CEREBRAL PALSY

DR. ANDI DHEDIE P. SAM, M.KES, SP.OT

MAIN DISCUSSIONS
Definition, Etiology and Epidemiology
Pathophysiology
Classification
Clinical Manifestations
Treatment Options
Definition, Etiology and Epidemiology
Cerebral Palsy, first described by William Little (1862), was called Little’s disease
Cerebral Palsy is a heterogenous group of permanent disorders of the development of
movement and posture, causing limitation of activity that are attributable to non-progressive
disturbances that occurred in the developing fetal or infant brain
The motor disorders are often accompanied by disturbances of sensation, perception, cognition,
communication and behavior, epilepsy and secondary musculoskeletal problems
Epidemiology : 2-2.5/1000 births
In Short, Cerebral Palsy is …
A Permanent Disorder, caused by
Non-progressive Disturbance (Static encephalopathy), of
Developing Fetal or Infant Brain, causing
Permananent Disorders of Movement and Posture.
Cerebral Palsy causes include..
Congenital brain malformations (5-15%)
Pre-natal causes (50-70%)
◦ Intra-uterine infections, placental malformations, complications of prematurity, brain hemorrhages and
stroke (pre- or neonatal)

Peri-natal causes (10%)

◦ Hypoxic-ischemic encephalopathy

Post-natal causes (10-25%)

◦ Head injury, metabolic encephalopathy, hyperbilirubinemia and infections
Cerebral Palsy risk factors include..
Prematurity (the most common risk factor for Cerebral Palsy)
◦ Fragile cerebral vasculature = Immature autoregulation of cerebral blood flow = Vulnerable cerebral
parenchyma

Low birth weight

Multiple births
Intra-uterine infections
APGAR scores <5 at 5 minutes
Post-natal hyperbilirubinaemia
Maternal Disorders (diabetes)
Beware.
“Knowing the exact cause of cerebral palsy does not
alter the management of treatment”
Pathophysiology
Brain lesion produce specific abnormalities of tone and movement depending on the location of
lesion (spastic, dyskinetic, etc)
◦ Upper Motor Neuron disorders : Hypertonia, Hyper-reflexia and co-contractions
◦ Loss of connections to Lower Motor Neurone : Weakness, loss of selective motor control, deficits in
balance and coordinations

Decreased activities associated with developmental delay, along with hypertonia that impairs
muscle growth relative to the growing skeleton, resulting in static or fixed contractures
Diagnosis
Classification (Clinical Classification)
Classification (Physiopathological Perspective)
CORTICOSPINAL / PYRAMIDAL VS EXTRAPYRAMIDAL
Spastic Athethoid
Choreiform
Ataxic
Rigid
Hypotonic
Motoric Problems
Classification (Physiopathological Perspective)
CORTICOSPINAL / PYRAMIDAL MANIFESTATIONS
Spastic Fatigue
Loss of dexterity and coordination
Balance disorders
Contractures
Joint subluxations
Classification (Physiopathological Perspective)
MANIFESTATIONS
EXTRAPYRAMIDAL
Dyskinetic movements augmented by
Athethoid external stimulus
Choreiform May be associated with dystonia or
hypotonia
Ataxic
Rigid
Hypotonic
Classification (Physiopathological Perspective)
EXTRAPYRAMIDAL
MANIFESTATIONS
Athethoid
Chaotic movements of the fingers,
Choreiform hands, ankles
Ataxic Voluntary movements are very hard to
finalize
Rigid
Hypotonic
Classification (Physiopathological Perspective)
EXTRAPYRAMIDAL
Athethoid
Choreiform MANIFESTATIONS
Uncoordinated movements
Ataxic
Cerebellum damage results in gait
Rigid disturbances
Hypotonic
Classification (Physiopathological Perspective)
EXTRAPYRAMIDAL
Athethoid
Choreiform
MANIFESTATIONS
Ataxic
Can be final or transient (until ataxic or
Hypotonic spastic forms appears)
Determines difficulties in maintaining
the correct body position, or balance
disorders
Classification (International Multidisciplinary Group)
Gross Motor Functional Classification System (GMFCS)
Level I (Ambulatory) – can perfom all activities with some difficulties with speed, balance, and
coordination
Level II (Ambulatory) – can perform all functional abilities on flat and familiar surface but need
support on uneven surfaces or when climbing stairs
Level III (Ambulatory) – independent walkers but require assistive device (crutch or walkers) and
may use wheelchairs for longer distances
Level IV (Non-ambulatory) – may bear weight for transfers and use a walker for exercise
purpose
Level V (Non-ambulatory) – cannot achieve any functional weight bearing and totally
dependent of caregivers
Gross Motor Functional Classification System (GMFCS)
Clinical Manifestations
1. Posture and Movement Disorders
2. Abnormal gait patterns
3. Secondary Scoliosis and hip instability
4. Disorders of sensation, perception, cognition, communication and behavior, epilepsy and
secondary musculoskeletal problems
Clinical Manifestations
Clinical Manifestations
Gait Disturbances. The Specific Types.
BILATERAL CEREBRAL PALSY UNILATERAL CEREBRAL PALSY
True Equinus Drop Foot
Jump Gait / Jump Knee True Equinus
Apparent Equinus Equinus/Jump Knee
Crouch Gait Equinus/Jump Knee/Hip Flexion
Bilateral Cerebral Palsy Gait Bilateral.
Group I : True Equinus (equinus
ankle, extended knee, extended hip)

Group II : Jump Knee (equinus ankle,

flexed knee, flexed hip)

Group III : Apparent Equinus (up on

toes despite neutral ankle to
accommodate flexed knee and hip)

Group IV : Crouch Gait (dorsiflexed

foot segment relative to tibia
occurring either because of
calcaneus at the ankle or because of
midfoot break, flexed knee and hip)
Group I : Drop Foot Patter (Equinus
in swing phase only)

Group II : True Equinus (equinus in

swing and stance phase

Group III : Equinus/Jump Knee (the

knee is involved, showing abnormal
flexion (jump) or stiff knee pattern)

Group IV : Equinus/Jump Knee/Hip

Flexion (Additional proximal
involvement at the hip)
Treatment Priorities
AMBULATORY CHILDREN NON-AMBULATORY CHILDREN
Preserve or improve Gait Efficiency (decrease Prevent and relief pain (often present with
energy consumption) seizure disorders, visual and hearing
impairments, cognitive delay, communication
Increase activities and participation difficulties, swallowing difficulties, aspiration ,
Improve gait appearance constipation and incontinence)
Facilitate caregiving
Preserve or improve quality of life
Treatment Options
1. Management of spasticity in the cerebral palsies
2. Managing weakness in the cerebral palsies
3. Orthopaedic surgery for fixed deformities
 Spastic Hemiplegia
 Spastic Diplegia
 Spastic Quadriplegia
Management of spasticity in the cerebral palsies
 Treatment can be classified as temporary or permanent and as focal of generalized
 Temporary and Focal management
 Intramuscular injections
 Phenol (neurolytic agent)
 BTX-A (potent neurotoxin, Clostridium botulinum)
 binds to cholinergic nerve endings and inhibits release of the neurotransmitter
acethylcholine by blocking the binding of acetylcholine vesicles to the plasma membrane
of the motor endplate)
 Completely reversible in around three months
Management of spasticity in the cerebral palsies

 Temporary and Generalized management

 Intrathecal Baclofen (ITB)
 Mainly for children with severe spastic quadriplegia with whole-body involvement
 Expensive, invasive and associated with high incidence of life-threatening complications
 Reports of rapidly progressing scoliosis
Management of spasticity in the cerebral palsies

 Permanent and Generalized management

 Selective Dorsal Rhizotomy (SDR)
 Laminoplasty from L1 to S1 and section of 20% to 40% of the dorsal rootlets
 Results in immediate and marked reduction in spasticity accompanied by weakness of the
lower limb
 Intensive physiotherapy needed to regain strength and function
 Reduction of spasticity is followed by marked improvement in range of movement of joints
and dynamic gait function
Managing weakness in the cerebral palsies
 Often neglected
 Traditional views :
“Muscle strengthening in children with cerebral palsy was neither possible
nor desirable because it might increase spasticity”
 Research has shown that children who participate in strengthening programmes demonstrate
increases in muscle power and improvements in function
Orthopaedic surgery for fixed deformities : Spastic Hemiplegia

 Fixed deformities of the upper limb are usually corrected in a one-stage multilevel approach by
combination of management of spasticity, lengthening of a fixed muscle-tendon contractures
and correction of dynamic imbalance by tendon transfers
 Group I and II gait patterns (Spastic Hemiplegia) dan be managed by lengthening of the
gastrocsoleus and ankle-foot orthosis application
 Group III and IV gait patterns (Spastic Hemiplegia) may benefit from multilevel surgery with a
combination of tendon-lengthening and tendon transfers
Orthopaedic surgery for fixed
deformities : Spastic Diplegia

 Most will develop progressive musculoskeletal

deformities as they grow
 Correction of fixed contractures of muscle-
tendon units is achieved by muscle-tendon
recession or fractional lengthenings
Orthopaedic surgery for fixed deformities : Spastic Quadriplegia

 Management is particularly challenging

 Hip displacement and spinal deformities are common
 Surgery should only be done in a multidisciplinary team
 The standard of care for severe spinal deformity is a long, instrumented posterior fusion to the
pelvis
Orthopaedic Procedures – List.
HIP KNEE CALF, ANKLE AND FOOT
 Psoas Lengthening  Hamstring Lengthening  Gastrocnemius and soleus
lengthening
 Adductor Lengthening  Distal femoral
extension osteotomy  Tibialis posterior split tendon
 Femoral derotational or transfer or lengthening
varus derotational  Patellar tendon
osteotomies shortening or  Distal tibial (supramalleolar)
advancement derotational osteotomies
 Periacetabular pelvic
osteotomies  Rectus Femoris transfer  Calcaneal osteotomies
Prognosis
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