets of
information. The first concerns objec-
tive information about what the per-
son should do. This might b e infor-
mation about the position in space to
which the person should move o r
about the load to be moved. Variables
that define what a person should do
have been defined as task
variables.1(1.'90) The second set of in-
formation refers to how the task
should be performed and is usually
presented in the form of verbal in-
structions. Verbal instructions include
information about such factors as the
speed and accuracy of the movement.
Therefore, a task refers "to the union
of the task variables and instructions:
those things necessary for a subject to
make a specific mo~ement."~(pl9~)
When a person performs a task, many
variables can be measured that de-
scribe this performance. Examples are
movement speed, movement time,
and movement accuracy. These varia-
bles are called performunce variables.
A movement task gives rise to a moue-
ment strategy, defined as "a set of
rules between a movement task and
measured variables, sufficient to
perform the task."l(~l92)The impor-
tant point is that there are at least
two sets of rules and hence two.
strategies for controlling movement.
This point can also b e inferred from
the equilibrium-point hypothesis, in
which o n e parameter (A) is related
to the control of the final limb posi-
tion and the other parameter (o) to
the speed at which the movement is
performed.
Nearly all of the studies that will be
discussed in this article have used
tasks in which individuals made
movements at only one joint. This is
because such movements are much
easier to analyze compared with multi-
joint movements using EMG tech-
niques. For a more comprehensive
review of theories underlying the
control of movements with one me-
chanical degree of freedom, see the
article by Gottlieb et a1.l It should,
however, also be possible to apply
the principles derived from the analy-
sis of such movements to the perfor-
mance of tasks that require using
more than one degree of freedom, as
will be discussed in the section o n
organizing principles. For further dis-
cussion o n this issue, see the article
by Corcos and colleagues.12For a re-
view of studies using other tasks, see
the chapter by Campbell.l3(1'~22&22*)
See the article by Wolf et a114(l~r1729-73u)
for a discussion of the problems in-
herent in relating EMG and kinematic
measures to treatment efficacy.
Physiology
The electrical signal that can be mea-
sured o n the surface of muscles is
 Task

Action Potentkl Trains

Figure 2. ,Wodeling the rectfied and

,filtered electromyographic (FiMG) signal,
with a linear first-order difkrential equa-
tion jollowed by a n amplitude-li~niting
nonlinearity, shows systematic changes
when one of the two parameters of a
rectangmlar pulse input is zlaried.
(A) Changes in the intensity of the rectan-
gular input pulses lead to a familv of
EMG wat~efomzsthat rise at rates propor-
tional to amplitude Areas and peaks
(until limiting both scale with the inten-
sity o f the input, hut rhe durations o f
these-^^^ s&nals are not unambg;
Figure 1. Selected portions of the motor control svstem. The motoneuron pool is uomsly dtfferent. (B) Changes in the dura-
the final common pathwaj' to the muscle, o n ulhich the excitarion pulse acts. Two d$ tions of the rectangular input pulses Lead
ferent kinds of penpherallv obsen~ahlephenomena are caused by the action potentials to afamilj of^^^ waueforms that all
produced b y the e.xcitation pulse, ujhich can be induced by input from both supers%- rise at the same rate, dez~iating,fromthe
mental commands and feedback. The electromj~ographic(EhIG) activi[y arises from the common pathway when the input pulse
electn'cal responses in the muscle membranes;forces and movements arise,from me- ends. These changes gizle rise to hystematic
chanical responses of the contractile elements. (Reproduced u~ithpermission from Cor-
cos et aI.l2)
-
changes in the area ofthe EMG ujazle-
form and, until limiting is reached, in the
peak EMG amplrtude as well. Even
called the EMG signal and is shown in toneuron pools. The low-pass filtering though the EhfG wavefotn~does not hate
assumption is required because the a zuell-defined end point, changes in its
the bottom left section of Figure 1,
duration are reliahlj distinguishable. The
which captures selected features of motoneuron pool serves to smooth X axis represents time, and the Y a.~isrep-
the motor control system. The figure the many inputs that converge on it. resents milliz~olts(Reproduced with per-
depicts how a movement task deter- The EMG is analyzed because the exci- mission from Gottlieb et al.')
mines a movement strategy that gives tation pulse per se is not measurable
rise to an "excitation pulse," which is in the intact human organism.' The a rectangular pulse that can be modu-
the input to the motoneuron pool, and schematic diagram in Figure 2 depicts lated in height or width. If the height
ultimately prcduces the EMG signal. a simple model of the rectified, fil- is altered, then the EMG signal rises
tered EMG signal. The model is a first- more steeply. If the duration is modu-
The EMG is one of the principal tools order differential equation with an lated, the EMG signal rises at the same
for identifying mechanisms underlying amplitude-limiting nonlinearity. The rate. A more detailed account of the
motor control and motor dysfunction. amplitude-limiting nonlinearity is re- filtering effects of the motoneuron
In the dual-strategy hypothesis of mo- quired because there are only a given pool and muscle can be found in the
tor control, the EMG is interpreted as number of motor units and they can article by Gottlieb et al.5
a low-pass filtered version of an excita- only fire up to a certain frequency.
tion pulse that is the input to the mo- The excitation pulse is assumed to be

38 / 27 Physical Therapy /Volume 71, Number 1/January 1991

Biomechanics

The schematic diagram in Figure I

shows that one consequence of the 1.60.
action potential train is that contractile 2.50
elements; generate torques that may 0 .
o r may not lead to movement, de- 5 0
pending on whether the contraction
is isometric o r isotonic.' The analysis
C
d
. 5
4
of movement impairment also re-
quires information about the motion -0.005 . . , . , , . . . 2
of limbs, the forces generating the -0.005
0.80-
motion, :and the forces generated by 1
the motiton, a very real problem for 0
I
- n 2.50
patients ,with central nervous system
dysfunction. Such information can be
W II
4 '

in the form of forces and torques (ki- $ I\ W

d
netics) a,s well as position, velocity,
and acceleration (kinematics). Such
C
1 It , ill :
knowledge can allow one to deduce
-0.005 , :, , . . . , ,
-0.005
1, ; .V
;( i q !I:3i
I 1,
!
factors albout the control of move- 30.004
ment. In the study of patients with
hyperactive stretch reflexes, for exam-
ple, the :analysis of position and veloc- c
ity records can allow the researcher .--
,- .
to deduce the presence of a move- 8
0.
ment deficit. So, for example, Corcos
and colleagues15 showed that when
individuials with hyperreflexia (spastic- -22.00 ... ... . . . . . ., , ,
ity) makce dorsiflexion movements,
their movement may be impeded by 325.
the presence of a hyperactive stretch
reflex that momentarily reverses -
.-A .
--
.A
moveme:nt direction. This reversal can
most clearly be seen in the position
-3
C
U

record of Figure 3A. This phenome-
non is somewhat difficult to observe
without equipment to record EMG
and kinematic data. However, it may
sometimes be s o obvious that the in-
dividual will report having noticed it
upon detailed questioning. For exam-
ple, the data in Figure 3B depict a
plantar-flexion movement to a target.
The movement slightly overshot the
target. When the limb started to dorsi-
flex back to the target, the patient ex-
perienced clonus. Upon noticing this
phenomenon, I asked the patient
whether he drives a car, and to my
astonishment he replied that he does!
He often has to manually lift his foot
off the a.ccelerator, because he fre-
quently experiences clonus upon
making dorsiflexion movements to
ease up on the accelerator.
.
-8
9
-60 . . . . , , . , -350
0 200 400 ms 0 200 400 600 ms
Time Time
A B
Figure 3. (A) Recordings of agonist (tibialis anterior muscle) (TA EIMC) and antag-
onist (soleus muscle) (SOL EMG) electromvographic activity and position and velocity
data. Dashed lines refer to a 24-degree movement with no target, dotted lines to a 24-
degree movement with a 4-degree target, and solid lines to a 12-degree mouement with
a 4-degree target. (B) Recordings of agonist (SOL EMG) and antagonist (TA EMG) elec-
tromyographic activity and position and velocip data. Recordings show four 12-degree
ankle plantar-jlexion movements, which ot~ershoota 4-degree target and then go into
clonus upon returning to the target. The data are from the same individuals as in Fig-
ure 3A. (Reproduced with permission from Corcos et ~ 1 . ~ 5 )
Organizing Principles ciples for the study of motor con-
trol, as follows:
Based on the relationship between
movement tasks, physiological prin- I. Elements of a movement task lead to
ciples, and biomechanics, Gottlieb a strategy governing its control. We
et a1 generated four organizing prin- have identified two strategies ro de-
scribe how single-joinr movements

Physical Therapy /Volume 71, Number 1 /January 1991 28 / 39

 are accomplished for a variety of
tasks.
11. Strategies consist of sets of rules
that determine the patterns of mus-
cle activation.
111. Rules for muscle activation lead
to patterns of muscle torques
and EMGs. Well-chosen scalar
measures of torque and EMG
will be highly and consistently
correlated irrespective of task
because of their shared causal,
neural activation.
N. Muscle torques interact with limb
loads to generate kinematics (an-
gle, its derivatives, and movement
intervals). Because of the role of
load in determining kinematics, no
general correlations between EMG
and purely kinematic measures are
~~1~ible.2(1'~~42-343)
Based on these organizing principles,
Gottlieb et a12 demonstrated the pres-
ence of two strategies (sets of rules)
for performing movements and also
the relationship of the EMG measure
to selected measures of torque. Figure
4 depicts two sets of movements that
are performed by using the two dif-
ferent strategies. The data represented
by the dark dashed lines are for o n e
subject moving four different distances.
The inertial torques (acceleration mul-
tiplied by moment of inertia) rise at
approximately the same rate and are
independent of the distance moved.
The same observation is true for the
EMG activity. This finding should b e
contrasted with the plot of the data
represented by the lighter dashed
lines. In this case, in which the subject
was asked to move one distance at
four different speeds, both EMG activ-
ity and inertial torque diverge early in
the trajectory. The movements are con-
trolled in the first case by changes in
the duration of the excitation pulse
(speed-insensitive strategy) and in the
second by changes in the intensity
(speed-sensitivity strategy), as was
shown in Figure 2. The differences
in the two control schemes are de-
picted in Figure 5. It is important to
note that the speed-insensitive strat-
egy can b e used with any value of
intensity1" and that the presentation
in Figure 5 is not meant to imply
different sets of rules underlie the
control and regulation
- of movement.
These sets of rules are dependent on
the type of task to b e performed but
are not limited to single-degree-of-
freedom tasks. For example, Wadman
et all7 had subjects perform diverse
tasks including playing simple tunes
o n the violin and trombone. (See
Wadman et al's'' Figure 15, which
depicts trombone slide velocities dur-
i!
ing movements of different slide dis-
,,,.---."-""------' tances, using what appears to b e a
speed-insensitive strategy based o n
;I,.;:#;---:--- the uniform rate of rise of velocities.
,# '
f ;-..,;*;,'/,
-.
:
-*-
Their Figure 17 shows bow move-
%
,.;
*t ;.A<,, r--
j f i A,,'
,,
,,,,.--.-,,,. ments during violin playing at three
different tempos, using what appears
2 @*,
4,;;.
#*,
:&;.&
';
:? -.----.
-----------. to b e a speed-sensitive strategy.) Lee
and colleagues~Olooked at horizontal
- tr
-30
50
A?.*, , : , , , , , , pulls o n a cable and found patterns of
ground-reaction forces and hand-pull
tensions that can b e described using
- the terminology of the dual-strategy
E hypothesis. These data are presented
z, -
in Figure 6. The dual-strategy hypoth-
3 -
e esis can, in principle, also b e applied
e - to gait.19.20 In this gait study, subjects
-e -- t
were asked t o walk at three different
speeds and ground-reaction forces
- ~ . l l l l l l , l I l l were measured. The force records at
Time (ms) en the three different speeds had dif-
ferent rates of rise and are distinc-
Flgure 4. Time-seriesplots of aver- tively speed-sensitive in nature, as can
aged (10 trials) biceps muscle electromyo- b e seen in Figure 7. The data in these
graphic (EMG) activity, angle, and iner-
tial torque jor two sets of movements studies all suggest that insight into the
performed by the same subject. The mozle- control of more complex movement
ments drawn in thick lines represent tasks can b e obtained through parti-
movements of 18,34 54, and 7 2 degrees tioning tasks into speed-insensitive
to a Pdegree-wide target. The move- and speed-sensitive categories.
ments drawn in thin lines correspond to
54-degree movements to a Pdegree-u~ide
target at ,four subject-selected speeds. The From the perspective of physical they-
EMG signals,from the fle.xor (biceps mus- apy, the observation that there are at
cle) are shown aJer full-ulave rectzjica- least two sets of rules for activating
tion and smoothing with a 25- muscles implies that movement im-
millisecond moving atlerage digital,filter.
The arrows on the inertial torque plot pairment can b e characterized by an
correspond to the torque generated dur- inability to modulate the intensity of
ing maximal voluntary contractions in the excitation pulse to the agonist
each direction. (Angle origin is with the and/or antagonist muscle, an inability
elbouj at a ri&t angfe,flexion positive.) to modulate the duration of the exci-
(Reproduced ufithpermission from Corcos
et a[,.$) tation pulse to the agonist and/or an-
tagonist muscle, and inappropriate
that speed-sensitive movements scaling of the latency of the antagonist
have larger values of intensity than muscle. These three possibilities are
speed-insensitive movements. not mutually exclusive.
The essential feature of the dual- This description also needs to b e
strategy hypothesis is that at least two evaluated in light of a distinction
drawn between "reduced output pare-
Physical Therapy /Volume 71, Number 1/January 1991
 sis" and "subtraction paresis."2' Cer-
tain disorders of movement can be
characterized by diminished input to
SPEED-INSENS I T I V E SPEED-SENSITIVE
motoneuron pools, whereas others
can be characterized by excessive out-
Excitation
Ir, AL
put. h~such, motor dysfunction can
lag occur either because of a diminished
*
excitation to motoneuron pools o r
Agonist because the timing and/or size of the

1 Dag 4 b T
b
excitation is excessive.

The causes of inappropriate levels of

Iant excitation to motoneuron pools can
A
originate from either supraspinal
I Antagonist mechanisms o r spinal mechanisms, o r
/ Lat
3 from a combination of both. In many
Dant disorders, the actual cause of the
b v
b movement deficit is difficult to iden-
T ime Timce tify because damage to parts of the
brain can lead to changes in the deli-
cate balance between inhibition and
excitation that exist in the spinal cord
Figure 5. Schematic diagrams illustrating how speed-insensitive and speed-sensitive as well as to long-term changes in the
strategies majl he operationalized by controlling ( I ) the duration (D,,) or intensip
(I,,) of the excitation pulse to the agonist muscle, (2) the latency (Laf) of antagonist
structure of muscle. The distinction
activation, and (3) the duration (D,,,) or intensiol (I,,,,) of the antagonist. (Modijed between supraspinal and spinal mech-
from Gottlieh et ~ 1 . ~ ) anisms refers to the primary source of
the problem and becomes important
when certain types of therapeutic in-
tervention are considered.

Application of Motor Control

Theories to Movement
Impairment

In this section, three disorders of

movement will be discussed in which
the primary cause is a supraspinal
deficit in the ability to control move-
ment. Down syndrome and Parkin-
son's disease will be discussed from
the perspective of the dual-strategy
hypothesis because several studies
have been conducted that can easily
be interpreted within this framework.
Motor dysfunction arising from cere-
brovascular accidents will be dis-
cussed in more general terms be-
cause n o studies have been identified
by the author that provide data that
can be clearly interpreted within this
framework. For a study to be easily
interpreted within the framework of
the dual-strategy hypothesis, EMG and
TIME ( s e c ) kinematic data must be analyzed for
at least two different tasks. The inter-
pretation of the data is also greatly
Flgure 6. Overlaid indiuidual trial records of ankle torque and pulling torque for
one subject, at all percentages of maximal pulling force (MPF),synchronized to the on- facilitated if data plots of the tasks are
set of the pull. Arrows indicate trials of increasing percentage of MPF. (Reproduced with superimposed. This section will con-
permission ,from Lee et al.IX) clude with a subsection on spasticity,

Physical Therapy/Volume 71, Number 1 /January 1991


Figure 7. Thirty vertical ground-reactionforce cuwes (10 trials at each of three
speed conditions). (Reproduced with permission from Copland.19)
which occurs in a wide variety of dis-
orders of movement.
Down Syndrome
The individual with Down syndrome
can be characterized as moving and
reacting slowly. Several reasons have
been postulated for these characteris-
tics, including hypotonicity and an
inability to generate normal levels of
f o r ~ e . ~ 'The
, ~ 3 key findings from the
perspective of the dual-strategy hy-
pothesis are that individuals with
Down syndrome might lack the ability
to modulate the intensity with which
they activate motoneuron pools. This
evidence comes from work by Latash
and Corcos (unpublished research)
and Cole et aLZ4In the study by Cole
42 / 31
et al,z4individuals were asked to lift a
200-g object with a sandpaper or a
satin finish, which would necessitate
different grip forces to lift. Individuals
in the control group modulated the
rate of grip force required to lift the
object. In contrast, individuals with
Down syndrome reached the appro-
priate levels of force, but did so by
"increasing the duration of grip force
appli~ation."~*(~75~) The data in Fig-
ures 8A and 8B illustrate this point.
Latash and Corcos (unpublished re-
search) had individuals with Down
syndrome generate movements of
different distances. They found that
the pattern of activation of the mus-
cles was very similar to that of con-
trol subjects (compare this pattern
with the dark dashed lines of Fig. 4)
Physical Therapy /Volume 71, Number 1/January 1991
but that the movements were much
slower. The implication of this find-
ing is that the intensity of activation
is less in individuals with Down syn-
drome than in control individuals,
but that individuals with Down syn-
drome modulate duration of activa-
tion in a normal manner to accom-
plish movements over different
distances (Fig. 8C).
Parkinson's Disease
The movement deficits of patients
with Parkinson's disease are numer-
ous. However, one deficit that ties in
with the dual-strategy hypothesis is
that of an inability to modulate the
rate at which different levels of force
are generated in isometric tasks or an
inability to accelerate at different rates
in isotonic tasks. For example, Hallett
and Khoshbin25 had patients with Par-
kinson's disease and healthy subjects
generate movements over different
distances. The healthy subjects
showed an early divergence of the
angle trace for longer movements.
This type of trajectory implies that a
speed-sensitive strategy was being
used and that the subjects were accel-
erating much more quickly for long
movements than for short move-
ments. However, the parkinsonian
patients tended to follow the same
trajectory for both long movements
and short movements. Both sets of
data are presented in Figure 9.
Although the pattern demonstrated
in the parkinsonian patients is fre-
quently observed in healthy individ-
uals and has been termed "de-
fault,"lG the question of interest is
whether parkinsonian patients have
access to both strategies. This issue
awaits further research.
Similar arguments can be applied to
isometric contractions as studied by
Stelmach and W ~ r r i n g h a mThey
.~~
had individuals with Parkinson's dis-
ease and healthy subjects generate
isometric contractions to different lev-
els of their maximal voluntary con-
traction. They observed that the major
difference between the groups was
not in the maximum levels of force
that could be generated, but in the
 '\
-
-
\

t.
Y*\
'-.
----
- Y*,
\'=,
\ "..------
\
\

0 2 1 d A L O 0 2 .4 .I .I LO
SZCOPB 8ECQP8
0
A B - VEL
-
-
-
-
-
-
-
-
-150 I I I I I , I I I .\ .-,:' I , , , , ,

1
-
TrLon 400 -
- ACC
-
-
-
,

I I I I I 1 l I I I 1 I I I I I l l l i

0 1000
TIME

-700 l l l l l l l l l l l , , l l l r , l l

Figure 8. Aleraged torque signals for trialsfrom (A) three control subjects (NI, N3, 1V5jand (B) three individuals with Doan syndrome
(DS2, DS& DS5) for lifring objects co~leredwith sandpaper (thick line) and satin (thin line). Object weighed 200 g Traces illustrate thefail-
ure of the p u p of individuals with DOZWsyndrome to increase rate of grip force (N=newtons) to achieve greater force needed to lift ob-
ject with more slippety (satin) s u ~ a c e(Reproduced
. with permissionSfom Cole et alJ4) (0 Averaged electromyographic (EMG) and kine-
matic data for a n individual with Down syndrome who was pei$omting mouements of 1836 54, and 72 degrees (6 of each amplitude).
Note coinciding initial agonist (biceps muscle [BIC])Eh4G and kinematic trajectoriq especialb apparent in the acceleration trace (ACC)
Time scab is in milliseconds; angle, ueloci&, and acceleration scales are in degrees, degrees per second, and degrees per second per second,
respectic~eb.fie Eh4G scales are in millivolts. TrLon refers to the long head of the triceps muscle.

Physical Therapy /Volume 71, Number 1/January 1991 32/ 43

 Figure 9. (a) Attempted ballistic
movements of 10 degrees (A), 20 degrees
(B), and 40 degrees (C) by a healthy 83-
year-old woman. In graphs 4 B, and C,
the traces are gram top downward) bi-
ceps muscle electromyographic (EMG)
activity, triceps muscle EMG activity, and
position of'the elbow. Graph D shows the
three position traces supe&nposed The
parts of the jigure were altyned so that
the movements all began at the same
time from the beginning of the traces. The
dashed vertical lines are discontinuous
straight lines indicating the correspon-
dence of the timing of EMG bursts in the
dtfferent movements. (b) Ballistic move-
ments of a 68-.year-old man with Parkin-
son's disease. The organization of the
jigure is the same as in Figure 9a. Note
the additional cycles of bursts; the third
and fourth agonist bursts are labeled Ag
3 and Ag 4, respectively, and the second
and third anta'qonist bursts are labeled
An 2 and An 3,respectively. In graph D,
the initial part of the position traces are
similar, indicating similar velocities of the
dzfferent movements. In graph A, the suh-
ject did not sustain the attempted 10-
degree position, but returned quickly to
near the starting point. (Reproduced with
permission from Hallett and k%~shbin.~'-)

rate at which the force could be de-

veloped. This difference can also be
seen in the work of Wing," who
showed lower rates of force increase
and also force decrease in parkinson-
ian individuals.

Cerebrovascular Accidents

Cerebrovascular accidents frequently

lead to "upper motoneuron syn-
drome." The movement disabilities
associated with this syndrome include
weakness, slowness, clumsiness, spas-
ticity, and abnormal movement syner-
gies. Berardelli et alZ8investigated
how patients (aged 50-65 years) with
upper motoneuron lesions of vascular
origin make movements of different
distances. They had healthy individu-
als and patients make elbow flexion
movements over 10, 20, and 30 de-
grees. Their main finding was that the
agonist and antagonist EMG activity
durations of the patients were pro-
longed compared with those of the
healthy individuals. They suggest that
prolonged duration of muscle activity
is a compensatory mechanism for
generating sufficient force to per-
form the task. Again, these data are

Physical Therapy /Volume 71, Number 1 /January 1991

 *i
A B
100, C

1 t 1 TILO" 40 1 AHOLE
:: i i
!
&
/ : I
e.
a
0
* ]b_""...
--..--."...-
TtL.1
-40 -h,
i
.-
L..",.""

1 ERR O i ! !

1...-. -..---
500
k h .............. ..,......,..-h .,I 2s0

'
0 TIME 3000
,&,hv
i ;& ............ .. -2000 --".. ".""""_
0 1800

Figure 10. Attempts at voluntay dors$exion before (A) and I 2 0 minutes afrer (B) the adnzinistration of baclofen. Note the dis-
appearance o f soleus (SOL) and hamstring (HAM) muscle coactivation. (QUAD=quadriceps femoris muscles, TA=tihialis anterior mus-
cle.) (Keproduced with permissionfi.om Latash et al.-<-'J(C) Averaged records o f j t l e trials at tloluntary elbow Jexion (agonists, biceps
muscle [HIC]and brachioradialis muscle [BM])in a patient with supraspinal trauma before (thin line) and afrer (thick line) intrathe-
cal buclojkn. Peak electromyographic (EMG) levels of the agonists were practicallv unchanged. Long-lasting coactivation component
of antagonist (long [TrLon]and lateral [TrLat]heads o f triceps muscle) activity decreased, retlealirzg phasic "normal-looking" antago-
nist burst. As a result, the peak speed increased twofold and the oscillations in t h e j n a l positiotz were damped. Full EMG scales corre-
spond to the maximal leziels obsewed during maximal zioluntary isometric contractiotzs; time scale is in milliseconds. (Reproduced
with permission from Latash et aC.ii)

consistent with the view that these
individuals d o not have the capacity
to generate excitation pulses of
large intensities.
Spasticity
Increased muscle tone and muscle
spasms are major problems facing the
physical [:herapist in delivering appro-
priate tht:rapy in many disorders that
are associated with spasticity. As such,
careful consideration should first he
given to the use of antispastic medica-
tion in alleviating these unwanted
signs of spasticity. The advent of drug-
pump technology has allowed for the
delivery of antispastic medications that
have considerably more effect than
oral medicat1on.~9-3~
Latash and colleague~3~,33 have shown
that reflexes can be abolished 2 to 3
hours after a bolus injection of ba-
clofen and that voluntary movement
can be improved. This finding is
shown in Figure 10A, in which vol-
untary dorsiflexion movements are
plotted before and after the admin-
istration of baclofen, and in Figure
10B, in which elbow flexion move-
ments are depicted.
Latash and c o l l e a g u e ~ 3 ~attribute
~~3
these dramatic changes in EMG activ-
ity, kinematics, and the consequent
capacity to generate voluntary move-
ment to changes that occur in the
spinal cord and not to the central re-
organization of motor commands. In
terms of the dual-strategy hypothesis
of motor control, this finding suggests
that improved performance is d u e to
diminished input to the motoneuron
pools of antagonist muscles. Further
studies o n these patients and others
also showed an improvement in their
activities of daily living.34
Synopsis
Van der Kamp et a135 have summa-
rized several studies of rapid move-
ments that have been performed on
different patient populations. The re-
sults are presented in the Table and
show that the EMG and kinematic
parameters of certain disorders of
movement differ from the EMG and
kinematic profiles of healthy individu-
als.25.3540However, the limited differ-
ential diagnostic value of using only
one task for the assessment of dys-
function can b e seen when compari-
sons are made among the various
disorders. A clearer description of the
differences between movement disor-
ders may emerge when tasks requir-
ing speed-sensitive and speed-
insensitive strategies are used. Any
deficits observed, however, should
also b e evaluated after individuals
have had considerable opportunity to
practice the task that is being used to
determine the deficit.+l One of the

Physical 'Therapy /Volume 71, Number 1/January 1991 34 / 45

Table. Comparison of Mouernents in Patients zuith Dzfferent Disorders of MouernenP

Upper
motor Cerebellar Parkinson's Huntington's
neurone ataxia disease disease Athetosis Dystonia

Amplitude variability NK *Increased N Increased Increased Increased (15" only)

Peak velocity Slow Slow Slow Slow Slow Slow
Velocity profile NK *Asyrnm tN NK NK N
Duration Ag 1 Prolonged Prolonged N Prolonged Prolonged Prolonged
AgiAnt pattern N Variable N Cocontracting Cocontracting Cocontracting

"All movements were self-paced and self-terminated elbow o r wrist flexion movements made as rapidly as possible. Measured mechanical variables are
(1) variability in peak amplitude from trial to trial, (2) average peak velocity, and (3) velocity profile with relative duration of acceleration and deceler-
ation phases of the movement. Measured electromyographic (EMG) parameters are the average duration of the first burst of agonist (flexor) EMG activ-
ity (Ag 1) and the approximate time relations of agonist and antagonist EMG activity (Ag/Ant pattern). Descriptions refer to comparison with data from
healthy subjects executing movements of the same extent under the same instructions. These results are taken from a variety o f studies.z5.35-" (NK=
not known, N=normal, Asymm=asymmetrical profile. Asterisk indicates personal communication between van der Kamp et a1 and Fiallett. Dagger
indicates calculated from a reexamination by van der Kamp et a1 of the data of Berardelli ct al.-i7) (Reproduced with permission from van d e r Kamp
et al.35)

factors that makes individuals with
movement deficits unique is the dif-
ferent degrees of experience they
bring to performing the types of
movements that are used in therapy.
There is a tendency in the literature
on disorders of movement to not only
fail to differentiate movement tasks,
but also to group disorders into ho-
mogenous classifications.41 For exam-
ple, there are three genetically dif-
ferent forms of Down syndrome that
are seldom alluded to in the literature
on motor control. In the case of cere-
bral palsy, there are several types and
numerous associated deficits, all of
which have been poorly controlled
for (or alternatively represented in
insufficient numbers to allow for sep-
arate analyses) and poorly analyzed in
the few studies on physical therapy
efficacy that have been conducted.42
Few assumptions, therefore, should
be made about whether a deficit ex-
ists in any mechanism in any particu-
lar individual before he or she has
been assessed over a wide variety of
movement experiences.
Implications for
Physical Therapy
In the previous sections, it has been
suggested that disorders of movement
can be characterized by abnormalities
in how muscles are activated. This
section will discuss how extensive
practice over a wide variety of move-
ment tasks, exercise and strength
training, and principles of transfer of
training can be applied to improving
the quality of movement in individu-
als with disorders of movement.
These implications are either derived
from o r are congruent with the dual-
strategy hypothesis. However, these
implications are not meant to be con-
sidered in isolation. They are simply
meant a5 another factor to consider
when designing treatment programs.
Consideration will also be given to
situations in which the most expedient
therapeutic approach might be deter-
mined functionally, because there are
many other factors to consider when
comparing the design of a treatment
program for an elderly individual who
has Parkinson's disease o r is suffering
from a cardiovascular accident with the
design of a treatment program for a
young individual with Down syndrome
o r cerebral palsy. These factors include
economic, social, and developmental
considerations.
In addition, even when motor con-
trol theory can identify causal links
between movement impairment and
resultant consequences, it does not
address the issues that arise from
indirect effects such as cardiopul-
monary problems. Thus, the optimal
way in which to use motor control
theory is in conjunction with a
model for multisystem evaluati0n.~3
The scheduling of treatments and
the provision of feedback between
and within treatment sessions are
also crucial for the optimal imple-
mentation of physical therapy, and
these aspects of treatment have re-
cently been reviewed by Winstein.44
Practice
One of the very few agreed upon ob-
servations in the motor learning liter-
ature is that appropriate practice leads
to improved motor performance. The
implication for physical therapy is that
patients should be encouraged wher-
ever possible to practice making
movements. As obvious as this may
seem, it is not always recognized how
many movements are required to ob-
tain changes in motor performance o r
for how long such improvements can
take place.45 In a study of healthy in-
dividuals, Corcos et a14Qhowed that
performance enhancement (as de-
fined by the ability to move more
quickly and more accurately) can take
place over at least 1,400 repetitions.
The causes for this improvement are
primarily related to the ability to in-
crease the intensity of activation to
motoneuron pools.

46 / 35 Physical Therapy /Volume 71, Number 1/January 1991

In the study of mental retardation,
many studies have shown that ex-
tended practice can lead to great im-
provements in performance such that
there is little difference between the
practicecl group and the healthy con-
trol group. The point to be stressed
in this article is that motor skills
should be chosen that encourage pa-
tients to practice aspects of the move-
ment in which they are deficient. For
example, in the case of Down syn-
drome and Parkinson's disease, the
inability to modulate the intensity of
excitatiol~to the motoneuron pools
seems a potential problem. As such,
the same movement task should be
practicecl at a wide variety of speeds.
Strength Training and Exercise
One of the points to emerge from the
dual-strategy hypothesis of motor con-
trol is that substantial forces are in-
volved in the generation of move-
ments. This fact is demonstrated in
Figure 4, in which the peak inertial
torque is plotted for a healthy subject.
The values of peak inertial torque are
a large percentage of the person's
maximal voluntary contraction, which
is shown by the arrows on the inertial
torque plot. Many disorders of move-
ment art: characterized by weakness
that some investigators believe is re-
lated to {:hediminished functional
capacity of the patient (for example,
see artic1.e by Bohannon and accom-
panying commentary by Rothstein et
a143.Strength training and exercise
would therefore seem to have the
potential to play an important role in
facilitating improved movement ca-
pacity in disorders of movement.48
Evidence: in support of using strength
training can also be derived from the
findings of Colebatch et a1,49who
have shown that the strength of the
elbow flexors was relatively more
weakened than that of the extensors
on the hemiparetic side of the indi-
viduals they studied. This finding was
true for hemiparetic patients suffering
from strokes as well as those with
cerebral tumors.
The folbwing factors, however,
should be considered before using
exercise and strength training. The
Physical Therapy /Volume 71, Number 1 / January 1991
therapist should ensure that move-
ment restraint is not caused by hyper-
excitable reflexes, for example as in
the data in Figure 3. If it is, any form
of exercise that induces activation of
the antagonist muscles could be coun-
terproductive. The following caveat
should also always be kept in mind.
As pointed out by Hashimoto and Paty
in discussing multiple sclerosis
Physiotherapy has an important part to
play. The problem is that it can b e
counterproductive if pushed too hard.
In a patient with limited energy re-
sources, it does not make sense to
have them squander that energy on
exercises when it could b e better used
doing work o r some other activity that
is important in maintaining self-esteem.
On the other hand, it is vely important
for a patient's self-esteem to continue
to push and to see results from that
striving.50(Pl~579-5HO)
Transfer of Training
Any program of movement therapy
should work on the premise that a
wide variety of different movements
should be practiced, because what is
learned in performing one movement
will not necessarily have a major ef-
fect in learning another movement.
For example, Gottlieb et a151 had
healthy individuals practice move-
ments at one distance and then gener-
ate movements to three distances in-
cluding the practiced distance.
Movements to the practiced distance
were faster and more accurate than
movements to the nonpracticed dis-
tance, suggesting only partial transfer
of what is learned. These findings are
in general agreement with the views
of Schmidt and Y0ung,5~who also
argue that the amount of transfer wit-
nessed in motor tasks is low.
Theory Versus Function
The issue of how best to determine
physical therapy intervention princi-
ples is far from resolved. Craik and
Oatis53 provide a detailed discussion of
the appropriate times to use normal
gait as a means for understanding
"gait deviations" and also when to use
standards derived from patients. Many
of the points they address apply to
determining the appropriate move-
ment pattern desired for all types of
movement, and not just gait. So far in
this article, it has been argued that
there are certain situations in which
physical therapy intervention should
be based on theories of motor con-
trol derived primarily from studies on
healthy individuals. However, many
times this may not be the most suit-
able approach. One such situation is
when the disorder of movement is
primarily involuntary. For example,
the predominant disabling feature of
athetoid cerebral palsy is excessive
involuntary movement. As such, the
best therapeutic approach would
seem to be to identify key functional
tasks that a person needs to perform
and experiment with ways in which to
perform such tasks so that there is
minimum involvement of extraneous
movements. This suggests that individ-
uals with disorders of movement
need to be observed closely and that
they need different types of treatment,
depending on whether the primary
cause of their disability stems from
the voluntary o r the involuntary as-
pect of the disorder.
It is also important to observe
whether movement impairment is
related to extraneous muscle activity
or whether impaired movement and
extranecius activity are both signs of
the underlying movement pathology.
For example, some studies have
shown causal relations between spas-
ticity and movement impairment,l5,54
whereas others have not.55 Equally,
some studies have shown that treat-
ment alleviates spasticity and im-
proves movement,jOwhereas others
have n0t.5~The reason for these dif-
ferent findings may be that insufficient
care has been taken to document the
primary causes of spasticity, whether
more than one mechanism may be
responsible o r whether the spastic-
ity is related to the movement def-
icit. So, for example, McLellan et
aP7 have shown that the antispastic
medication tizanidine did not abol-
ish abnormal EMG activity for one
of their spastic patients. This finding
led them to conclude that the ab-
normal patterns of muscle activation
were centrally determined. Simi-
larly, Nashnerss has argued that
spasticity is secondary to a func-
tional loss in central and spinal pro-
grams. In such cases, treatments
based on the premise of developing
"normal" movements should not
necessarily be expected to work
because the normal mechanisms are
absent. However, in cases in which
the negative signs of spasticity im-
pede movement and can be sup-
pressed by medication o r therapy
based on principles of inhibition,
physical therapy should be very
effective and lead to even greater
functional improvement by enabling
more productive work on factors
such as strength, endurance, and
range of motion that are predicated
o n motor control theory. In this sit-
uation, normal mechanisms will
now be able to produce coordi-
nated movement.
Conclusion
When a person performs a task, an
analysis of a wide variety of motor
disorders suggests that they share
many characteristics. Most disorders
are characterized by (1) slow reac-
tion times, (2) slow movement
times, (3) increased variability in
performance, and (4) movement
trajectories with discontinuities. In
addition, many disorders of movc-
ment can b e characterized by a rate
limitation on their ability to pro-
duce force o r generate movements.
("Rate limitation" refers to the
speed at which a person can gener-
ate a force o r make a movement.)
This article has suggested that the
dual-strategy hypothesis can b e used
to identify particular causes of some
of these movement deficiencies. Defi-
ciencies can result from a failure to
appropriately modulate the intensity,
duration, o r latency of muscular acti-
vation. The therapist, therefore, needs
to carefully observe how movement
tasks are performed, because this per-
formance can give insight into the
underlying disorder. For example,
subtle changes in instructional em-
phasis between speed and accuracy
can reveal whether a patient has the
ability to modulate the speed and pre-
cision with which movements are
made. Treatment programs can then
be selected that specifically address
the particular deficiency. One particu-
lar treatment principle would b e to
identify the range of speeds over
which patients can make movements.
This information can most easily b e
obtained by varying movement dis-
tance. Then the therapist should iden-
ti% the degree to which patients can
move at different speeds within that
range. Once it has been established
that the person cannot move quickly
and cannot change speed intention-
ally, the next step is to identify
whether the cause of this inability is
limited input to the agonist muscle,
excessive input to the antagonist mus-
cle, o r both. (Identification of the
cause of the movement restraint is
difficult without the use of electromy-
ography.) Structured practice o f dif-
ferent types of movements, the use of
exercise programs, biofeedback and
motor copy training,lhnd appropri-
ate medication can then b e chosen to
increase agonist activity o r to decrease
antagonist and unwanted synergistic
activity.
Acknowledgments
This article would never have been
possible without the ideas and experi-
mental data of Gerry Gottlieb and
Mark Latash and the software develop-
ment of Om Paul. I would like to
thank Dr Suzann Campbell for her
thorough and thought-provoking re-
view of the manuscript and for help-
ing me to clarify several of the ideas
expressed in it. I would also like to
thank Roni Cromwell and Gil Almeida
for their review of the manuscript and
Dick Penn for giving me the opportu-
nity to d o clinical research.
References
1 Gottlieb GL, Corcos DM, Agarwal GC. Strate-
gies for the control of single nlechanical de-
gree of freedom voluntary movements. Behav
Brain Sci. 1989;12:189-2 10.
2 Gottlieb GL, Corcos DM, Agarwal GC. Orga-
nizing principles for single joint movements, I:
a speed-insensitive strategy, ,J Neuroph)aiol.
1989;62:34?-357.
3 Corcos DM, Gottlieb GL, Agarwal GC. Orga-
nizing principles for- single joint movements.
Physical Ther-apy /Volume 71, Number 1/January 1991
11: a speed-sensitive straresy. ,J Areurop~!~'siol.
1989;62:358-368.
4 Feldman AG. Once more o n rhe
equilibrium-point hypothesis ( A model) for
motor control. ,Journal of ,).lolor Behavior:
1986;18:17-54.
5 Gottlieb GL, Corcos DM, Latash ML, Agawal
GC. Principles under-lying single joint move-
ment strategies. In: Winters J, \YrooS, eds. Mul-
liple Must-le .Svslerns: Biomechanics and Mol~e-
men1 OKanizaliorz. New York, NY Springer-
Verlag New York Inc; 1990:236-250.
6 Hallett M, Shahani BT, Young RR. EMG anal-
ysis of stereotyped voluntary movements in
man, ,J Neurol Neurosup Pg'chia~ry.
1975;38:1154-1162.
7 Angel RW. Electromyography during volun-
tat? movement: the two-burst pattern. Eleciro-
rrzcrphalogr Clin Neurol 1974;36:493498.
8 Hannaford B, Stark L. Roles of the elements
of the triphasic control signal. Exp Neurol.
1985;90:619-634.
9 Beradelli A, Rothwcll JC. Day BL, et al. Du-
ration of the first agonist burst in ballistic arm
movements. Brain Kes. 1984:304:183-187.
10 Brown SH, Cooke Jn, Initial agonist burst
duration depends on movement amplitude.
&p Brain Res 1984;55:523-527.
11 Kelso JAS. The process approach to untler-
sranding human behavior: an introduction. In:
Kelso JAS, ed. IIuman Molor Hehal'ior: An 112-
~roduciiorz.Hillsdale, NJ: Lawrence Erlbaum
hsociatcs Inc; 1982:3-19.
12 Corcos DM, Gottlieb GL, Agarwal GC. Does
constraining movements constrain [he devel-
opment of movement theories? Rrhav Bmin
Sci. 198%12:237-246.
13 Campbell SK. Assessment of the child with
CNS dysfunction. In: Rothstein JM, ed. Mea-
suremen! in Physical Therapy. New York, NY:
Churchill Livingstone Inc; 1985:207-228.
14 Wolf SL, LeCraw DE, Barton LA. Compari-
son of motor copy and targeted biofeedback
training techniclues for restitution of upper
extremity function among patients with neuro-
l o g ~ cdisorders. Phys Ther. 1989,69:719-735.
15 Corcos DM. Gottlieb GI., Penn RD, et al.
Movement deficits caused by hyperexcitable
stretch reflexes in spastic humans. Brain
1986;109.1043-1058.
16 Gottlieb GL, Corcos DM, Agawal GC,
Latash ML. Organizing principles for single
joint movements, 111: the s1)eed-insensitive
strategy as default.,J Nezrroph~aiol
1990:63:625-636,
17 Wadman W), Denier van d e r Con JJ, Geuze
mi, Mol CR. Control of fast goal-directed arm
movements. ,Journal of'Hurnun Moz~emeni
Sludies 1979,5.3- 17.
18 Lee WA, Michaels CF, Pai Y. The organiza-
tion of torque and EMG activity during bilat-
eral handle pulls by standing humans. Exp
Brain Rec. In press.
19 Copland C. Kelalirw Force Invariance Uur-
ing rhe Stance Phase o f ' f f u m a nWalking a!
Three Dlflerenl Speeds. Carbondale, Ill. South-
ern Illinois University; 1989. Master's thes~s.
20 Fischman MG, Copland C. De Vita P. Rela-
tive force invariance during the stance phase
of human walking at three direrent speeds.
Presented at the annual conference of the
North American Society for the Physiology of
Sport and Physical Activity; May 17-20, 1990;
Houston. Tex.
21 Freund HJ. The pathophysiology of central
paresis. In: Struppler A, Weindl A, eds. Electro-
myography a n d Evoked Potentials. Berlin, Fed-
eral Republic of Germany: Springer-Verlag;
1985:19-20.
22 Rarick GL, Dobbins DA, Broadhead GC.
The Motor Domain a n d Its Correlates in Edu-
cationally Eiandicapped Children. Englewood
Cliffs, NJ: Prentice Hall; 1976.
23 Morris AF, Vaughan SE, Vaccaro P. Mea-
surements of neuromuscular tone and strength
in Down's syndrome children. J Ment DeJic
Res 1982;26:41-46.
24 Cole Kj, Abbs JH, Turner GS. Deficits in
the production of grip force in Down Syn-
drome. Dev Med Child Neurol 1988;30:752-
758.
25 Hallett M. Khoshbin S. A physiological
mechanism of bradykinesia. Brain.
1980;103:301-314.
26 Stelmach GE, Worringham CJ. The prepara-
tion and production of isometric force in Par-
kinson's disease. Acta Pg~chologica.
1988;26:93-103.
27 Wing Pd.A comparison of the rate of
pinch grip force increases and decreases in
Parkinsonian bradykinesia. Acta Psychologica.
1988;26:479-482.
28 Berardelli A, Accornero N, Hallett M, et al.
EMG burs1 duration during fast arm move-
ments in patients with the upper motor neu-
rone syndrome. In: Delwaide PJ, Young RR,
eds. Restorative Neurology. Amsterdam, the
Netherlands: Elsevier Science Publishers BV;
1985377-82.
29 Penn FD, Kroin JS. Continuous intrathecal
baclofen for severe spasticity. Lancet.
1985;2:125-127.
30 Penn FD, Savoy SM, Corcos DM, et al. In-
trathecal baclofen for severe spinal spasticity.
N Engl J hled. 1989;320:1517-1521.
31 Ochs (;, Struppler A, Meyerson BA, et al.
Inrrathecal baclofen for long-term treatment of
spasticity: :a multi-centre study.J Neurol Neu-
rosurg P.ychiafy. 1989;52:933-939.
32 Latash ML, Penn RD, Corcos DM, Gottlieb
GL. Shon-~ermeffects of intrathecal baclofen
in spasticity. Exp Neurol 1989;103:165-172.
33 Latash ML, Penn RD, Corcos DM, et al. Ef-
fects of inrrathecal baclofen on voluntary mo-
tor contro:l in spastic paresis. J Neurosurg.
1990;72:388-392.
Physical Therapy /Volume 71, Number 1 /January 1991
34 Parke B, Penn RD, Savoy SM, Corcos DM.
Functional outcome after delivery of intrathe-
cal baclofen. Arch Pbys Med Rehabil.
1989;70:30-32.
35 van der Kamp W, Berardelli A, Rothwell JC,
et al. Rapid elbow movements in patients with
torsion dystonia. J Neurol Neurosurg Psycbia-
t v . 1989;52:1043-1049.
36 Halle~tM, Alvarez N. Attempted rapid el-
bow flexion movements in patients with athe-
tosis. J Neurol Neurosurg Psychiatv.
1983;46:745-750.
37 Berardelli A, Dick JPR, Rothwell JC, et al.
Scaling of the size of the first agonist EMG
burst during rapid wrist movements in pa-
tients with Parkinson's disease. J Neurol Neu-
rosurg Psychiatv. 1986;49:1273-1279.
38 Thompson PD, Berardelli A, Rothwell JC, et
al. The coexistence of bmdykinesia and chorea
in Huntington's disease and its implications for
theories of the basal ganglia and control of
movement. Brain. 1988;111:233-244.
3 9 Hallett M. Ballistic elbow flexion move-
ments in patients with amyotrophic lateral
sclerosis.J Neurol Neurosurg Psychiatry
1979;42:232-237.
40 Fagioli S, Berardelli A, Hallett M, et al. The
first agonist and antagonist burst in patients
with an upper motor neuron syndrome. Move-
ment Disorders. 1988;3:126132.
41 Newel1 KM. Down's syndrome and motor
control: comments and notes. Presented at the
first conference of motor control in Down syn-
drome; 1989; Chicago, Ill.
42 Tirosh E, Rabino S. Physiotherapy for chil-
dren with cerebral palsy. Am JDis Child.
1989;143552-555.
43 Schenkman M, Butler RB. A model for
multisystem evaluation, interpretation, and
treatment of individuals with neurologic dys-
function. Phys Ther. 1989;69:538-547.
44 Winstein CJ. Motor learning considerations
in stroke rehabilitation. In: Duncan PW, Badke
MD, eds. Stroke Rehabilitation: The Recoveql of
Motor Control. Chicago, Ill: Year Book Medical
Publishers Inc; 1987:109-134.
45 Kottke FJ, Halpern D, Easton JKM, et al.
The training of coordination. Arch Phys Med
Rebabil 1978;59567-572.
46 Corcos DM, Gottlieb GL, Jaric S, et al. Or-
ganizing principles underlying motor skill ac-
quisition. In: Winters J , Woo S, e d ~Multiple
.
Muscle Svstems: Bionrechanics a n d Movement
Opanization. New l'ork, NY: Springer-Vcrlag
New York Inc; 1990:;!51-267.
47 Bohannon RW. 1: [he measurement of
muscle strength appt.opriate in patients with
brain lesions? A special communication. Pbvs
Ther. 1989;69:225-236.
48 Campbell SK. Api~licationof Exercise Prin-
ciples to Treatment of Cerebral Palsy. Forum
Medicum/American F'hysical Therapy Associa-
tion Self-Study Cour:e. Berqwille, Va; 1988.
49 Colebatch JG, Gandevia SC, Spira PJ, et al.
Voluntary muscle strength in hemiparesis: dis-
tribution of weaknes.i at the elbow. JNeurol
Neurosurg Psychiatq'. 1986;49:1019-1024.
50 Hashinioto SA, Paty DW. Multiplc sclerosis.
Disease-A-Month. 1916;32:523-589.
51 Gottlieb GL, Corc.os DM, Jaric S, Aganval
GC. Practice improvt.s even the simplest move-
ments. &p Brain Re:; 1988;73:436440.
52 Schmidt R4,Young DE. Transfer of move-
ment control in motor skill learning. In: Cor-
mier SM, Hagnian JC, e d ~Tranger
. oj'Learn-
ing. Orlando, Fla: Acidemic Press Inc;
1987:47-79.
53 Craik RL, Oatis C4. Gait assessment in the
clinic: issues and approaches. In: Rothstein JM,
ed. Measurement in Physical Therapv New
York, NY: Churchill 1.ivingstone Inc; 1985:169-
205.
54 Mizrahi EM, Angc.1 RW. Impairment of vol-
untary movement by spasticity. Ann Neurol.
1979;5:594-595.
55 Sahrmann SA, Norton BJ. The relarionship
of voluntary movemcmt to spasticity in the up-
per motor syndrome. Ann Neurol. 1977;2:460-
46 5.
56 Landau WM. Spasicity: What is it? What is it
not? In: Feldman RG Young RR. Koella WF',
eds. Spasticity: Dison fered Motor Control. Mi-
ami, Fla: Symposia Sl>ecialists Inc; 1980:17-24.
57 McLellan DL, Hasan N, Hodgson J.4. Track-
ing tasks in the assessment of spasticity. In:
Delwaide PJ, Young RR, eds. Restorative Neu-
rologv. Amsterdam, the Netherlands: Elsevier
Science Publishers BV; 1985:131-139.
58 Nashner LM. A f~nctionalapproach to un-
derstanding spasticit::. In: Struppler A, Weindl
A, eds. Electromyogr~zphya n d Evoked Poten-
tials. Berlin, Federal Republic of Germany:
Springer-Verlag; 198522-29.