Gait abnormalities in children with cp final

PRESENTED BY: MOHAMMAD KHAYATZADEH MAHANI
ASSISTANT PROFESSOR IN OT
AHVAZ JUNDISHAPUR UNIVERSITY OF MEDICAL
SCIENCES
FEB 2018
TEHRAN
Gait Abnormalities in
Children with Cerebral Palsy
‫در‬ ‫شده‬ ‫ارائه‬
‫تخصصی‬‫کارگاه‬‫کودکان‬‫در‬‫رفتن‬‫اه‬‫ر‬‫مشکالت‬‫انبخشی‬‫و‬‫ت‬‫و‬‫ارزیابی‬‫مغزی‬‫فلج‬ ‫به‬‫مبتال‬

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

CP Types
 There are three main types of CP: Spastic,
Dyskinetic, Ataxic, and Mixed.
 Spastic CP is the most common, affecting
approximately 87% of children with CP, while
dyskinetic CP affects approximately 7.5%, ataxic CP
affects approximately 4%, and mixed type affects
approximately 1.5% .
3

Spastic CP
4
 Spastic CP present with varying degrees of :
Weakness
 Short muscle-tendon unit
 Spasticity
Impaired SMC.

Diskinetic CP
5
 The definition of dyskinetic CP has evolved recently
to include dystonic and choreoathetoid CP.
 Severe fine motor impairment and a GMFCS level
of IV or V, representing severe CP with reduced or
absent independent mobility

Dyskinetic CP
6
 Dyskinetic CP is characterized by:
 Involuntary, uncontrolled hyperkinetic movements
 Repetitive and occasionally stereotyped dystonic
limb movements
 Muscle tone fluctuates
 Primitive reflex patterns predominate

Ataxic CP
7
 Ataxic CP is characterized by:
 Hypotonia
Impaired limb coordination during voluntary
movements
Balance and stability problems
Speech impairments.

Walking and Gait
8
 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?
 The word “Gait” describes the manner or style of
walking.

Gait Regulation
9
 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 Cycle
10
 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
11

Stance Phase
13

Swing Phase
14

Gait Terminology
15
 Stride length/Duration
 Step Length/Duration
 Step Width
 Cadence
 Walking Speed/Velocity
 Degree of Toe-out
 Kinematics
 Kinetics

Determinants of Gait
16
 Pelvic Rotation
 Pelvic Tilt
 Lateral Displacement of the Pelvis
 Knee Flexion
 Foot and Ankle Motion

Kinematics
17
 Kinematics is the
study of the
positions, angles,
velocities, and
accelerations of
body segments and
joints during
motion

Kinetics
18
 Ground Reaction Force
 Center of Pressure
 Muscle Activity
 Moments

Gait Requirement
19
 Control System
 Energy Source
 Levers Providing Movement
 Forces to Move the Levers.

Factors affecting the Gait
20
 The problems in standing will affect the gait
 Fears of falling may increase abnormal gait patterns
 Poor or absent stability and counterpoising
 Absence of anteroposterior shift
 Absence of lateral sway
 Lack of tilt reactions in standing
 Lack of protective reaction

Gait Prerequisites
21
 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
22
 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
23
 Normal walking is regulated to minimize energy
expenditure, and an abnormal gait pattern tends to
be more energy demanding.
 This often results in reduced velocity and limited
walking distance.
 The abnormal gait pattern puts a heavy strain on
joints, ligaments and muscles , which can lead to
pain in the long run, as has been reported in adults
with CP.

Gait in Young Children
24
 The walking base is Wider
 The stride length and speed are lower and the cycle
time shorter (higher cadence)
 Small children have No heelstrike, initial contact
being made by the flat foot
 There is very little stance phase knee flexion
 The whole leg is externally rotated during the swing
phase
 There is an absence of reciprocal arm swinging.

Gait in CP
25
 Population based studies show that about 70% of
children with CP are classified as walking with or
without assistive devices.
 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.
 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.

Gait Problems in Children with CP
26
 Children with CP have been reported to have
shorter stride length than peers, and consequent
reduced velocity compared with normal children.

Gait in Adolescents and Adults with CP
27
 There is a decrease in walking ability and decrease
in gait velocity, stride length over time in
adolescence
 Surveys of adults with CP show decreased walking
ability or ceased walking in 44%, mainly between 15
and 35 years of age.

Ambulation Prognosis in Children with CP
28
 Primitive Reflexes and Reactions
 Gross Motor Skills
 CP Type
 Co morbidities(Seizure, Intellectual Disability,
Blindness)
 GMFCS

GMFCS and Prognosis
29

GMFCS and CP Type
30

Neuromuscular and Musculoskeletal problems
in CP
31
 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.

Neuromuscular and Musculoskeletal Deficits in
Spastic CP
32
 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
33
 Loss of excitatory motor signals descending in the
CST results in reduced muscle activation and
reduced muscle size.
 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
34
 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
35
 Spasticity particularly influence biarticular
muscles, such as the rectus femoris, hamstrings,
and gastrocnemius, which require greater excursion
across two joints.

Impaired SMC in Spastic CP
36
 Impaired SMC occurs when flexor or extensor
synergies interfere with isolated joint movements,
resulting in impaired functional movements, such
as gait.
 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.

Muscle Co-Contraction
37
 Co-contraction occurs when agonist and antagonist
muscles contract simultaneously around a joint
causing it to hold a certain position.
 This can happen normally to stabilize joints and is
more prevalent in the early stages of learning new
motor skills.
 When co-contraction is excessive and relatively
constant it is considered to be a pathological sign.
 For example hamstring/quadriceps co-contraction
can cause a flexed Stiff Knee Gait.

Bone Mass and Deformities
38
 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.

Sensory Deficits
39
 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
40

Neuromuscular Deficits and Gait Abnormalities
41

42
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‫کارگاه‬‫تخصصی‬
‫ارزیابی‬‫مغزی‬‫فلج‬‫به‬‫مبتال‬ ‫کودکان‬‫در‬‫رفتن‬‫اه‬‫ر‬‫مشکالت‬‫انبخشی‬‫و‬‫ت‬‫و‬
‫اریم‬‫ز‬‫سپاسگ‬

Gait abnormalities in children with cp final

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