ORIGINAL ARTICLE
Observation and
Following hemiplegic stroke, many people
present with one or more clinically significant
kinematic deviations from normal gait.
Significant kinematic deviations observed in
swing phase include decreased peak hip flexion,
decreased peak knee flexion, decreased knee
extension for heel strike and decreased ankle
dorsiflexion throughout swing. In this paper the
causes of these kinematic deviations are
discussed in terms ofthe forces produced by the
inappropriate activation and adaptive shortening
of particular muscle groups.
[Moore S, Schurr K, Wales A. Moseley A and
Herbert R: Observation and analysis of
hemiplegic gait: swing phase. AustralianJournal
of Physiotherapy 39: 271-278]
Key words: Cerebrovascular
Disorders, stroke; Gait;
Physical Therapy
Sally Moore BAppSc(Phtyl. MHScEd is the
physiotherapy neurological programme co-
ordinator at the Mt Wilga private hospital,
Hornsby.
Karl Schurr BAppSc(Phty) is a physiotherapy
clinical unit supervisor at Lidcombe Hospital.
Amanda Wales BAppSc{Phty), MEd is a
physiotherapy student unit supervisor at
Lidcombe Hospital.
Anne Moseley BAppSc(Phty), GradDip
AppSc(ExSpSc) is the physiotherapy clinical unit
supervisor in the Lidcombe Hospital Head Injury
Unit.
Rob Herbert BAppSc(Phtyl. MAppSc is a lecturer
in the School of Physiotherapy, The University
of Sydney, Lidcombe.
Correspondence: Rob Herbert, School of
Physiotherapy, Faculty of Health Sciences, The
University of Sydney, PO Box 170, Lidcombe,
NSW 2141.
analysis of hemiplegic gait:
swing phase
wing phase begins at toe-off and
ends at heel strike. At normal
walking speeds, it occupies about
40 per cent of the duration of the gait
cycle. In swing phase, the foot is
moved forward to a point which is in
front of the hips, complementing
stance phase in which the hips are
moved forward to a point which is in
front of the foot. Together, the stance
and swing phases transport the body
forward in space.
There are specific physical
requirements for swing phase to be
successful. The foot must be
transported forward, and the lower
limb must shorten sufficiently to
enable the swinging foot to clear the
ground. The important kinematic
characteristics which enable this to
occur are hip flexion, knee flexion then
extension, and ankle dorsiflexion.
The temporal sequence of these
kinematic characteristics in normal
walking seems to be virtually invariant
(Winter 1987, Figure 1), perhaps
reflecting the precision required to
swing the foot through at high
velocities and clear the ground by less
than a few centimetres. The knee
begins to flex in the last third of stance
phase and continues flexing for the
first quarter of swing phase.
Thereafter, the knee is extended until
just prior to heel strike, when slight
flexion occurs in preparation for the
next stance phase. The hip begins to
flex in the latter part of stance phase
and it completes its flexion in the first
half of swing phase. Ankle dorsiflexion
begins just after toe-off and peak
dorsiflexion is attained by about mid-
swing. This position is then
maintained by the ankle throughout
the remainder of swing (Winter 1987).
Although there is a large amount of
published data on the kinetics of swing
phase (eg Cavanagh and Gregor 1975,
Winter 1987, Figure 2) the
intersegmental dynamics of swing are
not well understood. As with the stance
leg, it has been suggested that the
motion of the swing leg is
predominantly pendular in nature
(Mena et al 1981, Mochon and
McMahon 1980), involving a complex
interaction of motion-dependent and
gravitational moments and only
relatively small muscle moments
(Zernicke et aI1991). Kinematic events
which occur in pre-swing (ie in the
period immediately preceding swing
phase, Skinner et aI1985), particularly
extension of the hip at the end of
stance phase and the large hip flexion
angular velocity at the beginning of
swing phase, appear to be critical in
establishing these interactions.
The mechanics of normal gait
provide a template against which the
mechanics of hemiplegic gait can be
compared. Table 1 summarises some
of the kinematic deviations of the
swing phase of gait commonly
observed after hemiplegic stroke, and
their most probable causes. [The
preceding paper (Moseley et a11993)
has presented an analysis of the stance
phase of hemiplegic gait]. The
remainder of the paper is divided into
four main sections. Each section
provides a description of a clinically
significant kinematic deviation from

the normal kinematics of swing phase,
and a discussion of possible causes of
that kinematic deviation. In addition,
each section includes a description of
associated kinematic deviations.
Associated kinematic deviations occur
either as a direct consequence of the
motor problem, or as an adaptive
strategy which is learned in order to
compensate for the motor problem
(Carr and Shepherd 1987).
Decreased peak hip flexion
The hip joint reaches a mean peak
extension of about 11 degrees (SD 8
degrees) before it begins to flex in late
stance (Winter 1987). At this stage,
knee flexion and ankle plantarflexion
have already commenced. By toe-off
the hip has flexed to about 8 degrees
(SD 7 degrees) of extension and it
continues to flex to a peak of about 19
degrees (SD 5 degrees) of flexion by
mid-swing.
In pre-swing, the hip accelerates into
flexion at least partly under the
influence of a net hip flexor muscle
moment (Winter 1987), and probably
also under the influence of
gravitational moments (Zernicke et al
1991). The resulting hip flexion
continues into swing phase, but
progressively more slowly (Winter
1987). That is, because the hip flexion
angular velocity is decreasing, the hip
is actually accelerating towards
extension in the period just after toe-
off. This acceleration occurs under the
influence of large motion-dependent
moments, attributable particularly to
the angular acceleration of the leg
(Zernicke et aI1991). The tendency of
the hip to accelerate towards extension
under the influence of these motion-
dependent moments is counteracted by
the net hip flexor muscle moment
which persists for about the first
quarter of swing phase (Winter 1987,
Zernicke et aI1991). The flexor muscle
moment observed in early swing, like
the flexor muscle moment in pre-
swing, is produced by a concentric
contraction of the rectus femoris
(Shiavi et a11987, Winter 1987), and
probably by the iliopsoas muscles as
well.
ORIGINAL ARTIClE
The concentric contraction of the hip
flexors which occurs in pre-swing and
early swing phase probably provides a
critical contribution to normal swing
phase dynamics. Evidence for this
comes from mathematical models
which have been used to investigate
the dynamics of swing phase in normal
walking (Mena et al 1981, Mochon and
McMahon 1980). These models
illustrate that the thigh behaves
essentially as a constrained compound
pendulum during swing phase; that is,
its motion is determined largely by
gravitational and motion-dependent
forces, requiring relatively little
muscular control in the middle part of
swing. The models show that the
kinematics of the swinging leg depend
largely on the initial thigh angular
velocity and on the amount of hip
extension achieved late in stance phase
(Mena et al 1981, Mochon and
McMahon 1980). This suggests that
the concentric hip flexor muscle
activity in pre-swing is important
because it establishes an appropriate
thigh angular velocity and an
appropriate angular displacement of
the hip at the beginning of swing
phase.
Peak hip flexion has been reported to
be both increased and decreased in
people with hemiplegic stroke (Burdett
et a11988, Knutsson and Richards
1979, Malezic et a11987, Pinzur et al
1987). In the absence of detailed
kinetic data on the swing phase of
hemiplegic gait, it is difficult to know
what causes these deviations of hip
kinematics. Given that the hip flexor
muscles have an important role in the
setting up of normal swing phase
dynamics, it seems plausible that an
inability to appropriately activate the
hip flexor muscles in pre-swing could
cause a decrease in the hip flexion
velocity in early swing, which in turn
could result in a decrease in peak hip
flexion. Alternatively, it is possible that
any of the causes of decreased peak hip
extension discussed in the preceding
paper (Moseley et a11993) could lessen
the gravitational moments which act to
flex the hip in late stance and early
swing so that normal peak hip flexion
is not attained. Also, alterations in knee
flexion kinematics during swing could
alter the motion-dependent moments
which normally act to produce
continuing hip flexion at the end of
swing phase in the presence of
substantial hip extensor muscle
moments (Zernicke et aI1991). The
causes put forward here can only be
speculative; more experimental data is
required before any certainty can be
attached to them.
A decrease in the peak hip flexion
achieved in swing phase may
contribute to a decrease in step length,
because decreasing hip flexion
decreases the extent to which the swing
foot can be moved in front of the hips.
Following hemiplegic stroke, some
people learn to compensate for an
inability to adequately flex the hip by
inclining the trunk and pelvis
backwards at the end of swing phase.
This enables them to get the swing
foot in front of the hips at the end of
swing phase, and thus increase step
length, without the normal amount of
hip flexion. People who employ this
compensatory strategy may also
excessively dorsiflex the contralateral
ankle and flex the contralateral knee in
stance phase, to further increase step
length.
An increase in peak hip flexion
sometimes occurs as a compensation
for an inability to extend the knee in
late swing. If the knee is not
sufficiently extended at the end of
swing, step length will be diminished.
In these circumstances, some people
learn to increase their step length by
increasing the amount of hip flexion at
the end of swing.
Decreased peak knee flexion
The knee begins to flex about two-
thirds of the way through stance in
preparation for swing phase. At this
time, the hip is still extending and the
ankle has not yet begun to plantarflex
(Skinner et a11985, Winter 1987). A
peak knee flexion angle of
approximately 65 degrees (SD 5
degrees) is attained in the first third of
swing phase. Importantly, about half of
the total knee flexion occurs during the
latter part of stance phase (Cavanagh
and Gregor 1975, Cerny 1984,
 ORIGINAL ARTICLE

Table 1.
Commonly observed swing phase kinematic deviations and some of their possible causes.

Kinematic deviation Potential causes

Decreased peak hip flexion in swing phase Inability to produce sufficient active tension with the hip flexor
muscles in pre-swing or early swing
Decreased peak hip extension in late stance phase

Decreased peak knee flexion Inability to produce sufficient active tension with the knee flexor
in early swing phase muscles in pre-swing
Production of excessive active tension with the knee extensor
muscles in pre-swing or early swing
Production of excessive active tension with the plantarflexor
muscles in pre-swing
Adaptive shortening of the plantarflexor muscles
Decreased peak hip extension in late stance phase

Decreased knee extension Inability to produce sufficient active tension with the knee
prior to heel strike extensor muscles in early swing
Production of excessive active tension with the knee flexor
muscles in swing
Adaptive shortening of the knee flexor ml,lscles, ora loss of
compliance of other tissues on the flexor aspect of the knee
Decreased knee flexion in early swing

Decreased dorsiflexion in swing phase
Inability to produce sufficient active tension with the dorsiflexor
muscles in swing
Production of excessive active tension with the plantarflexor
muscles in swing
Adaptive shortening of the plantarflexor muscles

Kettlekamp et a11970, Winter 1987).
That is, a substantial part of the
shortening of the leg which needs to
occur for the successful execution of
swing phase occurs prior to toe-off.
Pre-swing events need to be
considered, therefore, when examining
the possible causes of the inability to
sufficiendy flex the knee in swing
phase.
Winter's studies of normal subjects
indicate that a small net flexor muscle
moment usually acts at the knee from
approximately 40 to 54 per cent of the
gait cycle at slow walking speeds,
although this is quite variable (Winter
1987). This implies that knee flexor
muscles contribute to the initial
acceleration of the knee into flexion in
late stance. EMG studies suggest that
the knee flexor moment is produced
predominandy by the gastrocnemius
muscle (Shiavi et al 1987, Winter
1987); the hamstring muscles are
relatively quiescent at and immediately
preceding this time (Cappozzo et al
1976, Knutsson and Richards 1979,
Shiavi et al 1987, Winter 1987 , Yang
and Winter 1985). At the very end of
stance, the knee flexion velocity begins
to decrease and the net knee flexor
moment diminishes or changes to a net
extensor moment (Winter 1987).
However, at very slow walking speeds
(for example speeds ofless than
0.5 m.s- I ), the normal limb dynamics
can be quite variable - in some people
the net flexor muscle moment persists
until toe-off (Cavanagh and Gregor
1975).
Kinetic studies of normal walking
consistendy show that, at least at slow
normal walking speeds, knee flexion in
early swing phase is not usually
accompanied by a knee flexor muscle
moment (Cavanagh and Gregor 1975,
Winter 1987, Zernicke et aI1991).
Perhaps this should not be surprising
because even though the knee is
flexing, it is accelerating into extension
in this part of swing (Winter 1987). At
and after toe-off in normal walking, a
small net extensor muscle moment acts
at the knee (Cavanagh and Gregor
1976, Winter 1987, Zernicke et al
 ORIGINAL ARTICLE

1991). This is in addition to the weight

moment, which is also acting to extend F
the knee at this time. Only the motion-
dependent moments attributable to the
angular acceleration of the leg tend to
flex the knee in early swing (Zernicke
et aI1991).
A decreased knee flexion during
swing is commonly observed in people
with hemiplegic stroke. There are
reports in the literature of decreased
knee flexion during pre-swing
(Knutsson and Richards 1979, E
Lehmann et al 1987, Olney et al 1988
and 1989, Takebe and Basmajian
1976), at toe-off (Brandell 1977,
Burdett et al 1988, Finley and F
Karpovich 1964, Knutsson and
Richards 1979, Lehmann et a11987,
Olney et al1986 and 1988, Takebe and
Basmajian 1976) and during swing
phase (Knutsson and Richards 1979,
Lehmann et a11987, Olney et al 1986,
1988, and 1989, Takebe and Basmajian
1976, Van Griethuysen et al 1982).
People who fail to adequately flex the
knee in early swing often scrape the
foot on the ground during swing, or E
they may exhibit marked compensatory
strategies, suggesting that the
decreased knee flexion cannot be
explained simply by reduced walking OF
speeds.
Several possible causes exist for the :'
.~ ...............
failure to adequately flex the knee in
swing phase. These causes first
manifest late in stance phase as an
inability to initiate knee flexion during
the pre-swing part of the gait cycle.
The authors' clinical observations and
the observations reported by Carr and
Shepherd (1987) suggest that many -20
people are unable to sufficiently PF
activate the knee flexor muscles
following stroke. It is possible that an o 20 40 80 80 100
inability to provide the necessary initial Time <" of cycle)
burst of concentric knee flexor muscle
activity in pre-swing is a common
cause of a lack of knee flexion at toe-
off and in swing. Conversely, excessive Stance Swing
activation of knee extensor muscles,
especially the rectus femoris, can
prevent the knee flexion which Figure
normally occurs at the end of stance or Normal sagittal Imee ami ankle displacements \fersus time
early in swing. le\fe! walking at a slow cadence (redraw!! from the data of Winter 1987 with permissioll
Altered muscle moments acting at the from tile <luthor). Graphs are of mealls alia Orie standard deviation about the meal!.
 AUSTRAliAN PHYSIOTHERAPY ORIGINAL ARTICLE

ankle joint in pre-swing constitute

0.8 another possible cause of a lack of knee
E flexion in swing. In normal walking,
...
0;
.......
0.6 the knee flexion initiated in pre-swing
E continues to occur into the first third
0.4
~ of swing phase due to the significant
•a• 0.2 '.~ ............. ...., ..
~
inertia of the leg. However, increases
in plantarflexor muscle activity and
E
,., 0.0 adaptive changes in the length and
"0
0
.AI compliance of plantarflexor muscles
::::- -0.2 can produce excessive plantarflexor
'"•
E
........... ...".

'. .... }' muscle moments which inhibit the

0 -0.4 /l
E ...... 1 initiation of knee flexion by preventing
Q.
-0.6 the leg from moving forward over the
X ' .. foot in late stance. If knee flexion is not
-0.8 F initiated in pre-swing, the normal peak
1.0 knee flexion cannot be attained
......
,.."
E without the production of unusually
0.8
....... large knee flexor moments in early
E swing.
0.6
3 Aberrant segmental alignment in late
••a 0.4
stance, caused by one or more of a
E
,., 0.2 number of common problems, may be
"0
another cause of the failure to initiate
..•
.........
0

c
0.0

-0.2
knee flexion. Lehmann et al (1987)
reported that the vertical component
E
0 of the ground reaction force of seven
E -0.4
people with hemiparetic stroke tended
•• -0.6 to pass more anterior to the knee
'"
:.0:
F during stance phase than in age and
-0.8
speed matched normals. This indicates
2.0 that the body's centre of mass was
positioned further in front of the knee
...
0;
.......
........
. . '
PF
than normal, and probably also that
E 1.:1
.'.'
.' the mass of segments superior to the
z
..... knee induced a larger than normal
•a• 1.0 ,
gravitational moment which acted to
,.,E extend the knee. Such a situation
"0 would be expected to occur whenever
...
0

...
....... 0.:1 the hip failed to extend adequately in
stance phase. Several possible causes of
•'"E decreased hip extension have been
0
E 0.0 .. .:
'
discussed in the accompanying paper
•
:; '.' (Moseley et aI1993). Theoretically,
c
-< OF the large external knee extensor
-0.5 moments associated with decreased hip
0 20 40 60 80 100
extension could inhibit the initiation of
Time (S of cycle) knee flexion in pre-swing. Clinical
observations of people who have
difficulty in achieving adequate knee
flexion during swing phase are
Stance Swing consistent with this idea. It has been
_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _-----.l
observed that once an appropriate
2. segmental alignment is established (ie
!mee and ankle muscle moments fever walking at a slow cadence
once the hip is sufficiently extended in
stance phase) these people sometimes
tt16 data of 19811.IVith permission from tile author). Graphs are of
become more able to initiate knee
means and Olle stimdard deviation about -Ine meim.

flexion in preparation for swing phase.
This illustrates that the causes of the
failure to flex the knee adequately in
swing may lie in the inability to set up
swing phase during stance.
The compensations which are likely
to be associated with decreased knee
flexion are those which effectively
shorten the lower limb. These include
elevation of the pelvis on the side of
the swinging leg (ie abduction of the
contralateral leg) and occasionally
abduction (or circumduction) of the
swing leg (Knutsson and Richardson
1979, Lehmann et aI1987). Elevation
of the pelvis is usually accompanied by
inclination of the trunk towards the
contralateral side, and stability
requirements dictate that this, in turn,
be accompanied by a decreased lateral
displacement of the pelvis to the
contralateral side during contralateral
stance.
Decreased knee extension
prior to heel strike
Peak knee flexion occurs at about one
third of the way through swing phase,
after which the knee extends, usually
until just prior to heel strike. The knee
extends from approximately 65 degrees
(SD 5 degrees) of flexion to about 2
degrees (SD 3 degrees) of flexion
(Winter 1987). It is during this latter
two-thirds of swing phase that the
motion of the limb most closely
resembles that of a compound
pendulum (Mena et al 1981, Mochon
and McMahon 1980).
The knee begins to extend about one
third of the way through swing phase,
primarily under the influence of
gravitational forces and a knee extensor
muscle moment. It continues to
accelerate towards extension under the
influence of a diminishing knee
extensor muscle moment until about
two thirds of the way through swing.
Thereafter, a small net knee flexor
moment (Winter 1987, Zernicke 1991)
attributable to eccentric knee flexor
muscle activity (Knutsson and Richards
1979, Winter 1987) begins to
decelerate the knee so that it is no
longer extending at heel strike (Winter
1987). In this part of swing, motion-
ORIGINAL ARTICLE
dependent moments, primarily those
attributable to the angular
accelerations of the leg and thigh,
produce an external extensor moment
(Aleshinsky 1986, Zernicke et aI1991).
A lack of knee extension prior to heel
strike has commonly been reported in
the literature on hemiplegic gait
(Finley and Karpovich 1964, Knutsson
and Richards 1979, Lehmann et al
1987, Olney et al1988 and 1989, Van
Griethuysen et al 1982). A probable
cause of a decreased peak knee
extension is likely to be the inability to
sufficiently activate the knee extensor
muscles in the first third of swing
phase. Failure to sufficiently activate
the knee extensor muscles may mean
that the knee does not adequately
accelerate towards extension, or
accelerates towards flexion, in the early
part of swing. Also, failure to attain a
normal peak knee flexion at the
beginning of swing phase may
diminish the gravitational forces which
tend to accelerate the knee towards
extension. In addition, the knee may
fail to extend adequately if there is
insufficient acceleration of the thigh or
leg in mid to late swing to generate the
motion-dependent moments which
normally tend to extend the knee.
Finally, a lack of knee extension prior
to heel strike may also result from an
excessive knee flexor muscle moment
due either to excessive activation of the
knee flexor muscles or to changes in
the length and stiffness of the tissues
on the flexor aspect of the knee. A
substantial number of people who are
unable to extend the knee at the end of
swing phase have significant
shortening of the hamstring or
gastrocnemius muscles.
Occasionally, people with hemiplegic
stroke have been observed
hyperextending the knee prior to heel
strike. Perhaps some of these people
are unable to control the motion-
dependent moments which act to
extend the knee and which are
normally controlled by eccentric knee
flexor activity (Zernicke et al 1991).
Failure to extend the knee at the end
of swing phase will have the effect of
decreasing step length unless
compensations are employed. Simple
calculations show that failure to extend
the knee the last 20 degrees could
decrease step length by as much as one
quarter. Commonly, people who are
unable to extend the knee at the end of
swing phase compensate by increasing
their cadence, excessively extending
the contralateral hip, and excessively
flexing the contralateral knee during
stance phase.
Decreased peak
ankle dorsiflexion
At the end of stance, the ankle
undergoes rapid plantarflexion and it
continues to plantarflex briefly after
toe-off, reaching a maximum of about
18 degrees (SD 5 degrees) at
approximately 66 per cent of the gait
cycle (Winter 1987). The ankle then
dorsiflexes to an approximately
plantargrade position by about half
way through swing phase, and it
essentially maintains this position until
heel strike (Winter 1987). It is
important that the ankle achieves this
degree of dorsiflexion by about 85 per
cent of the gait cycle because it is at
this time that the ankle joint passes
closest to the ground; a plantargrade
position of the ankle is necessary at this
point in the gait cycle in order to
prevent the toes hitting the ground as
the leg swings through. Although the
net muscle moments acting at the
ankle during swing phase are very
small (Winter 1987), EMG recordings
of tibialis anterior muscle activity show
peaks of activity at the beginning and
end of swing (Shiavi et al1987, Winter
1987). Presumably the tibialis anterior
muscle produces a dorsiflexion
moment which prevents the ankle
accelerating into plantarflexion under
the influence of motion-dependent
moments early in swing phase (Mena
et alI981).
Lack of dorsiflexion in swing phase
and at heel strike is a commonly
reported kinematic deviation in people
with hemiplegic stroke (Berger et al
1984, Burdett et al1988, Colaso and
Joshi 1971, Finley and Karpovich
1964, Guiliani 1990, Knutsson and
Richards 1979, Lehmann et al1987,
Olney et al1986, 1988, and 1989,
Wolf and Minkiwitz 1989). When a

lack of dorsiflexion is evident
throughout swing phase, it is likely to
be due to an inability to generate a
sufficiently large dorsiflexor muscle
moment. EMG studies indicate that,
following stroke, many people are
capable of only reduced levels of
activation of their dorsiflexor muscles
during swing (Dimetrejevic 1981, Peat
1976). Also, and perhaps even more
commonly, a reduced dorsiflexion in
swing phase may be caused by an
increased plantarflexor muscle moment
attributable either to adaptive
shortening or excessive activation of
the plantarflexor muscles. Numerous
studies have documented EMG
findings and findings of changes in the
passive mechanical properties of the
ankle in people with hemiplegic stroke
(eg Berger et al 1981, Dimetrejevic
1981, ThilmannetaI1991). These
changes would be expected to reduce
the ability to dorsiflex the ankle during
swing phase.
As the foot normally clears the
ground by less than a few centimetres
during swing phase, a failure to
dorsiflex the ankle during swing will
effectively lengthen the lower limb.
Unless compensations are made, this is
likely to result in the foot hitting the
ground as the hip flexes and the knee
extends. To compensate for this
increased lower limb length, people
with hemiplegic stroke may excessively
elevate the pelvis on the side of the
swinging leg (ie abduct the
contralateral hip in stance) and perhaps
also abduct the swing hip, and they
may laterally flex the trunk towards the
unaffected side and restrict the lateral
pelvic displacement towards the stance
leg in much the same way as discussed
under decreased peak knee flexion
above.
Conclusion
The science of clinical gait analysis is
one that is still evolving under the
influence of a rapidly expanding
research base. Pertinent research could
have a substantial impact on clinical
practices. More research into the
incidence and significance of individual
kinematic deviations and the causes of
these common kinematic deviations
ORIGINAL ARTICLE
would be particularly useful, because it
would enable physiotherapists to more
objectively structure intervention
around key problems. Another area yet
to be addressed is the intersegmental
dynamics of gait. Currently, there are
no data available on the intersegmental
dynamics of stance phase, yet this
information is critical for the
understanding of normal walking
mechanics. Finally, there is enormous
potential value in mathematical models
of both normal and pathological gait
(eg Yamaguchi et al 1991) because such
models can potentially provide
objective answers to questions such as
how a particular person's gait might be
expected to improve if they were to
become more able to generate
plantarflexor moments, or if they had
longer hip flexor muscles. Clearly the
field of biomechanics has much to
contribute to the clinical practice of
gait observation and analysis.
Acknowledgements
The authors wish to thank Jack
Crosbie, Michael Lee,Janet Carr,
Roberta Shepherd and Pat Pamphlett
for their comments on earlier drafts of
the manuscript.
References
Aleshinsky SU (1986): An energy "sources" and
"fractions" approach to the mechanical energy
expenditure problem - I. Basic concepts,
description of the model, analysis of a one-
link system of movement. Journal of
Biomechanics 19: 287-293.
Berger W, Horstman G and Dietz V (1984):
Tension development and muscle activation
in the leg during gait in spastic hemiparesis:
independence of muscle hypertonia and
exaggerated stretch reflexes. Journal of
Neurology, Neurosurgery and Psychiatry 47:
1029-1033.
Brandell BR (1977): Functional roles of the calfand
vastus muscles in locomotion. American
Journal ofPhysical Medicine 56: 59-74.
Burdett RG, Birello-France D, Blatchly C and
Potter C (1988): Gait comparison of subjects
with hemiplegia walkingunbraced, with ankle-
foot orthosis and with air-stirrup brace.
Physical Therapy 68: 1197-1203.
Carr JH and Shepherd RB (1987): A Motor
Relearning Programme for Stroke (2nd ed.)
London: Heinemann, pp. 29-42, 125-148.
Cappozzo A, Figura F and Marchetti M (1976):
The interplay of muscular forces in human
ambulation. Journal ofBiomechanics 9: 35 -43.
Cavanagh PR and Gregor RJ (1975): Knee joint
during the swing phase of normal treadmill
walking. Journal of Biomechanics 8: 337-344.
Cerny K (1984): Pathomechanics ofstance: clinical
concepts for analysis. Physical Therapy 64:
1851-1859.
Colaso M and Joshi J. (1971): Variation of gait
pattern in adult hemiplegia. Neurology India
(Bombay) 19: 212-216.
Dimitrijevic MR, Faganel J, Sherwood AM and
McKay WE (1981): Activation of paralysed
leg flexors and extensors during gait in patients
after stroke. Scandinavian Journal of
Rehabilitation Medicine 13: 109-115.
Finley FR and Karpovich PV (1964):
Electrogoniometric analysis of normal and
pathological gaits. Research Quarterly 35: 379-
384.
Guiliani CA(1990): Adult hemiplegic gait. In Smidt
GL (Ed.) Gait Rehabilitation. New York:
Churchill Livingstone, pp. 253-266.
Kettlekamp DB, Johnson RJ, Smidt GL, Chao
EYS and Walker M (1970): An
electrogoniometric study of knee motion in
normal gait. Journal ofBone and Joint Surgery
52: 775-790.
Knutsson E and Richards C (1979): Different types
of disturbed motor control in gait of
hemiplegic patients. Brain 102: 405- 430.
Lehmann JF, Condon SM, Price Rand deLatour
BJ (1987): Gait abnormalities in hemiplegia:
their correction by ankle-foot orthoses.
Archives ofPhysical Medicine and Rehabilitation
68: 763-771.
Malezic M, Klajic M, Acimovic-Janezic R, Gros N,
Krajnik J and Stenic U (1987): Therapeutic
effects of multisite electric stimulation of gait
in motor-disabled patients. Archives ofPhysical
Medicine and Rehabilitation 68: 553-560.
Mena D, Mansour JM and Simon SR (1981):
Analysis and synthesis of human swing leg
motion during gait and its clinical applications.
Journal of Biomechanics 14: 823-832.
Mochon S and McMahon TA (1980): Ballistic
walking. Journal ofBiomechanics 13: 49-57.
Moseley A, Wales A, Herbert R, Schurr K and
Moore S (1993): Observation and analysis of
hemiplegic gait: stance phase. Australian
Journal of Physiotherapy 39: 259-267
Olney S, Colborne GR and Martin CS (1989):
J oint angle feedback and biomechanical gait
analysis in stroke patients: a case report.
Physical Therapy 69: 863-870.
Olney SJ,Jackson VG and George SR (1988): Gait
re-education guidelines for stroke patients
with hemiplegia using mechanical energy and
power analyses. Physiotherapy Canada 40: 242-
248.
Olney SJ, Monga TN and Costigan PA (1986):
Mechanical energy of walking of stroke
patients. Archives of Physical Medicine and
Rehahilitation 67: 92-98.
Peat M, Dubo HIC, Winter DA, Quanbury AO,
Steinke T and Graham R (1976):
Electromyographic analysis of gait:
~
 ORIGINAL ARTICLE

hemiplegic locomotion. Archives ofPhysical Medicine andRehahilitation 57:

421-425.
Pinzur MS, Sherman R, DIMonte-Levine P and Trimble J (1987): Gait
changes in adult onset hemiplegia. American Journal ofPhysical Medicine
66: 228-237.
Shiavi R, Bugle HJ and Limbird T (1987): Electromyographicgaitassessment,
part I: adult EMG profiles and walking speed. Journal of Rehabilitation
Research and Development 24: 13-23.
Skinner SR, Antonelli D, Perry J and Lester DK (1985): Functional demands
on the stance limb in walking. Orthopedics 8: 355-36l.
Takebe K and BasmajianJV (1976): Gait analysis in stroke patients to assess
treatments of foot-drop. Archives of Physical Medicine and Rehabilitation
57: 305-310.
Thilmann AF, Fellow SJ and Ross HF (1991): Biomechanical changes at the
ankle joint after stroke. Journal ofNeurology, Neurosurgery and Psychiatry
54: 134-139.
Van Griethuysen CM, PauIJP, Andrews BJ and NicolAC (1982): Biomechanics
of functional electrical stimulation. Prosthetics and Orthotics International
6: 152-156.
Winter DA (1987): The Biomechanics and Motor Control of Human Gait.
Waterloo, Canada: University of Waterloo Press.
Wolf SL and MinkiwitzJA (1989): Topical anesthetics: effects on the Achilles
tendon and H-reflexes II. Stroke patients. Archives of Physical Medicine
and Rehabilitation 70: 673-677.
Yamaguchi GT, Pandy MG and Zajac FE (1991): Dynamic musculo-skeletal
models of human locomotion: perspectives on model formulation and
control. In Pacia AE (Ed.): Adaptability of Human Gait. Amsterdam:
North-HollandlElsevier, pp. 205-240.
Yang JF and Winter DA (1985): Surface EMG profiles during different
cadences in humans. Electroencephalography and Clinical Neurophysiology
60: 485-491.
Zernicke RF, Schnieder K and Buford JA (1991): Intersegmental dynamics
during gait: implications for control. In Pacia AE (Ed.): Adaptability of
Human Gait. Amsterdam: North-HollandlElsevier, pp. 187-202.