Gait abnormalities in children with cp final

PRESENTED BY: MOHAMMAD KHAYATZADEH MAHANI
ASSISTANT PROFESSOR IN OT
AHVAZ JUNDISHAPUR UNIVERSITY OF MEDICAL
SCIENCES
DEC 2017
TEHRAN
Gait Abnormalities in
Children with Cerebral Palsy
‫در‬ ‫شده‬ ‫ارائه‬:
‫در‬ ‫رفتن‬ ‫راه‬ ‫مشکالت‬ ‫توانبخشی‬ ‫و‬ ‫ارزیابی‬ ‫تخصصی‬ ‫کارگاه‬
‫مغزی‬ ‫فلج‬ ‫به‬ ‫مبتال‬ ‫کودکان‬

Cerebral Palsy
 Cerebral palsy describes “a group of permanent disorders
affecting the development of movement and posture,
causing activity limitation, that are attributed to non-
progressive disturbances that occurred in the developing
fetal or infant brain” .
 Although the initial brain injury is non-progressive, the
musculoskeletal impairments and functional limitations
associated with CP are indeed progressive.
 A diagnosis of CP is often made based on abnormal
muscle tone or posture, a delay in reaching motor
milestones, or the presence of gait abnormalities in
young children, which range from mild, i.e., toe-walking,
to severe, i.e., crouched, internally rotated gait.
2
Gait Abnormalities in CP

Walking and Gait
3
 Walking on two legs distinguishes humans from other
mammals.
 The importance of the ability to walk is highlighted by
the fact that the first question from parents of children
with CP is often: will s/he be able to walk?
 Disturbance of motor function affecting walking is a
major obstacle for the individual, and much time and
effort and many different methods are utilized to achieve
and maintain walking ability.
 The word “walking” is used to describe if, where and how
you can walk, whereas the word “Gait” describes the
manner or style of walking.

Gait Cycle
4
 The normal Gait cycle consists of two phases: the Stance
phase, when some part of the foot is in contact with the
floor, which makes up about 60% of the gait cycle, and a
Swing phase, when the foot is not in contact with the
floor, which makes up the remaining 40%.
 There are two periods of double support occurring
between the time one limb makes initial contact and the
other one leaves the floor at toe off.
 At a normal walking speed, each period of double
support occupies about 11% of the gait cycle, which
makes a total of approximately 22% for a full cycle.

Gait Cycle
5

Stance Phase
7

Swing Phase
8

Gait Terminology
9
 Stride length/Duration
 Step Length/Duration
 Step Width
 Cadence
 Walking Speed/Velocity
 Degree of Toe-out

Determinants of Gait
10
 Pelvic Rotation
 Pelvic Tilt
 Knee Flexion
 Foot and Ankle Motion
 Lateral Displacement of the Pelvis

Kinematics
11
 Kinematics is the
study of the
positions, angles,
velocities, and
accelerations of
body segments and
joints during
motion

Kinetics
12
 Ground Reaction Force
 Center of Pressure
 Muscle Activity
 Moments

Initial Contact
13

Loading Response
14

Mid Stance
15

Terminal Stance
16

Pre Swing
17

Initial Swing
18

Mid Swing
19

Terminal Swing
20

Clinical Gait Assessment
21
 History: Surgery, BTX, Orthosis, Mobility Aids, Therapy
 Physical Examination
o Anthropometry
o PROM and AROM
o Muscle Strength/ Weakness
o Muscle/Postural Tone
o Selective Movement Control
• Laboratory Gait Analysis
o Kinematics via Motion Capture
o Kinetics via Force Plate
o Muscle Activity via EMG
• Functional Assessment Tests

Laboratory Gait Analysis
22
 Assessment via high
tech motion capture
and computerized
software then
interpretation by :
1. Gait Deviation Index
2. Gillette Gait Index

Laboratory Gait Analysis
23
 Although walking is an activity most of us can manage
without thinking, it is difficult to analyze.
 The eight distinctive phases described by Gage all take
place within about one second, the normal time for one
gait cycle.
 The complex of actions on several levels of the body
(ankle, knee, hip, pelvis, trunk and arms) that take place
in each phase give us a large amount of data, 96 variables
per second, to analyze.
 In a gait lab it is possible to sample and store such data at
a high frequency for further analysis and make
comparison between groups of individuals or/and on
individual basis.

Kinematics and Kinetic
24
 Kinematics: Describes the movements
of the body segments (segment
positions and joint angles), 3-D Joint
Motion
8 Digital Motion Capture Cameras
Record Position of Light Reflective
Markers
 Kinetics: Calculates the forces
controlling the movements, described
in terms of Moments and Power
Force Plate Embedded in the Floor
Records Ground Reaction Force
Vectors

Kinematics
25
 Nearly normal hip motion
 Increased knee flexion at IC and stance
 Reduced peak knee flexion in swing
 Increased plantar flexion in terminal
stance
 Internally rotated foot progression

Kinetics
26

Kinetics
27
 Normal ankle plantar flexor moment
peaks in terminal stance
 Increased plantar flexor moment in
loading response “double bump”
associated with increased plantar
flexion at IC
 Decreased moment in terminal
stance associated with a reduced
forefoot rocker

Muscle EMG Timing During Gait
28

Postural Balance
29
 Force Plate Center of Pressure
 Postural Sway with Eyes Open / Closed

Energy Expenditure Index
30

Functional Assessment Tests
31
 Whilst instrumented gait assessment that provides
quantitative measures of 3D gait kinematics and
kinetics and the electrical activity of muscles remains
the gold standard for gait assessment, in the context
of routine clinical practice it is still restricted by the
fact that it is laboratory based, expensive, time-
consuming and requires a high-level of
interpretation skills.

( without videotaping)
32
TUG and Modified TUG
 SIX Minute Walk Test/One MWT/
10 Meter Walk Test
 GMFM band D and E
 Dynamic Gait Index

GMFM band D
33

GMFM band E
34

Dynamic Gait Index
35

( with videotaping)
36
Observational Gait Scale (adapted from Physicians
Rating Scale)
Edinburgh Visual Gait Analysis Interval Testing
(GAIT)
 Gillette Functional Assessment Questionnaire

Edinburgh Visual Gait Analysis Interval
Testing (GAIT)
42

Edinburgh Visual Gait Analysis Interval Testing
(GAIT)
43

Gillette Functional Assessment Questionnaire
44

Gait Requirement
45
 Control System
 Energy Source
 Levers Providing Movement
 Forces to Move the Levers.

Gait Regulation
46
 Walking involves a complex interplay between
automated neural activation patterns and voluntary
muscle control.
 At the level of the spinal cord there are afferent and
efferent nerves linked together in a web of
interconnections called a Central Pattern Generator
(CPG) , which can produce walking movements in
the legs.
 This circuitry is controlled by supraspinal centers in
the nervous system and by information from sensory
systems to adapt the walking movements to the
voluntary control and to the environmental demands

Gait Prerequisites
47
 Gage (Gage 2004) formulates five prerequisites for
normal walking:
1. Stability in Stance
2. Foot Clearance in Swing
3. Pre-positioning of the Foot for Initial Contact
4. Adequate Step length
5. Energy Conservation

Energy Conservation
48
 Eccentric muscle forces (as opposed to concentric)
are used to the greatest extent possible during gait
 Stretch energy in tendons and muscles is returned as
kinetic energy, since in normal gait muscles tend to
be ‘pre-stretched’ before they fire concentrically
 Biarticular muscles serve to transfer energy from one
segment to another

Abnormal Gait and Energy Expenditure
49
 Normal walking is regulated to minimize energy
expenditure, and an abnormal gait pattern tends to be
more energy demanding (Waters and Mulroy 1999).
 This often results in reduced velocity and limited walking
distance. Kerr, Parkes et al. (2008) found a correlation
between energy cost and activity limitation in children
with CP, and that energy cost increased with severity.
 The abnormal gait pattern puts a heavy strain on joints,
ligaments and muscles (McNee, Shortland et al. 2004),
which can lead to pain in the long run, as has been
reported in adults with CP.

Gait in CP
50
 Population based studies show that about 70% of
children with CP are classified as walking with or without
assistive devices (Himmelmann, Beckung et al. 2006;
Beckung, Hagberg et al. 2008).
 Age at start of walking is often delayed; the median age
for walking debut has been found to be two years of age
for all children with CP and four years in the group with
CP spastic diplegia (Jahnsen,Villien et al. 2004).
 Rosenbaum, Walter et al. (2002) reported that for
children at GMFCS I-III, 90% of their motor
development potential was reached between 3.7 and 4.8
years of age. Development then levels off and optimal
function is reached about the age of seven (Rosenbaum,
Walter et al. 2002; Beckung, Carlsson et al. 2007).

Gait in Adolescents and Adults with CP
51
 There is a decrease in walking ability and gait
pattern through adolescence expressed as a decrease
in gait velocity, stride length and sagittal joint
excursions over time (Johnson, Damiano et al. 1997;
Bell, Öunpuu et al. 2002).
 Surveys of adults with CP show decreased walking
ability or ceased walking in 44% (Andersson and
Mattsson 2001), mainly between 15 and 35 years of
age (Jahnsen, Villien et al. 2004).

Ambulation Prognosis in Children with CP
52
 Primitive Reflexes and Reactions
 Gross Motor Skills
 CP Type
 Co morbidities(Seizure, Intellectual Disability,
Blindness)
 GMFCS

GMFCS and Prognosis
53

GMFCS and CP Type
54

Gait Problems in Children with CP
55
 Children with CP have been reported to have shorter
stride length than peers, and consequent reduced
velocity compared with normal children (Abel and
Damiano 1996).
 Other frequent problems have been described as Stiff
Knee in Swing, Equinus, In-Toeing, Increased Hip
Flexion and Crouch, all seen in over 50% of children
in the diplegic and quadriplegic group (Wren,
Rethlefsen et al. 2005).

Neuromuscular and Musculoskeletal problems in
CP
56
 Neuromuscular deficits differ among spastic,
dyskinetic, and ataxic CP and involve abnormal
motor drive, muscle tone, motor patterns, and
coordination caused by the original brain injury.
 In addition, subsequent Musculoskeletal changes
result from chronic abnormal muscle activation,
biomechanical imbalance around joints, neglect,
and/or disuse.
 These factors, combined with Rapid Limb Growth
and Increasing Body Weight in children, contribute
to gait abnormalities in CP (Meyns et al., 2016).

Neuromuscular and Musculoskeletal Deficits in
Spastic CP
57
 Muscle Weakness
 Shortened Muscle-Tendon Unit
 Spastic and Passive Resistance to Stretch
 Impaired SMC
 Muscle Co-Contraction
 Bone Mass and Deformities (e.g., femoral anteversion)
 Joint Subluxations/Dislocations (e.g., hip subluxation)
 Joint Stiffness and Joint Contractures
 Sensory Deficits

Weakness in Spastic CP
58
 Loss of excitatory motor signals descending in the
CST results in reduced muscle activation and
reduced muscle size, which is aggravated further by
pathological changes in the elasticity of the muscle.
 Medial and lateral gastrocnemius, soleus, tibialis
anterior, rectus femoris, semimembranosus, and
semitendinosus of patients with CP had reduced
volumes compared to TD children.
 Surgical procedures, Posture and disuse, orthoses or
serial casting, BTX, ITB, SDR cause Weakness

Shortened Muscle-Tendon Unit
59
 Impaired muscle growth and muscle fiber changes
result in a shortened muscle-tendon unit in the
muscles affected by spastic CP.
 The failure of muscle growth to keep pace with bone
growth is most evident in the bi-articular muscles,
e.g., the gastrocnemius, hamstrings, and rectus
femoris, and contributes to joint contractures and
gait abnormalities such as toe-walking and flexed-
knee gait.
 The short muscle-tendon unit also likely contributes
to Weakness.

Spasticity in Spastic CP
60
 Spasticity and passive resistance to muscle stretch
particularly influence biarticular muscles, such as
the rectus femoris, hamstrings, and gastrocnemius,
which require greater excursion across two joints.

Impaired Selective Motor Control in Spastic CP
61
 Impaired SMC occurs when flexor or extensor
synergies interfere with isolated joint movements,
resulting in impaired functional movements, such as
gait (Rose, 2009; Cahill- Rowley and Rose, 2014).
 Children with mild to severe spastic CP consistently
demonstrate co-activation of the quadriceps and
gastrocnemius on EMG, distinguishing spastic CP
from idiopathic toe walking (Rose et al., 1999; Policy
et al., 2001).

Muscle Co-Contraction
62
 Co-contraction occurs when agonist and antagonist
muscles contract simultaneously around a joint causing it
to hold a certain position (Lewis et al. 2011).
 This can happen normally to stabilize joints and is more
prevalent in the early stages of learning new motor skills
(Osu et al. 2002).
 When co-contraction is excessive and relatively constant
it is considered to be a pathological sign.
 Muscle co-contraction during active movements and
during gait have been investigated (Pierce et al. 2008),
for example hamstring/quadriceps co-contraction can
cause a flexed Stiff Knee Gait (Rodda & Graham 2001).

Bone Mass and Deformities
63
 Bone growth is dependent on the size and direction
of forces applied to the bone
 Muscle contracture, spasticity and altered forces
associated with differences in weight-bearing posture
and mobility can cause changes in the bone growth
and bony deformity in CP.
 Abnormal tibial torsion and abnormal femoral
anteversion are known to cause rotational gait
problems

Sensory Deficits
64
 In addition to changes of muscles, bones and joints,
CP can affect sensory processing as well.
 Young children with CP can have altered Vestibular,
Kinaesthetic, Tactile and Proprioceptive awareness.

Neuromuscular Deficits and Gait Abnormalities
65

Neuromuscular Deficits and Gait Abnormalities
66

Gait Patterns in Children with CP
67
 Abnormal gait pattern at one level may be
attributable to a primary problem located around the
joint, but it may also be a compensatory strategy for
problems at other levels of the body.
 In order to be able to differentiate the abnormal
pattern as a primary problem or a secondary
strategy, the gait analysis has to be supplemented
with a clinical examination including ROM,
Spasticity, Muscle Strength, and SMC.
 These measurements together can help to identify
abnormal patterns and weaknesses.

Gait Classification
68
 The diversity of gait deviations observed in children
with CP has led to repeated efforts to develop a valid
and reliable gait classification system to assist in the
diagnostic process, clinical decision making and the
communication of a child’s presentation between
clinicians

Sagittal Plane Gait Classification in Spastic
Hemiplegia
69
 Type 1 – Weak or paralyzed/silent dorsiflexors (=
drop foot)
 Type 2 – Type 1 + Triceps surae contracture
 Type 3 – Type 2 + Hamstrings and/or Rectus
Femoris spasticity
 Type 4 – Type 3 + Spastic hip flexors and adductors

Drop Foot
70
 In Type 1 hemiplegia there is a `drop foot'
which is noted most clearly in the Swing
phase of gait due to inability to selectively
control the ankle dorsiflexors during this
part of the gait cycle.
 There is no calf contracture and therefore
during stance phase, ankle dorsiflexion is
relatively normal.
 This gait pattern is rare, unless there has
already been a calf lengthening procedure.

Drop Foot
71
 The compensation for this defect is
an increase in knee flexion at mid
and terminal swing, initial contact
and load acceptance.
 The only management maybe
needed is a leaf spring or hinged
ankle foot orthosis (AFO).
 Spasticity management and
contracture surgery are clearly not
required.

True Equinus
72
 Type 2 hemiplegia is the most common type in
clinical practice.
 True equinus is noted in the stance phase of gait
because of the spasticity and / or contracture of the
gastroc-soleus muscles.
 There are two sub-catagories to type 2:

Type 2 Management
73
 Once a significant fixed contracture develops,
lengthening of the gastrocnemius and soleus may be
indicated.
 Type 2 hemiplegia with a fixed contracture of the
gastroc-soleus constitutes the only indication for
isolated lengthening of the tendon Achilles.
 If the knee is in recurvatum, a hinged AFO with
plantar flexion stop is the most appropriate choice. A
plantar flexion stop or posterior stop in an AFO is
designed to substitute for inadequate strength of the
ankle dorsiflexors during swing phase of gait.

Jump Knee
74
 Type 3 hemiplegia is characterized
by gastroc-soleus spasticity or
contracture, impaired ankle
dorsiflexion in swing and a flexed,
`stiff€knee gait' as the result of
hamstring/quadriceps co
contraction.
 At a later stage, management may
consist of muscle tendon
lengthening for gastroc-soleus
contracture.

Equinus/Jump Knee
75
 In Type 4 hemiplegia there is much
more marked proximal involvement
and the pattern is similar to that seen
in spastic diplegia.
 However, because involvement is
unilateral, there will be marked
asymmetry, including pelvic
retraction.

Equinus/Jump Knee
76
 In the sagittal plane there is
equinus, a flexed stiff€knee, a
flexed hip and an anterior pelvic
tilt.
 In the coronal plane, there is hip
adduction and in the transverse
plane, internal rotation.

Other
Classifications
77
 Hip Hiking
 Circumduction
 Steppage
 Vaulting
 In-toeing (Pes
Varus, Int Tib
Torsion)
 Stiff Knee

Common Postural/Gait Patterns in
Diplegic Spastic CP
78
 Torsional deformities of the
long bones and foot
deformities are frequently
found in diplegic spastic CP,
in association with musculo-
tendinous contractures.
 The most common bony
problems are medial
femoral torsion, lateral
tibial torsion, mid foot
breaching, with foot valgus
and abduction.

Sagittal Plane Gait Classification in Spastic
Diplegia
79
 Type 1: True Equinus
 Type 2: Jump Gait
 Type 3. Apparent Equinus
 Type 4. Crouch Gait
 Type 5: Stiff Knee Gait
 Type 6: Asymmetric Gait

True Equinus
80
 When the younger child with Diplegic
CP begins to walk with or without
assistance, calf spasticity is frequently
dominant resulting in a True Equinus
gait with the ankle in plantar flexion
throughout stance and the hips and
knees extended.
 The patient can stand with the foot flat
and the knee in recurvatum. The
equinus is real but hidden.

True Equinus
81
•A few children with diplegic
cerebral palsy remain with a
True Equinus pattern
throughout childhood .
• The persistence of this pattern
is unusual and seen in only a
small minority of children with
bilateral CP.

Idiopathic Toe-Walking
82
 Rarely, an asymmetric toe-
walking can be dystonic and
transient and an explanation for
Idiopathic Toe-Walking.
 Under 2 years of age, toe
walking may not be pathologic;
when persistent after the age of
2 years and in the absence of
neurological or orthopedic
abnormalities, toe- walking is
referred to as idiopathic.

Jump Gait
83
 The jump gait pattern is very commonly
seen in children with diplegia.
 The ankle is in equinus, the knee and hip
are in flexion, there is an anterior pelvic
tilt and an increased lumbar
lordosis. There is often a stiff knee
because of rectus femoris activity in the
swing phase of gait.
 In younger children, this pattern can be
managed e€ffectively by BTX injections to
the gastrocnemius and hamstrings and
the provision of an AFO.

Jump Gait
84
 In older children
musculotendinous
lengthening of the
gastrocnemius, hamstrings
and iliopsoas may be indicated
with transfer of the rectus
femoris to semi-tendinosus for
co-contraction at the knee.

Apparent Equinus
85
 It defined by a foot position that is normal
in relationship to the tibia, however heel
strike does not occur due to more
proximal deviations (flexion of the knee
most common)
 As the child gets older and heavier, this
pattern may be progress.
 Equinus may gradually decrease as hip
and knee flexion increase.
 Sagittal plane kinematics will show that
the ankle has a normal range of
dorsiflexion but the hip and knee are in
excessive flexion throughout the stance
phase of gait.

Apparent Equinus
86
 Redirection of the
ground reaction vector
in front of the knee can
best be achieved by the
use of a solid or a
ground reaction AFO.

Crouch Gait
87
 Crouch gait is defined as excessive
dorsiflexion or calcaneus at the ankle
in combination with excessive flexion
at the knee and hip.
 This pattern is part of the natural
history of the gait disorder in children
with more severe diplegia and in the
majority of children with spastic
quadriplegia.

Crouch Gait
88
 Regrettably, the
commonest cause of
crouch gait in children
with spastic diplegia is
isolated lengthening of
the heel cord in the
younger child.

Crouch Gait
89
 This gait is an unattractive,
energy-expensive gait pattern,
followed by anterior knee pain
and patellar pathology in
adolescence
 Crouch gait is always difficult to
manage and usually requires
lengthening of the hamstrings
and iliopsoas, a ground reaction
AFO and adequate correction of
bony problems such as medial
femoral torsion, lateral tibial
torsion and stabilization of the
foot.

Stiff Knee Gait
90
 The characteristic for SKG is delayed and/or reduced
peak knee flexion during swing phase due to rectus
femoris firing out of phase.
 Gait analysis reveals quadriceps activity from terminal
stance throughout swing phase.
 SKG is associated with reduced walking speeds and an
increased incidence of tripping and falls.
 Rectus femoris transfer, where the distal attachment of
the extensor muscle is transferred to become a flexor of
the knee.
 SKG could be caused by multiple factors including
weakness in the ankle plantarflexors and hip flexors and
stiffness in the knee extensors.

Asymmetric Gait
91
 The gait pattern is
asymmetrical to the degree
that the subject’s two lower
limbs are classified as
belonging to different groups;
e.g. right lower limb apparent
equinus and left lower limb
jump gait

Other Classifications
92
 Scissoring Gait
 In-Toeing Gait

Scissoring Gait
93
 Leg crossing in swing causing
problems with foot clearance.
 Sometimes coexists with crouch
gait and some authors consider it
as a part of crouch gait.
 Excessive hip adduction and
scissoring is common in
Quadriplegic CP.

In-toeing Gait
94
 In-toeing is a frequent gait problem
in children with cerebral palsy.
 The most common causes of in-
toeing in the subjects with bilateral
involvement were internal hip
rotation ,internal tibial torsion ,and
internal pelvic rotation.
 The most common causes in the
hemiplegic children were internal
tibial torsion , Pes Varus , internal hip
rotation, and metatarsus adductus.

System Approach to Gait Training
95

 Strength Training
 Deformity Control
 Spasticity
Management
 Motor Learning
 Balance and Postural
Control Training
 Sensory Regulation
 Treadmill Training
 Weight Supported
Locomotor Training
 Robot-Assisted Gait
Training/ Virtual gait
training
 FES
 Biofeedback
 Hippotherapy
 Aquatic Therapy
 Space Suit Therapy
96
Focusing on Individual

Strength Training
Tehran CP Workshop, May 2017
97
Progressive resisted exercise improves
muscle performance & functional
outcomes in CP children.
 Closed chain V open chain
 Use of theraband, Springs, weight cuff,
Bike, stationary bike, treadmill
 Aerobic
 Plyometric
 Core stability: Ball, TRX
 Circuit Training: Treadmill walking,
step-ups, sit-to-stands and leg presses.

Strength Training Effectiveness
98
 Blundell et al (2002): task-specific
strengthening exercise, run as a group
circuit class, resulted in improved
strength and functional performance that
was maintained over time.
 Verschuren et al (2007): An exercise
training improves physical fitness,
participation level, and quality of life in
children with CP
 It could be used as a target treatment
specifically anticipating temporary
muscle weakness, such as before or after
BTX-A or surgical treatment.

Strength Training Effectiveness
99
 Dodd et al (2002)[sys review]:
training can increase strength and
may improve motor activity in people
with CP without adverse effects.
 Verschuren et al(2008) [sys review]:
Children with CP may benefit from
improved exercise programs that
focus on LE muscle strength,
cardiovascular fitness, or a
combination.
 Vanessa et al (2012): Muscle
strength increased significantly in the
training group compared to the
control group, but walking ability and
participation did not change.
Spasticity remained unchanged

Deformity Control
100
 Manual Stretch
 Casting
 BTX-A
 Orthosis
 Surgery
(SEMLS)

Deformity Control (Orthotic Management)
101
 6 hours a day for muscle enlargement
 As a general rule the use of KAFOs is not indicated for
children with CP and fixed knee are poorly tolerated.
 Anterior Floor Reaction AFOs that prevent dorsiflexion
at the ankle can prevent knee flexion during stance by
realigning the GRF in front of the knee.
 Twister orthoses incorporating a flexible torque cable
extending from a waistband to an AFO create active
rotational forces and can alter the foot-progression angle.
 Different kinds of AFO such as Solid, hinged, PLS,
supramalleolar , and FR AFO are prescribed.

AFO Effectiveness
102
Wingstrand et al(2014): 2200 cases
 The use of AFO is most frequent at 4–6 years of age
in children with lower levels of gross motor function.
 Three quarters of the children treated with AFO
attained the treatment goals.

FR AFO and Solid AFO
103

PL AFO and Hinged AFO
104

AFO Effectiveness
105
Results of 28 studies and more than 450 children
concluded :
 Preventing plantarflexion improved gait efficiency
(Morris 2002).
 Clearance in swing phase (Õunpuu et al. 1996)
 Pre-positioning in terminal swing (Romskes and
Brunner 2000),
 Increase step length and walking speed (Abel et al. 1998).
 Improving energy expenditure based on oxygen
consumption (Maltais et al. 2001).

AFO Effectiveness
106
 Energy expenditure was shown to decrease with the
use of AFOs
 Gait velocity was shown to increase in some studies
but did not change for others due to a slower cadence
 Functional measures (e.g. ability to walk long
distances or navigate over curbs), significant
improvements were only shown in few studies.

Spasticity Management
107

Tehran CP Workshop, May 2017 108
Casting
 Serial casting in the CP population
has been shown to improve ROM.(
Brouwer 2000)
 Novak proposed that Casting is a
good method of contracture
management in UE and LE (2013)

BTX-A
109

Tehran CP Workshop, May 2017 110
BTX-A
 Target muscles in LE
 In more severe cases: medial hamstrings and adductors
 in less severe cases: hamstrings or calf, or occasionally
adductors and calf
 In hemiplegia: 1. calf 2. hamstring
 In diplegia: 1. hamstrings 2. calf
 In quadriplegia: 1. adductors 2. calf and hamstrings
 Repeated exposure to BTX-A can lead to
immunoresistance
 Novak proposed that BTX-A is a good method of
spasticity management in children with CP(2013)
 BTX-A reduces spasticity and improves ambulatory
status.(Flett 1999)

Focusing on Task
111
 Task Modification
 Compensation
 Assistive mobility Devices

Focusing on Environment
112
 Physical Context Modification
 Social Context Modification

Individual-Task-Environment Interaction
113
 The task itself can also be modified, such as walking
and carrying an object, or turning while walking.
 Environmental characteristics such as the incline
and texture of the support surface can also be varied.
 Adjusting gradually the complexity of a task (e.g.,
walking with and without turning) and the
characteristics of environment (e.g., the degree of
slope changes) will allow patients to adapt to their
individual capability while training their problem-
solving skills.

Gait Abnormalities in CP 115
‫تخصصی‬ ‫کارگاه‬
‫راه‬ ‫مشکالت‬ ‫توانبخشی‬ ‫و‬ ‫ارزیابی‬
‫فلج‬ ‫به‬ ‫مبتال‬ ‫کودکان‬ ‫در‬ ‫رفتن‬
‫مغزی‬
‫سپاسگزاریم‬www.farvardin-group.com
@farvardin_group_channel
@neuroscience4family
@farvardin_group96

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