Hemiplegic Gait

HEMIPLEGIC
GAIT
Presented By: Himani Kaushik
1

INTRODUCTION
Hemiplegia is a paralysis of one side of the
body due to corticospinal tract lesion at any
point from its origin in the cerebral cortex
down to the fifth cervical segment.
In hemiplegia, shoulder is adducted; the elbow
is flexed; the forearm is pronated, and the wrist;
fingers are flexed; knee is held in extension and
the ankle is plantar flexed. 2

Causes
➢ Vascular: Stroke, diabetic neuropathy
➢ Infective: encephalitis, meningitis, brain abscess
➢ Neoplastic: glioma-meningioma
➢ Multiple sclerosis
➢ Traumatic brain injuries
➢ Congenital: cerebral palsy
➢ Psychological: parasomnia (nocturnal hemiplegia)
➢ Brown sequard syndrome
3

Hemiplegic type of gait of a person who has had a brain insult and
depends on which area of the brain is affected.
Walking is the phenomenon which is taken for granted by healthy
individuals but requires a complex control of the
neuromusculoskeletal system.
Walking is mainly a result of automatic process, involving the
spinal cord and brainstem mechanisms.
It is usually maintained without conscious awareness and cognitive
processing. 4

Gait abnormality is characterized by
pronounced clinical presentation of gait
asymmetry, as compared to healthy
subjects (Olney and Richards, 1996).
Hemiplegic gait usually have:
1. Decreased stance phase and
prolonged swing phase of the
paretic side.
2. Decreased walking speed and
shorter stride length 5

There are 5 biomechanical modules or muscle synergies that are
required to perform sub-tasks of gait in a organized and coordinated
patterns:
Module 1: includes gluteus medius, vasti, and rectus femoris
muscles, primarily contributing to body support in early stance.
Module 2: soleus and gastrocnemius is activated during both body
support and propulsion in late stance.
Biomechanics and Neural Control of the Hemiplegic Gait
6

Module 3: rectus femoris and tibialis anterior acts to decelerate the
leg in early and late swing phase.
Module 4: consists of the hamstrings muscles, activation of these
muscles decelerates the ipsilateral leg prior to heel strike.
Module 3 & 5: iliopsoas act together to accelerate the ipsilateral
leg forward in early swing.
7

These modules represents a general repertoire of motor actions that
can be recruited in a variety of combinations and at different times
for different locomotion control and balance needs.
As compared to the normal gait, fewer modules are seen during
hemiplegic gait pattern.
8

Studies suggested that the number of modules was correlated to
preferred walking speed, speed modulation, step length asymmetry
and propulsive asymmetry (Routson et al., 2014) and for example,
demonstrated that abnormal pattern of muscle activation, joint
positions are altered at rest and joint movement are coupled during
walking as a result of reflex-mediated coupling between hip flexion
and knee extension in hemiplegic gait(Finley et al., 2008).
9

Mulroy et al., 2003 observed full spectrum of gait abnormality
clinically, depending on level of muscle weakness, severity of
spasticity, compensatory mechanisms, walking speed and their
interactions.
According to walking speeds which correspond to the muscle
weakness, they classified hemiplegic gait impairments into 4
different groups: Fast walker, Moderate walker, Slow-Extended
walker (circumductory gait), and Slow-Flexed walker.
10

Fast walker:
➢ 44% of walking speed is normal,
➢ Lack of heel rise is seen in the terminal stance due to plantarflexors
weakness,
➢ Knee hyperextension is observed in order to compensate the lack of
heel rise during terminal stance so that the body can roll forward onto
the forefoot,
➢ Step length is compromised secondary to lack of transition of
momentum from the unaffected limb
11

Moderate walker:
➢ 21% of walking speed is normal
➢ Weakness in gluteus maximus, quadriceps muscles is also seen and
plantarflexor start to show spastic characteristic
➢ Excessive knee and hip flexion occur at mid stance phase as a result
of extensors weakness
➢ Due to the lack of pre-swing forward progression over the toe rocker,
ankle plantar flexion, knee flexion, and heel-off are inadequate in the
terminal stance
➢ However, the survivor is still able to achieve a neutral foot position
for clearance in the mid swing phase without any assistance 12

Slow Extended walker: (Circumductory Gait)
➢ 11% of walking speed is normal
➢ Quadriceps muscles are further weakened, and are not able to support
the knee during the stance phase
➢ Though weak, the gluteus maximus muscle is still strong enough to
retract the femur into knee hyperextension to support the body
➢ During the swing phase, there is persistent gluteus maximus and
ankle plantarflexor spasticity.
➢ Hip hiking and leg circumduction occur for foot clearance and
usually requires a assistive device to walk
13

Slow flexed walker:
➢ 10% of walking speed is normal,
➢ Gluteus maximus muscle is weakened further and not able to retract
femur and stabilize the knee
➢ In mid stance, there is excessive hip and knee flexion, ankle
dorsiflexion and trunk forward leaning
➢ Step length is compromised secondary to lack of transition of
momentum from the unaffected limb, this posture persits in the swing
phase with assistance
15

Extensive neural structures and
pathways are also involved in
the process of gait control,
including the spinal cord,
brainstem, cerebellum, basal
ganglia, limbic system, and
cerebral cortex, as well as their
interactions with the
environment.
10min
5
15
20min
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4
25
30min
35
40min
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5
22
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On the other hand, brainstem descending pathways and the
intraspinal motor network are disinhibited and become
hyperexcitable in hemiplegic gait patterns.
This is mainly a phenomenon of disinhibition, or unmasking
effects.
The wide-range and hierarchy of hemiplegic gait impairments is a
reflection of mechanical consequences of muscle weakness,
spasticity, abnormal synergistic activation and their interactions.
17

Altered neural control for hemiplegic gait. 18

Temporal and Spatial Descriptors of the Hemiplegic Gait
Birol Balaban, Fatih Tok, 2013 concluded that hemiplegic gait
results in
1. Reduced walking speed ( 0.10m/sec to 0.76 m/sec)
2. Decreased Cadence: 98-99 steps/min
3. Decreased Step & Stride time: 0.62 & 1.22 sec.
4. Increased Step & Stride length: 17.7 & 37 inches
5. Increased double support time: 0.32 sec.
6. Decreased support time: 0.44 sec. 19

Stance Phase: (Moore et al.,1993)
➢ Decreased peak hip extension in late stance phase
● Inability to produce sufficient active tension with the hip extensor
muscles early in stance
● Adaptive shortening of hip flexor muscles
● Production of excessive active tension with the hip flexor muscles in
stance
● Production of excessive active tension with the ankle plantarflexor
muscles in stance
● A Adaptive shortening of ankle planterflexor muscles
Observed Kinematics of the Hemiplegic Gait
20

● Inability to produce sufficient active tension with the hip flexor
muscles late in stance
● Inability to produce sufficient active tension with the knee extensor
muscles throughout Stance
● Inability to produce sufficient active tension with ankle plantarflexor
muscles in stance
21

➢ Decreased peak lateral pelvic displacement in stance phase
● Inability to produce sufficient active tension with the hip adductor
muscles in early stance
● Inability to produce sufficient active tension with the hip abductor
muscles in early to mid stance
➢ Increased peak lateral pelvic displacement in stance phase
● Adaptive shortening of the hip adductor muscles
● Production of excessive active tension with the hip adductor muscles
in stance
● Inability to produce sufficient active tension with the hip abductor
muscles in early to mid stance
22

➢ Decreased knee flexion (or knee hyperextension) in stance
phase
● Inability to produce sufficient active tension with the knee flexor
muscles in mid stance
muscles in stance
● Production of excessive active tension with the ankle plantarflexor
muscles in early or mid stance
● Adaptive shortening of ankle plantarflexor muscles
23

➢ Increased knee flexion in stance phase
muscles in a shortened range during stance
● Adaptive shortening of the knee flexor muscles or decreases in the
compliance of other tissues on the flexor aspect of the knee
● Production of excessive active tension with the knee flexor muscles
in stance
➢ Decreased ankle plantarflexion at toe-off
● Inability to produce sufficient active tension with the ankle
plantarflexor muscles in late stance
● Unnecessary due to segmental alignment 24

Swing Phase: (Moore et al.,1993)
➢ 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 in early swing phase
● Inability to produce sufficient active tension with the knee flexor
muscles in pre-swing
Observed Kinematics of the Hemiplegic Gait
25

● 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 prior to heel strike
muscles in early swing
● Production of excessive active tension with the knee flexor muscles
in swing
26

● Adaptive shortening of the knee flexor muscles, or a 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
27

Kinematics of the gait: frontal plane, sagittal plane and horizontal plane. Graph represents the reduced
knee flexion during the swing phase, plantar-flexed ankle at initial contact, reduced dorsiflexion of the
ankle during the last third of the swing phase (the time that the foot passes closest to the ground), rotation
of the hip, knee, and ankle, increased pelvic obliquity, and knee varus are clearly observed (Birol
Balaban, Fatih Tok, 2013). 28

Trunk biomechanics during hemiplegic gait:
Tamaya Van Criekinge et al., 2017 suggests that patients with
hemiplegic gait shows:
● increased mediolateral‐anteroposterior trunk sway,
● larger sagittal motion of the lower trunk,
● rotation of the upper trunk is increased,
● more in‐phase coordination,
● increased instability and asymmetry as there are less movement
towards the paretic side.
29

Energy expenditure:
Birol Balaban, Fatih Tok, 2013 suggests that patients who have had
a hemiplegic walk shorter distances with greater oxygen consumption,
indicating that they walk with a greater oxygen cost (ie, a greater
volume of oxygen is consumed per unit distance traveled).
Energy expenditure during gait in hemiplegic patients varies with the
degree of weakness, spasticity, training, and bracing, but in general,
the oxygen cost of walking is greater in hemiplegic patients (a ratio of
50%-67%) than that in healthy control subjects with comparable body
weight and the same walking speed. 30

Kinetics of the gait: Graph represents the hip & knee flex/ext and ankle dorsiflexion moments and ankle
power generation bursts are lower in amplitude on the paretic side than on the non-paretic side in a
patient who has had a left hemiparesis (Birol Balaban, Fatih Tok, 2013). 31

Ground reaction forces during gait: Figure shows that patients who have had hemiplegic gait have an
asymmetric gait pattern and a decrease mean GRF profiles clearly reveal a significant difference in the
stance phase percentage between sides. The gait speed modifies the moment of the gait cycle where the
peak GRF values occur (Sylvie Nadeau et al., 2013).
.
32

Path of center of pressure during gait: a) stroke without FDS, b) stroke with FDS, c) healthy control.
Findings of the affected limb with the foot drop stimulator as compared to the affected limb without the
foot drop stimulator: 1) increased anterior/posterior maximum center of pressure excursion 8% during
stance; 2) center of pressure at initial contact was 6% more posterior; 3) medial/lateral mean, maximum
and minimum center of pressure position during stance all significantly decreased; 4) anterior/posterior
net displacement increased during stance and single support; and 5) anterior/posterior velocity of the
center of pressure increased during stance(Nolan, K.J., et al., 2015).
. 33

Electromyographic
Evaluation
(D. Patikas et al.,2005)
34

Electromyographic
Evaluation
(D. Patikas et al.,2005)
35

Influence of assistive devices
for hemiplegic gait
Patients walking with cane demonstrated more
improvement in spatial variables and joint motion than
temporal variables and those without cane.
The affected-side kinematics of hemiplegic gait with a cane
showed increased pelvic obliquity, hip abduction, and
ankle eversion during terminal stance phase; increased hip
extension, knee extension, and ankle plantarflexion during
pre-swing phase; and increased hip adduction, knee
flexion, and ankle dorsiflexion during swing phase as
compared with hemiplegic gait without a cane. 36

A cane thus improved the hemiplegic gait by assisting the affected limb to smoothly
shift the center of body mass toward the sound limb and to enhance push off during
preswing phase. It also improved circumduction gait during swing phase (Ta-Shen
Kuan, et al., 1999)
Ankle–foot orthoses (AFOs) are frequently used to improve gait stability, toe
clearance, and gait efficiency in individuals with hemiparesis. During the swing
phase, AFOs enhance lower limb advancement by facilitating the improvement of
toe clearance and the reduction of compensatory movements (Pongpipatpaiboon,
K., Mukaino, M., Matsuda, F. et al., 2018).
37

Assessment of the hemiplegic
gait
● Observational gait analysis
● Digital video recording
● Hemiplegic gait analysis form
● Foot scan
● Gait pressure mat
● Electromyography
38

Management of the
hemiplegic gait
● Conventional training
● Circuit training
● Treadmill training (BWSTT)
● Biofeedback
● FES
● Robotics assisted training
● Virtual reality
39

Click here to see the clip: HEMIPLEGIC GAIT
40

REFERENCES
Li S, Francisco GE and Zhou P (2018) Post-
stroke Hemiplegic Gait: New Perspective and
Insights. Front.
Physiol.9:1021.doi:10.3389/fphys.2018.01021
Nadeau, Sylvie & Betschart, Martina &
Béthoux, François. (2013). Gait Analysis for
Poststroke Rehabilitation The Relevance of
Biomechanical Analysis and the Impact of
Gait Speed. Physical medicine and
rehabilitation clinics of North America. 24.
265-276. 10.1016/j.pmr.2012.11.007.
41

Balaban, B., & Tok, F. (2014). Gait
disturbances in patients with stroke. PM &
R : the journal of injury, function, and
rehabilitation, 6(7), 635–642.
https://doi.org/10.1016/j.pmrj.2013.12.017
McGowan, C. P., Neptune, R. R., Clark, D. J.,
and Kautz, S. A. (2010). Modular control of
human walking: adaptations to altered
mechanical demands. J. Biomech. 43, 412–419.
doi: 10.1016/j.jbiomech.2009.10.009
Mulroy, S., Gronley, J., Weiss, W., Newsam,
C., and Perry, J. (2003). Use of cluster analysis
for gait pattern classification of patients in the
early and late recovery phases following stroke.
Gait Posture 18, 114–125. doi: 10.1016/S0966-
6362(02)00165-0
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