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to establish locomotion, communication and self-help, gain optimal appearance and integration of motor functions; correct associated defects as effectively as possible and provide educational opportunities based on the individual’s needs and capabilities
By: DR HARDEV SINGH
MODERATOR: DR SAMIR GROVER
• A motor function disorder
– caused by permanent, non-progressive brain lesion
– present at birth or shortly thereafter.
• Non-curable, life-long condition
• Damage doesn’t worsen
• May be congenital or acquired
A Heterogenous Group of Movement Disorders
Three distinctive features common to all patients with cerebral palsy
(1) Some degree of motor impairment is present,
(2) An insult to the developing brain has occurred,.
(3) A neurological deficit is present that is nonprogressive,
• Muscles are unaffected
• Brain is unable to send
signals necessary to
instruct muscles when
to contract and relax
An insult or injury to the brain
–Fixed, static lesion(s)
–In single or multiple
areas of the motor
centers of the brain
• Development Malformations
– The brain fails to develop correctly.
• Neurological damage
– Can occur before, during or after delivery
* Unknown in many instances
Severe deprivation of oxygen or
blood flow to the brain
• Prenatal factors
– Before birth
– Maternal characteristics
• Perinatal factors
– at the time of birth to 1mo
• Postnatal factors
– In the first 5 mos of life
1)Risk factors inherent to the
fetus (most commonly
2)Factors inherent to the
mother (seizure disorders,
mental retardation, and
previous pregnancy loss),
3)Factors inherent to the pregnancy itself (Rh
incompatibility, polyhydramnios, placental rupture,
and drug or alcohol exposure).
4)External factors, such as TORCH (toxoplasmosis,
other agents, rubella, cytomegalovirus, herpes
1)Typically is associated with asphyxia or trauma
that occurs during labor.
3)Umbilical cord prolapse,
4)Breech presentation all have been associated
with an increased occurrence of cerebral palsy.
5)Cerebral palsy often is associated with low
Apgar scores during this period
Low-birth-weight infants (<1500 g) are at dramatically
increased risk of cerebral palsy.
This increased incidence is believed to be due to the
fragility of the periventricular blood vessels, which are
highly susceptible to physiological fluctuations during
These fluctuations, which include hypoxic episodes,
placental pathology, maternal diabetes, and infection, can
injure these vessels and lead to subsequent intraventricular
Grading of Periventricular Lesions
I Bleeding confined to germinal matrix
II Bleeding extends into ventricles
III Bleeding into ventricles with dilation
IV Bleeding into brain substance
Trauma, head injury
Lack of oxygen
Stroke in the young
One extremity involved, usually lower
In hemiplegia, one side of the body is involved, with
the upper extremity usually more affected than the
Patients with hemiplegia, approximately 30% of
patients with cerebral palsy, typically have sensory
changes in the affected extremities as well.
• Hemiplegia on right side
–Hip and knee contractures
–Talipes equinus (“tip-toeing”
- sole permanently flexed)
–Asteriognosis may be present.
(inability to identify objects by
Diplegia is the most common anatomical type of
cerebral palsy, constituting approximately 50% of all
Patients with diplegia have motor abnormalities in
all four extremities, with the lower extremities more
affected than the upper.
The close proximity of the lower extremity tracts to
the ventricles most likely explains the more frequent
involvement of the lower extremities with
periventricular lesions .
•both legs•both legs w/ slight
May also have
hips and knees
This type of cerebral palsy is most common in
Intelligence usually is normal.
Most children with diplegia walk eventually,
although walking is delayed usually until around
age 4 years.
In quadriplegia, all four extremities are equally
involved, and many patients have significant
cognitive deficiencies that make care more difficult
Head and neck control usually are present, which
helps with communication, education, and seating.
• Increased muscle tone,
tense and contracted muscles
– Have stiff and jerky or
– limbs are usually underdeveloped
– increased deep tendon reflexes
• most common form
• 70-80% of all affected
Spastic is the most common form of cerebral palsy,
constituting approximately 80% of cases, and usually is
associated with injury to the pyramidal tracts in the
Booth showed histologically that this altered muscle
function leads to the deposition of type I collagen in the
endomysium of the affected muscle, leading to thickening
and fibrosis, the degree of which correlated to the severity
of the spasticity.
Joint contractures, subluxation, and degeneration are
common in patients with spastic cerebral palsy.
positions of lower limbs
due to adductor spasms.
Athetoid/ Dyskinetic CP
• Fluctuating tone
– involves abnormal involuntary
– that disappear during sleep and
increase with stress.
– Interferes with speaking, feeding,
reaching, grabbing, and any other
– 20% of the CP cases,
Athetoid cerebral palsy is caused by an injury to the
extrapyramidal tracts and is characterized by
dyskinetic, purposeless movements that may be
exacerbated by environmental stimulation.
Choreiform cerebral palsy is characterized by
continual purposeless movements of the
patient's wrists, fingers, toes, and ankles. This
continuous movement can make bracing and
Patients with rigid cerebral palsy are the most hypertonic
of all cerebral palsy patients.
These patients have a “cogwheel” or “lead pipe” muscle
stiffness that often requires surgical release.
• Poor balance and lack of coordination
– Wide-based gait
– Depth perception usually affected.
– Tendency to fall and stumble
– Inability to walk straight line.
– Least common 5-10% of cases
Ataxic cerebral palsy is very rare
As a result of an injury to the
It is important to distinguish true ataxia from
spasticity because with treatment many children
with ataxia are able to improve their gait function
• A common combination is
spastic and athetoid
• Spastic muscle tone and involuntary
• 25% of CP cases, fairly common
• Stiff or floppy posture
• Weak suck/ tongue thrust/
tonic bite/ feeding difficulties
• Poor head control
• Excessive lethargy or
irritability/ High pitched cry
Infancy (0-3 Months)
• Abnormal or prolonged
Asymmetric tonic neck reflex
• Inability to perform motor skills as indicated:
– Control hand grasp by 3 months
– Rolling over by 5 months
– Independent sitting by 7 months
• Abnormal Developmental Patterns:
– Hand preference by 12 months
– Excessive arching of back
– Log rolling
– Abnormal or prolonged parachute response
Abnormal Developmental Patterns after 1
year of age:
• “W sitting” – knees flexed,
legs extremely rotated
• “Bottom shuffling” Scoots along the floor
• Walking on tip toe or hopping
History and physical examination are the primary tools in
making the diagnosis of cerebral palsy.
The history should include a thorough investigation of the
pregnancy and delivery.
Ancillary studies, such as radiographs, hematological studies,
chromosomal analysis, CT, MRI, and positron emission
tomography, rarely are needed to make the diagnosis, but may
be helpful in determining the type and extent of cerebral palsy
Diagnosis of cerebral palsy before age 2 years can be
Nelson and Ellenberg found that 55% of children
diagnosed with cerebral palsy by 1 year of age did not
meet the criteria by age 7 years.
Transient dystonia of prematurity is a condition
characterized by increased tone in the lower
extremities between 4 and 14 months old and often is
confused with cerebral palsy.
P osturing / Poor muscle control and strength
O ropharyngeal problems
S trabismus/ Squint
T one (hyper-, hypotonia)
E volutional maldevelopment
R eflexes (e.g. increaseddeep tendon)
*Abnormalities 4/6 strongly point to CP
- No treatment to cure cerebral palsy.
- Brain damage cannot be corrected.
• Crucial for children with CP:
–Multidisciplinary Care; and
NON OPERATIVE TREATMENT
Commonly used as primary treatment or in
conjuction with surgery
Common agents - diazepam
- botulinum toxin
Dantrolene-acts at the level of skeletal muscle and
decreases muscle calcium ion release. It has an
affinity for fast twitch muscle fibers and selectively
decreases abnormal muscle stretch reflexes and
Diazepam- increases inhibitory neurotransmitter
Baclofen -inhibit abnormal monosynaptic extensor
activity and poly synaptic flexor activity and
decrease substance P levels
Intrathecal injection of baclofen requires 1/30 the dose of
oral baclofen to achieve a similar or better response.
An implantable programmable pump dramatically decreases
the dose required to affect spasticity and decreases some of
the side effects such as sedation. This pump typically is
implanted subcutaneously in the abdominal wall and requires
refilling approximately every 2 to 3 months.
Botulinum toxin type A (BTX-A) (Botox, Dysport) has
been used to weaken muscles selectively in patients with
BTX-A injected directly into the muscle acts at the level
of the motor end plate, blocking the release of the
neurotransmitter acetylcholine and inhibiting muscle
This effect begins approximately 24 hours after
injection and lasts 2 to 6 monthsCare
– Intra muscular botulinum toxin for 2-6 months
– Safe maximal dose 36-50 U/kg
Physical therapy typically is used as a primary treatment
modality and in conjunction with other modalities, such as
casting, bracing, BTX-A, and surgery.
Bracing in patients with cerebral palsy most commonly is used
to prevent or slow progression of deformity.
The most commonly used braces for the treatment of cerebral
palsy include ankle-foot orthoses, hip abduction braces, hand
and wrist splints, and spinal braces or jackets.
Operative treatment typically is indicated when
contractures or deformities decrease function,
cause pain, or interfere with activities of daily
living. It is the only effective treatment when
significant fixed contractures exist.
Selective posterior rhizotomy
In some cases nerves need to be severed to decrease
muscle tension of inappropriate contractions.
How it Works
• The sensory nerve fibers in the spinal cord, usually
between the bottom of the rib cage and the top of the
hips are divided
• The nerve fibers are then stimulated and the
responses of the leg muscles are observed.
• Those that have an abnormal or excessive response
• Those with a normal response are left intact.
• Intensive rehabilitation is required after the surgery,
usually up to six weeks, followed by physical therapy
on an ongoing basis
OPERATIVE MENAGEMENT HIP
contracture or deformities causing
Interfere with ADL
PREREQUISITES FOR EFFECTIVE
hemiplegics / diplegics : good results
quadriplegics : minimal improvement
Age : 3- 12 years
IQ : good
Good upper limb function : for walking
Underlying muscle power should be good
surgery hardly changes status in
walkers/nonwalker, but improves gait
Indication for surgery
Hip flexion deformity never decrease by
Hip flexion deformity > 20 needs surgery
Hip flexion contracture hip , knee & ankle contracture
15-30 deg flexion >30 deg flexion multi level correction
ilioPsoas lengthening more release of
-anterior fibers of Gl.minimus
Iliopsoas recession is most commonly used
than complete tenotomy to avoid excessive
Mild contracture severe contractures
Early hip subluxation
Adductor tenotomy more release of
Leave adductor brevis ( the major hip stabilizer )
MI > 30 % Soft tissue release for very young
Flexion adduction deformities
MI > 50% open reduction + femoral osteotomy
Correction of femoral valgus and anteversion
AI > 25 deg pelvic osteotomy
(Correction of acetabular deformities)
Femoral varus and derotational(external
Salter osteotomyredirection of the
acetabulum anterioly and laterally
Posterior dislocation (m.c)
TRETMENT OPTIONS IN HIP
Relocation procedure on femur and
Proximal femoral resection
Total hip arthroplasty
The most common deformity is ankle
equinus, with equinovarus and
equinovalgus deformities being equally
Equinus deformity is the most common foot deformity in
patients with cerebral palsy, affecting 70% of children.
Surgical Correction of Equinus Deformity
Open Lengthening of the Achilles Tendon
Z-Plasty Lengthening of the Achilles Tendon
Percutaneous Lengthening of the Achilles Tendon
Lengthening of the Gastrocnemius-Soleus Muscle
Varus deformity, which usually is accompanied by
equinus, is caused most commonly by an abnormal
posterior tibial muscle that is overactive or firing out
Lengthening of the Posterior Tibial Tendon
Z-Plasty Lengthening of the Posterior Tibial Tendon
Step-Cut Lengthening of the Posterior Tibial Tendon
Musculotendinous Recession of the Posterior
Flexion is the most common knee deformity in patients with
cerebral palsy and frequently occurs in ambulatory children
Spastic hamstrings, weak quadriceps, or a combination of both
can cause isolated knee flexion.
Fractional Lengthening of Hamstring Tendons
Combined Hamstring Lengthening, Posterior Capsular Release,
and Quadriceps Shortening
Distal Transfer of Rectus Femoris