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CEREBRAL PALSY

By
BEN DAVID PAJANUSTAN <3

It is a non-specific term applied to


neurologic disorders characterized
by
early
onset
and
impaired
movement and posture.
Most common permanent physical
disability of childhood.
ETIOLOGY
A variety of perinatal, postnatal and
prenatal factors can contribute to the
development of CP, singly or
multifactorially.
The
human
undergoes development during the
prenatal period up to 2 years of age
any injury or insult occurring in this
period may result in CP.
The prevalent traditional hypothesis
has been that CP results from
perinatal problems, especially birth
asphyxia (asphyxia neonatorum).
But now it is more often believed to
result from existing prenatal brain
abnormalities, but the exact cause of
these abnormalities remains elusive.
An estimation of 80% of all the cases
of CP is caused by unknown prenatal
factors.

PATHOPHYSIOLOGY
Because there is no characteristic
pathologic picture it is difficult to
establish a precise location of
neurologic lesions on the basis of
etiology or clinical signs.
Secondary causative mechanisms:

Intrauterine
Chorioamonionitis,
Infants born before 36 weeks
gestation,
Periventricular leukomalacia
Preterm births of EXTREME
LOW BIRTH WEIGHT and VERY
LOW BIRTH WEIGHT
Kernicterus

Gross malformations of the


brain
Evidence of vascular occlusion
Atrophy
Loss of neurons
Laminar degeneration
Narrower gyri
Wider sulci
Low brain weight

CLASSIFICATIONS
The most common:

Spastic CP

Clinical Manifestation

Some factors that have been


associated with increased risk of CP
are

Shaken baby syndrome


Bacterial meningitis
Viral encephalitis
Motor vehicle accidents
Child abuse
Neonatal encephalopathy

Delayed gross motor


movement
Abnormal
motor
performance
Alterations of muscle
tone
Abnormal postures
Reflex abnormalities
Associated
disabilities
and problems

Diagnostic Evaluation

MRI

Metabolic and genetic testing


Primitive reflexes
Hearing and vision deficits

Laboratories
are
recommended.

no

longer

THERAPEUTIC MANAGEMENT
Aims of therapy are:

Establish
locomotion,
communication and self-help
Gain optimum appearance and
integration of motor functions
Correct associated defects as
early
and
effectively
as
possible
Provide
educational
opportunities adapted to the
individual childs needs and
capabilities
Promote
socialization
experiences
with
other
affected
and
unaffected
children.

Mobilizing Devices
Ankle Foot Braces- molded to fit the
feet and worn inside the shoes, these
are used to:

Prevent or reduce deformity


Increase energy efficiency of
gait
Control alignment

Wheeled Scooter Boards- allow


children to propel themselves while
the abdomen or total body is
supported
and
the
legs
are
positioned with wedges to prevent
scissoring.

Wheeled Go Carts- provide good


sitting balance also serve as an early
wheelchair experience for young
children.
Surgery
Used primarily to improve function
rather than for cosmetic purposes
and is followed by physical therapy.
Indicated for:

Children
whose
spasticity
causes
progressive
deformities.
Contracture
or
spastic
deformities
Provide
stability
for
uncontrollable joint
Provide
balanced
muscle
power

Medication
Pharmacologic agents given orally:

Dantrolene Sodium (Dantrium)


Baclofen (lioresal)
Diazepam (Valium)

These are effective in decreasing


overall spasticity.
Botulinum Toxin A - is also used to
reduce
spasticity
in
targeted
muscles. (Commonly quadriceps,
gastrocnemius
or
medial
hamstrings.)The goal is to allow
stretching of muscles and permit
ambulation with an AFO.
AEDs
such
as
Carbamazepine
(Tegretol) and Divalproex (valproate
sodium and valproic acid; Depakote)
are prescribed for children who have
seizures.

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