Seminar on cerebral palsy ( akshay )

Seminar on cerebral palsy
Sbumitted Submitted to :
IAMR( CCS )
Akshya Raj Chandra
MPT 1st year Neurology

Defination: LATEST DEFINITION
OF CEREBRAL PALSY
 Cerebral palsy describes a group of
permanent disorders of 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.

History:
 William John Little 1861
Dr Little first noticed a group of children who
were later diagnosed as Spastic Diplegia
(1861)
 Orthopedic surgeon who observed that
children with tone and developmental
abnormalities often had prolonged labor,
prematurity or breech delivery.

History:
 William John Little 1861
 “Motor deformities resulted from
difficulties in the birth process.”

History:
 Sigmund Freud 1889
 “Cerebral palsy is not caused by a difficult
birthing process or perinatal difficulties.”
 “CP is the result of some injury to the brain that
occurred during pregnancy which leads to CP
and predisposes the infants to difficult
deliveries.”

History:
 It is not widely known that Sigmund Freud (1889)
was the leading European authority on CP of the
late 19th Century. He authored three Monographs
on CP in the 1890’s.
 Freud was the first to point out that prematurity
and birth asphyxia might reflect a fetus already
damaged in-utero

History:
 Even less well known is that William
Osler wrote the only 19th century
monograph on CP published in the US
 Osler’s special interest was in clinical
expression and brain pathology

Cerebral Palsy:
 Cerebral palsy (CP) is a heterogeneous group of movement disorders
with various etiologies.
 The primary functional difficulty is in movement and posture, i.e. the
movement disorder is not secondary to another neurofunctional disability.
 CP is associated with a permanent, non-progressive pathology that
formed in utero or early infancy (before 2-3 years of age).
 CP excludes transient disease processes.
 CP is often accompanied by disturbances of sensation, perception,
cognition, communication, behaviour, epilepsy, and secondary
musculoskeletal problems.

Prevalence:
 2-3 children out of every 1000
children
 Despite advances in medical science,
no decrease in prevalence

Classification:
A/C to Extent of damage in the brain
 Mild
 Moderate
 Severe
 Profound

Classification:
A/C to body Part Involvement
 Monoplegia
 Hemiplegia
 Diplegia
 Triplegia
 Quadriplegia

Classification:
A/C To Site of damage in the brain
 Spastic
 Dyskinetic
 Ataxia
 Rigidity
 Floppy
 Mixed

Manifestations:
 Malfunction of motor centers
 Postural and balance difficulties
 Normal life expectancy possible
 Early death respiratory involvement

Characteristics:
 100%Impaired movements
 65% speech defects
 50% are mentally retarded
 50% ocular defects
 25% hearing impairment
 40% seizure disorders
 20% seriously disabled

Cerebral Palsy Spastic:
 Extens 52% of total cerebral palsy population
Common Features
• Hyperirritability of muscles
• Arms flexed, legs internally rotated
• Difficulty bending into a sitting position
• Difficulty with head control
• Postural difficulty
• May not have protectiveion

Spastic Cerebral Palsy
• Speech impairment
• Swallowing impairment/drooling
• Spastic tongue thrust
• Primitive reflexes

Cerebral Palsy Spastic
Different Forms
 Spastic hemiplegia
 Spastic diplegia
 Spastic quadriplegia
 Spastic triplegia
 Spastic monoplegia

Spastic Hemiplegia:
 involvement of arm and leg on one side
(arm>leg)
 motor handicaps least likely to be disabling
 intelligence is normal to dull
 25–40% of all CP

Spastic Diplegia:
 involves legs more than arms
 often associated with premature births
 only 11-20% are severely impaired
 MR not so profound
 10–33% of all CP

Spastic Quadriplegia:
 aka double hemiparesis
 involves all four limbs, arms at least
severely affected as legs
 bilateral hemisphere involvement,
 severely impaired and MR
 often have bulbar symptomatology
 9–43% of all CP

Dyskinetic:
 25- 30% of all CP
 Uncontrollable writhing movements of opposing
muscle groups
 All four extremities involved, Neck and face
involved
 Voluntary movements are flailing
 Difficulty up righting and balancing
 May lack protective extension

Dyskinetic:
 Grimacing
 Drooling
 Speech defects
 Continuous mouth breathers
 Excessive head movements
 Tongue protrusion
 Primitive reflexes of varying severity

Ataxia:
 5 to 10 % of all CP
 Affects balance and coordination.
 They may walk with an unsteady gait with feet far
apart, and they have difficulty with motions that
require precise coordination,
 such as writing.

Etiology:
 Multifactorial but in most cases is unknown.
 Sometime Neuro-imaging may be entirely normal.
 An increasing amount of literature suggests a link between
various prenatal, perinatal, and postnatal factors and CP
 Prenatal factors play a significant role in the etiology of
CP.

Prenatal Risk Factor:
 Maternal thyroid disorder
 Long menstrual cycle
 Previous pregnancy loss
 Previous loss of newborn
 Maternal mental retardation
 Maternal seizure disorder
 History of delivering a child of less than 2000 g birth
weight or with motor deficit, mental retardation, or
sensory deficit

Factors during pregnancy:
 Polyhydramnios
 Treatment of the mother with thyroid hormone
 Treatment of the mother with estrogen or progesterone
 A fetus with congenital malformation
 Maternal seizure disorder, severe proteinuria, or high
blood pressure
 Bleeding in the third trimester
 Multiple gestations may be an added risk for CP

 Placentas show evidence of chorionitis were more
likely than others to have CP. Chorionitis is thought
to contribute either directly or indirectly by
increasing the risk of prematurity.
 . Neonatal asphyxia
Perinatal :

Postnatal Factors that lead to CP:
 Infection such as
meningitis
encephalitis
 Intracranial hemorrhage
 hypoxia- ischemia from meconium aspiration
 Coagulopathies
 Trauma

Possible causes of CP
Spastic Hemiplegia:
 70-90% are congenital and 10-30% acquired (eg,
vascular, inflammatory, traumatic).
 In unilateral lesions of the brain, the vascular
territory most commonly affected is the middle
cerebral artery; the left side is twice as commonly
involved as the right.

Spastic Hemiplegia:
 Other structural brain abnormalities include
hemi-brain atrophy and post-hemorrhagic
porencephaly.
 In the premature infant, this may result from
asymmetric periventricular leukomalacia.

Possible causes of CP by type:
Spastic diplegia
 In the premature infant, spastic diplegia may result
from parenchymal-intraventricular hemorrhage or
periventricular leukomalacia.
 In the term infant, no risk factors may be
identifiable or the etiology might be multifactorial.

Spastic quadriplegia
 50% of prenatal, 30% perinatal,20% postnatal in origin.
 This type is associated with cavities that communicate
with the lateral ventricles, multiple cystic lesions in the
white matter, diffuse cortical atrophy, and hydrocephalus.

Spastic quadriplegia:
 The patient often has a history of a difficult delivery with
evidence of perinatal asphyxia.
 Preterm infants may have periventricular leukomalacia.
 Full-term infants may have structural brain abnormalities
or cerebral hypoperfusion in a watershed

Dyskinetic (extrapyramidal)
 Associated with hyperbilirubinemia in the term infant or
prematurity without prominent hyperbilirubinemia.
 Hypoxia affecting the basal ganglia and thalamus may
affect the term infant more than the preterm infant.

Pathophysiology:
Arch Dis Child Fetal Neonatal
Ed. 2008 Mar;93(2):F153-61.
Pediatric Ophthalmology: Current
Thought and a Practical Guide, 1E
(Wilson)

Preterm infants:
The premature neonatal brain is
susceptible to two main
pathologies: intraventricular
hemorrhage
leukomalacia (PVL). Although both
pathologies increase the risk of CP,
PVL is more closely related to CP and
is the leading cause in preterm .

Conti:
 and is the leading cause in preterm infants.
The term PVL describes white matter in the
periventricular region that is underdeveloped
or damaged (“leukomalacia”). Both IVH and
PVL cause CP because the corticospinal
tracts, composed of descending motor axons,
course through the periventricular region.

Intraventricular hemorrhage (IVH):
IVH describes bleeding from the
subependymal matrix (the origin of
fetal brain cells) into the ventricles of
the brain. The blood vessels around
the ventricles develop late in the third
trimester, thus preterm infants have
underdeveloped periventricular blood
vessels, predisposing them to

Conti:
 predisposing them to increased risk of IVH.
The risk of CP increases with the severity of
IVH.

Periventricular leukomalacia (PVL):
IVH is a risk factor for PVL, but PVL is a
separate pathological process. The
pathogenesis of PVL arises from two
important factors:
(1)ischemia/hypoxia and
(2) infection/inflammation.

upper motor neurons :
Clinical features:
Nelson Textbook of Pediatrics, 18E
Eur J Neurol. 2002 May;9 Suppl 1:3-9;
discussion 53-61.
Neuroscience, 3E (Purves)
Clinical Neuroanatomy, 26E (Waxman)
Rosenbaum P, Rosenbloom L (2012).
Cerebral Palsy.

Clinical features:
 From Diagnosis to Adult Life. London: Mac Keith
Press.
 The clinical features of neurological disorders
depend on the location of damage to the nervous
system. The location of damage can be divided
into upper motor neuron or lower motor
neuron. The pathology in CP is in the upper
motor neuron

Upper motor neuron (UMN):
 Includes neurons in the brain and spinal
cord (central nervous system, CNS) that control
movement of muscles. UMN synapse onto
lower motor neurons at the ventral horn of the
spinal cord at the level which the neuron leaves
the cord. Upper motor neurons travel through
the pyramidal tracts (i.e., corticospinal tracts).

UMN LESION POSITIVE SIGN
 UMN lesions can cause positive or negative signs:
 Positive signs include muscle overactivity and spasticity, generally
due to reduced descending inhibitory signals from the brain.
 Negative signs include weakness or loss of dexterity, generally due to
reduced descending excitatory signals from the brain.
 Note that lesions in the extrapyramidal tracts do not cause these UMN
signs. The extrapyramidal tracts link the cerebellum and basal ganglia with
LMN. They function to modulate and refine movement rather than directly
cause movement, unlike the upper motor neurons in the pyramidal tracts

Spasticity:
 is defined as a velocity-dependent increase
in the tonic stretch reflex. It is characteristic
of an UMN lesion where there is
disturbance of the supraspinal excitatory
and inhibitory neurons, leading to a net
disinhibition of the spinal reflexes.
 .

Tonic stretch reflex:
Normally, passively stretching a muscle
group (e.g., stretching the biceps by passively
extending the elbow) causes contraction of
the same muscle group to prevent
overstretching and injury. This tonic stretch
reflex is a spinal reflex (i.e., it does not require
input from the brain). This reflex is normally
minimal or not present

Spasticity:
Injury to descending UMNs that
usually provide inhibitory signals to
the spinal reflexes causes net
disinhibition, which increases muscle
tone (contraction) as the muscle is
passively stretched. The faster the
velocity of stretching, the stronger the
reflex.

Lower motor neuron (LMN):
Includes neurons from ventral horn of
the spinal cord grey matter that exit
the spinal cord and attach to skeletal
muscles. The motor nuclei of cranial
nerves in the brainstem are also lower
motor neurons because they directly
attach to muscles in the head and
neck.

 LMNs relay signals from the UMNs to skeletal
muscles to initiate excitation-contraction coupling,
allowing individual units of a muscle to contract in
a synchronized manner

CONTI:
 Their function is to provide muscle tone to skeletal
muscles. In LMN lesions, there is no neural input to
muscles, which leads to flaccid paralysis due to lack
of resting muscle tone and subsequent atrophy from
disuse. The lack of excitation-contraction coupling
causes fasciculations in the muscles, where
individual sacromeres (contractile units in muscles)
fire and contract at random

Clinical manifestations:
• Delayed gross motor development
–A universal manifestation of CP
–The discrepancy between motor ability and expected
achievement tends to increase as growth advances.
–Delayed development of ability to balance slows milestones
–Delay in all motor accomplishments

Clinical Manifestations:
• Abnormal motor performance
– Preferential unilateral hand use may be apparent at 6
months.
– Hemiplegia, abnormal crawling or asymmetrical crawl;
spasticity may cause child to walk and stand on toes
– dyskinetic CP or uncoordinated or involuntary movements
(writhing tongue, fingers, and toes; facial grimacing), poor
sucking and feeding, persistent tongue thrust; head
staggering, tremor on reaching, truncal ataxia.

Alterations in muscle tone:
• Increased or decreased resistance to passive
movement (abnormal muscle tone).
• Opisthotonic postures or exaggerated back arching,
feel stiff on dressing.
• Difficulty diapering due to spastic hip adductor
muscles and lower extremities
• When pulled to a sitting position, child may extend
the entire body and be rigid at hip and knee. This is
an early sign of spasticity.

Abnormal postures:
• Children with spastic CP have abnormal posture at rest or
when position is changed
• Infantile lying prone may have hip higher than trunk with legs
and arms drawn in.
• Persistent infantile resting and sleeping position is a sign of
spasticity.
• Hemiparetic child may rest with affected arm adducted and
held against torso, with the elbow pronated and slightly flexed
and the hand closed

Primitive Reflexes:
• Palmar Grasp
• Sucking
• Search
• Moro
• Startle
• Asymmetric Tonic Neck
• Symmetric Tonic Neck
• Plantar Grasp
• Babinski
• Palmar Madibular
• Palmar Mental

Palmar Grasp:
The palmar grasp reflex is one of the most noticeable reflexes to emerge
 Appears in utero
 Endures through the 4th month postpartum
 Negative palmer grasp: neurological problems; spasticity
 Leads to voluntary reaching and grasping

Primitive Reflexes ~ Asymmetric Tonic
Neck

Primitive Reflexes ~ Symmetric Tonic
Neck

Primitive Reflexes ~ Plantar Grasp

Postural Reflexes:
Stepping
Crawling
Swimming
Head and Body Righting
Parachuting
Labyrinthine
Pull Up

Stereotypies:
 Common stereotypies
 Single leg kick
 Two-leg kick
 Alternate leg kick
 Arm wave
 Arm wave with object
 Arm banging against a surface
 Finger flexion

Associated Factors:
 Mental retardation
 Seizure disorders
 Delayed growth and development
 Spinal deformities
 Impaired vision
 Impaired hearing

Associated Factors:
 Impaired speech
 Dental
 drooling
 Incontinence
 Abnormal sensation
 Abnormal perception

Diagnosis Making :
 initial complaint is failure to meet early developmental
milestones
 no evidence of progressive disease
 no loss of milestones acquired previously
criteria
 delayed milestones
 persistence of primitive reflexes
 pathologic reflexes
 failure to develop protective reflexes

Diagnosis Making:
 Family member-First person to diagnose
(Mostly Grandmothers / Relatives)
- Motor delay- variation by more than 50%
- Abnormal movements
- Poor postural stability

Diagnosis Making:
 Associated disorders
-Epilepsy
-Visual deficits
-Drooling
-Hearing Deficits
-Feeding problems
-Poor Cognition

Diagnosis Making:
 Professional
* History Taking
-Pre-natal
-Peri-natal
-Post-natal
* Anthropometry

Diagnosis Making:
 Screening
 Investigation
- X-rays
- MRI / CT Scan
- Blood Tests
- Chromosomal Study

Diagnosis Making:
 Physical examination
- Tone
- Spasm, Tightness, Contracture, Deformity
- ROM
- Muscle Strength
- Sensation

Diagnosis Making:
 Base-line Evaluation
- Physical / Mobility Evaluation
- Fine Motor Evaluation
-Cognition Evaluation
-Communication Evaluation
-Social-Emotional Evaluation
-Activities of Daily Living

PHYSICAL EXAMINATION:
 The physical examination can be separated into 7 broad categories:
 1. Strength & selective motor control of isolated muscle groups
 2. Degree & type of muscle tone
 3. Degree of static muscle & joint contracture
 4. Torsional & other bone deformity
 5. Fixed & mobile foot deformities
 6. Balanced, equilibrium response & standing posture
 7. Gait by observation

MUSCLE STRENGTH:
 • Strength evaluation is necessary to assess appropriateness for
 intervention such as selective dorsal rhizotomy or lower limb surgery.
 • Children with CP are weak. Motor function and strength are directly
 related. Manual muscle testing (MMT) is the typical method for
 measuring muscle strength In child with CP.
 • Isometric assessment with a dynamometer is becoming more
 common in clinic and research studies.
 • Isokinetic evaluation are used when evaluating strength throught the
 range of motion (ROM). This assessment used to measure torque
 generated through an arc of movement.

SELECTIVE MOTOR CONTROL:
 Impaired ability to isolate and control movements confounds strength
 assessment and contributes to ambulatory and functional motor
 deficits.
 • Assessment of selective motor control involves isolating movements
 on request, appropriate timing , and maximal voluntary contraction
 without overflow movement.
 • A typical scale for muscle selectivity has 3 grades of control:
 GRADE 0- No ability / only patterned movement observed.
 1- Partially isolated movements observed.
 2- Completely isolated movements observed

MUSCLE TONE ASSESSMENT:
 • Tone is the resistance to passive stretch while a person is attempting
 to maintain a relaxed state of muscle activity.
 • Hypertonia is defined as abnormally increased resistance to an
 externally imposed movement about a joint. It can be caused by
 spasticity , dystonia ,rigidity or a combination of these.
 • Resting muscle tone can be influence by the degree of cooperation,
 apprehension, excitement of patient and position during assessment.
 • Muscle tone assessment on different occasions by different
 practitioners may be necessary to accurately check the nature of the
 child muscle tone.
 • SANGER AND COLLEAGUES recommend this process:

Conti:
 By using this process for evaluation, the consistency and
 completeness of tone abnormality documentation improve.
 • Spastic ( compared with dystonic) hypertonia causes an increase
 resistance felt at higher speeds of passive movement.
 • The ASHWORTH scale, modified ASHWORTH scale and an isokinetic
 dynamometer in conjunction with surface electromyography are
 methods used to assess severity of spastic hypertonia.

ASHWORTH SCALE:
 No increase in tone
 2. Slight increase in tone
 3. More marked increase in tone
 4. Considerable increase in tone
 5. Affected part rigid

MODIFIED ASHWORTH SCALE:
 GRADE 0 – No increase in muscle tone
 1 – Slight increase in muscle tone manifested by catch and
 release or by minimal resistance at the end of ROM when
 affected part is moved in flexion or extension.
 1+ – Slight increase in the muscle tone manifest by a catch
 followed by minimal resistance through out reminder of
 the ROM
 2 – More marked increase in muscle tone through most of the
 ROM but affected part easily moved.
 3 – Considerable increase in muscle tone, passive movement
 difficult.
 4 – Affected part rigid in flexion or extension.

ROM AND CONTRACTURE:
 Variation in ROM measurement between observer is common and
 frustrating.
 • Differentiation between static and dynamic deformity may be difficult
 in nonanesthetized patient. However static examination of muscle
 length provides some insight in to whether contracture are static or
 dynamic.
 • Comparison of joint ROM with slow and rapid stretch can be useful in
 evaluation of spasticity.
 • Dynamic contracture disappears under G.A. thus the ROM
 examination under G.A. can be used to help decide whether to inject
 botulinum toxin for spasticity in muscle or perform surgery to
 lengthen a contracture of the tendon.
 • Differentiation between contracted biarticular and monoarticular
 muscle is important.
 • The Silverskiold test assesses the difference between gastocnemius
 and soleus contracture.

Conti:
 Start by palpating the muscle in question to determine if
 there is muscle contracture at reMove the limb slowly to assess the available passive ROM
 The limb can then be moved through the available range at
 different speeds to assess the presence or absence of a catch and how
 this catch varies with a variety of speeds.
 Next is change the direction of motion of the joint at various
 speed and assess how the resistance varies.
 Last , observe the limb/ joint while asking the patient to move
 the same joint on contralateral side.st.

Silverskiold test:
The Silverskiold test: a) this test
differentiates tightness of
gastrocnemius and soleus. In this test
the knee is flexed to 90, hind
foot is positioned in varus, and
maximally dorsiflexed. B) As the knee
extented , if ankle moves towards
plantarflexion, contracture of
gastrocnemius present.

conti:
 The DUNCAN-ELY test differentiates between contracture of the
 monoarticular vasti and the biarticular rectus femoris.
 • Perry and colleagues have shown that when these test are performed
 with electromyography, both mono articular and bi articular muscle
 crossing the joint contract.
 • For example, in nonanesthetized person The DUNCAN-ELY test
 induce contraction of not only the rectus femoris but also iliopsoas
 and SILVERSKIOLD test induce contraction of both gastrcnemius and
 soleus. But under G.A. the biarticular muscle tests reliably
 differentiate the location of contraction. So this should routinely
 include as part of pre surgical examination under G.A.

Duncan-ely test:
The patient is positioned prone. As the knee
is flexed, a contracture of the rectus femoris causes the hip to
flex because rectus femoris is a hip flexor and knee extensor.

Hip:
 The Thomas test is used to measure the degree of hip flexor
 tightness.
 • It is preformed with patient supine position and pelvis held in such
 that the ASIS and PSIS are aligned vertically.
 • Defining the pelvis position consistently rather than using the
 flattened the lordosis method improves reliability.
 • Because of the origin and insertion points, the causes of limited hip
 abduction ROM can be distinguished by measuring hip abduction in
 various position of hip and knee with the patient in supine.
 The one joint adductors ( adductor longus, brevis , magnus) are
 isolated with the knee flexed. In this position, the gracilis is relaxedWith the knee in full extension the length
of 2 joint gracilis in a
 position of maximum stretch.
 • If the hip abduction is more limited when the knee is extended
 compare with the knee flexed, contracture of gracilis is the cause

Knee
 In child with CP capsular contracture causes knee flexion contracture.
 It is must to differentiate between true knee joint contracture and
 hamstring contracture.
 • Knee joint contracture is identify if knee extension is limited with hip
 extension (to relax hams) and ankle relax in position of equinus (to
 relax gastrocnemius) . Hamstring contracture is identified if knee extension is limited when
 the hip is flexed 90 (popliteal angle). normal values for popliteal
 angle are age and gender dependent, with boys tighter than girls and
 both tighter with increase with age, mainly at adolescent growth
 spurt.
 The bilateral popliteal angle measurement is performed with
 contralateral hip flexed until ASIS and PSIS aligned vertically.

Conti:
Unilateral and bilateral popliteal angle are measured to
calculate
the hamstring shift. A)The unilateral popliteal angle measured
with
typical lordosis, contralateral hip extended and ipsilateral hip
flex to
90. the number recorded is the degree missing from full
extension
at the point of first resistance. B) Bilateral popliteal angle
measured
with the pelvic position corrected. The contralateral hip is flexed
until the ASIS and PSIS are vertical.

Conti:
 A significant smaller popliteal angle with pelvis position corrected is
 referred as a HAMSTRING SHIFT.
 • The value popliteal angle with a neutral pelvis is a measure of true
 hams contracture and the value with the lordosis presents the
 functional hams contracture. The difference between this two
 represents the degree of HAMSTRING SHIFT.
 • Hamstring contracture is frequently implicated as a causes of crouch
 gait. However increased ant. Pelvic tilt is common in crouch gait
 caused by CP and this produce hamstring shift. In this situation,
 hamstring length may be normal or long, and hams lengthening
 surgery weakens hip extension and exacerbates the excessive
 hamstring length.

Conti:
 Because of difficulty in establishing dynamic hamstring length on
 physical examination, static hamstring length from supine physical
 examination should supplemented by estimation of hamstring length
 obtained from gait analysis before consideration of hamstring
 lengthening surgery.

BONE DEFORMITY:
 FEMORAL ANTEVERSION:
 • Femoral anteversion means the relationship between the axis of
 femoral neck and femoral condyles in transverse plane.
 • Femoral anteversion reported as the difference between the tibia
 and the vertical. Average normal value for adult men is 10 and for
 female is 15.
 • Femoral anteversion at birth is 45. If growth and development are
 typical, most infantile anteversion remodels b/n 1 to 4 year of age
 reaching normal value by 8 year.

Conti:
Femoral anteversion by palpation of maximum
trochanteric
prominence. In prone position with knee flex
90, rotate the
hip internally and externally until the GT is
maximally
prominent laterally. Femoral anteversion is the
difference
between the tibia and the vertical.

LEG LENGTH:
 Good assessment of limb length inequality can by complicated by
 scoliosis, hip subluxation, pelvic obliquity, unilateral contracture of
 hip adductors or abductors, or knee flexion contracture.
 • In the absence of an asymmetric hip or knee contracture, limb length
 can be measured clinically in supine using inferior border of ASIS and
 distal aspect of the medial malleolus.
 • Radiographic assessment is necessary if too many compounding
 factors are present.

POSTURE AND BALANCE:
 Assessment of posterior, anterior, medial and lateral equilibrium
 responses should not be neglected when planning treatment.
 • Many children with CP have delayed or deficient post equilibrium
 responses.
 • Assessment of posture including trunk, pelvis and lower extremity
 posture in static standing and during walking often gives insight to
 areas of weakness and poor motor control.

GAIT ANALYSIS:•
 Gait analysis consist of observing the patient with or without use of
 formal gait analysis equipment. Now a days computerized gait
 analysis is very much in use.
 • It is still an essential component for diagnosis. Clinical observation is
 done by repeatedly watching the child walk from sides, back and
 front. Attention should be paid at pelvis, hip, knee, ankle and foot.
 • Beginning with the feet , here several thing to be noted:
 1) Is the foot neutral or is it in varus or valgus position?
 2) Is the ankle in neutral position or in equinus?
 3) what portion of foot contacts the floor first?
 4) Is the arch maintain?
 5) At which point in the cycle does any deviation in the foot
occur?

Conti:
 At the knee following should be noted:
 1) what is the position of knee at initial contact?
 2) does knee hyper extended or extension controlled?
 3) does the knee comes in full extension at any point of stance?
 4) what is the maximum knee flexion in swing?
 5) is there varus or valgus motion during loading?
 • Following thing consider in general:
 1) is the pelvic position normal or it is ant. Or post.?
 2) is pelvic mal rotation or obliquity present?
 3) are the abnormal motions present?
 4) how are the arm moving during gait? Are they moving
 symmetrically and reciprocally or are they postured?
 5) does the child elevates his arms to assist with balance

Gait Cycle
 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 Terminilogy
 Stride length/Duration
 Step Length/Duration
 Step Width
 Cadence

Conti:
 Walking Speed/Velocity
 Degree of Toe-out
 Kinematics
 Kinetics

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

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

List of Pathological gait in cerebral palsy
 Type 1 – or dropped foot
 equinus foot
 equinus foot and genu recurvatum
 Jump gait
 Gait with apparent equinus
 Crouch gait

Coruch Gait
 It is determined by excessive dorsiflexion of the ankle and genu flexum with coxa flecta.
 Conservator treatment aims to maintain passive mobility, to avoid static activities like orthostatic or
supine position, to improve balance and coordination. Surgical treatment includes tenotomy,
elongation and transfer of hamstring, hip flexors and adductors. After surgery, there is a period of
casting, immobilization, and after that the child can begin physical therapy.
 Gait is a cyclical event, and Perry described it for the first time. The gait has two phases: stance (60%)
and swing (40%), each divided, so the stance phase includes pre swing, terminal stance, mid stance,
loading response and initial contact, and the swing phase includes terminal swing, mid swing and initial
swing. The stance phase allows body support and the swing phase allows limb movement. The lower
limb muscles are activated, one at a time, in the gait cycle

WHO MAKES THE DIAGNOSIS?
1.Takes a thorough history
2. Does a complete physical, orthopedic and neurological examination
3. Understands the diagnostic boundaries and the differential diagnosis
4. Applies the definition and classification accurately

ICF Model
International Classification of Functioning, Disability and Health
The ICF puts the notions of 'health' and 'disability' in a new light. It
acknowledges that every human being can experience a decrement in
health and thereby experience some degree of disability. Disability is
not something that only happens to a minority of humanity. The ICF
thus 'mainstreams' the experience of disability and recognizes it as a
universal human experience.”

ICF categories:
1. Body structure and functions and structures (anatomy and physiology)
2. Activities (carrying out daily living tasks)
3. Participation in home, work and community
4. Interactions with
 personal factors (e.g., age, motivation, desires) and
 environmental factors (e.g., settings of home or community, building
modifications)

Re / habilitation
Principles of proper habilitation
3.Holistic program
-Handling, carrying and transfer techniques
- Postural management
- Movement therapy
- Play therapy
4. Team work ( global dysfunction )
- Family support
- Professional support

Management Team
 Pediatrician ( Developmental Pediatrician)
 Neurologist (Pediatric Neurologist)
 Developmental Therapist
 Pediatric Occupational Therapist
 Pediatric Physiotherapist
 Pediatric Speech Therapist
 Special Educator

Conti:
 Clinical Psychologist
 Orthotician
 Specialized Carpenter
 Orthopedic Surgeon ( Trained for CP)
 Urologist
 Eye Specialist
 ENT Surgeon
 Others

Management Techniques:
Physiotherapy
Occupational therapy
Special Education
Speech Therapy
Aids / Appliances
= Drugs Therapy
= Chemodenervation
= Orthopedic Surgery

Components of rehabilitation
Physiotherapy
Occupational therapy
Bracing
Assistive devices
Adaptive technology
Sports and recreation
Environment modification

Rehabilitation planning Example:
Independent standing
State the necessary time period —Plan
the methods to achieve this goal
Evaluate the end state.
Revise the treatment program

Conventional exercises:
 Active passive range of motion exercise
 Stretching exercise
 Strengthening exercise
 Fitness exercise
 Postural oriented exercise
 Functional exercise

NEURO FACILITATION TECHNIQUE
Neurofacilitation techniques
 Sensory input to the CNS produces reflex motor output.
 Various neurofacilitation techniques are based on this
basic principle.
 All of the techniques aim to normalize muscle tone
 To establish advanced postural reactions and to
facilitate normal movement patterns.

Bobath neurodevelopmental therapy
 This is the most commonly used therapy method in CP worldwide.
It aims to
 Normalize muscle tone
 Inhibit abnormal primitive reflexes Stimulate normal movement.
 It uses the idea of reflex inhibitory positions to decrease spasticity and
stimulation to promote the development of advanced postural reactions.
 It is believed that through positioning and stimulation a sense of normal
movement will develop.
 To teach the mother how to position the child at home during feeding
and other activities.
 The baby is held in the antispastic position to prevent contracture
formation.

Constrient induced movement therapy
 Constraint induced movement
therapy Where the normal hand is
constrained Paralytic hand is forced to
function Useful in children with
hemiplegia.
 Begin therapy toward one year of age when the child can feed
himself using a spoon and play with toys.
 Teach the child age appropriate self care activities such as
dressing, bathing and brushing teeth.
 Encourage the child to help with part of these activities even if he is
unable to perform them independently

Use and goal OF Braces
 Increase function
 Prevent deformity
 Keep joint in a functional position
 Stabilize the trunk and extremities
 Facilitate selective motor control
 Decrease spasticity
 Protect extremity from injury in the postoperative phase

Braces in CP:
 Ankle foot orthoses
 Knee-ankle foot orthoses
 Hip abduction orthoses
 Thoracolumbosacral orthoses
 Supramalleolar orthoses
 Foot orthoses
 Hand splints

Function of the AFO
 Main function Keep the foot in a plantigrade
 position
 Stance phase Stable base of support
 Swing phase Prevent drop foot
 At night Prevent contracture

Spinal braces
 To slow the progression of deformity
 To delay surgery
 To allow skeletal growth
 To assist sitting balance
 To protect the surgical site from excessive loading after surgery

Mobility aids
Mobility aids
 Example
Standers
Walkers
Crutches
Canes
 Advantages of mobility aids
Develop balance
Decrease energy expenditure
Decrease loads on joints
Improve posture

Activity oriented excericse
Laying oriented
Sitting oriented
High sitting oriented
Kneeling oriented
Half kneeling oriented
Standing oriented

Rolling and twisting
 A child with cerebral palsy is often very stiff when it comes to twisting or rotating the main part of
her body. However, such twisting is necessary for learning to walk. Rolling also helps develop body
twisting.
 Help the child 'loosen up' by swinging her legs back and forth.

If the child is very stiff, first help
her 'loosen up' by swinging her
legs back and forth. Then help
her learn to twist her body and
roll.
Help her learn to twist her body
and roll.

sitting
 sit him with his legs apart and turned outward. Also lift his shoulders up and turn his arms out.
 Sit him with his legs apart and turned outward.

 Look for simple ways to help him stay and play in the improved position
without your help.

 Sitting with the legs in a ring helps turn hips outward.

 For the child with spasticity who has trouble sitting, you can control his legs like this. This leaves your
hands free to help him control and use his arms and hands. Help the child feel and grasp parts of his fa

 Sit the child on your belly with his legs spread and feet flat. Give support with your
knees as needed. As he begins to reach for his face, help his shoulders, arms, and
hands take more natural positions. Make a game out of touching or holding parts of
his face. MAKE IT FUN!

High sitting
 High sitting using high stool or bench
 High sitting using block or bloaster
 Catch and throw in high sitting
 Pick and drop in high sitting
 Reach out
 Lateral reach out both side
 Over head activity

Kneeling :
 Heel sitting
 Kneeling
 Dyanmic kneeling
 Lateral weight shifting
 Catch and throw
 Pic and drop

Half kneeling
 Kneeling to half kneeling
 Half kneeling
 Reach out in Half kneeling
 Hlf kneeling to standing vice versa

Standing :
 Step standing
 One foot standing
 stride standing
 Wide satnding
 Yard standing
 Dyanmic standing
 Pick and drop in satnding

Gait readucation exercise
 Jumping
 Hooping
 Tandem standing
 Tandem walking
 Walk over foot mark
 Figure of 8 walking

Institute of applied medicine and research( IAMR)
GHAZIABAAD (U P )
PH :7827068869
Email : physio.akshyarajchandra@gmail.com
submitted by : submitted to :
Akshya Raj chandra PT IAMR (CCSU)
MPT 1st year (Neurology )

Submitted Submitted to
Akshya Raj Chandra IAMR (CCSU )
MPT 1st year Neurology

Seminar on cerebral palsy ( akshay )

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