CEREBRAL PALSY o Breech/Face Delivery (r/t Hypoxia)

-gwaposiJHERBEN- o Intrauterine Asphyxia

o Asphyxia Neonatorum
History o Low APGAR Score
- William John Little = 1st to describe Cerebral Palsy o Seizures
- Sir William Osler = 1st to use the term Cerebral Palsy o Respiratory Distress Syndrome
derived from Cerebrale Kinderlahung. o Hyperbilirubinemia (Bilirubin crosses the
o Grouped Cerebral Palsy according to its Blood-Brain Barrier; therefore,
presumed etiology & speculated upon Hyperbilirubinemia causes damage to the
pathophysiological mechanisms. Basal Ganglia)
- Sigmund Freud = classified Cerebral Palsy as to Maternal Factors
anatomic lesions.
o Diabetes Mellitus
- National Orthopedic Hospital = 1st to establish
o Threatened Abortion
Cerebral Palsy Clinic in the Philippines (1954).
- Elks Cerebral Palsy Rehabilitation Center = o Pre-Eclampsia
comprehensive rehab program in the Philippines. o Twin Pregnancy (competition of twins; the 1st
twin will kick out the 2nd twin, possibility of
** In Leukomalacia, the Brain will not be able to function. Twin-Twin Transfusion)
** In Pre-Ventricular Leukomalacia, affected ventricle will not Post-Natal Factors
function. o Head Trauma (r/t Suction, Forceps, failure to
catch baby during delivery)
CEREBRAL PALSY o Intracranial Infection
- progressive disorder of movement & posture caused by o Toxic Encephalopathies
damage to the brain at the time of brain development. o Cerebrovascular Accident
- A disorder of movement & posture caused by a static
defect or lesion of the immature brain. Etiology
- Disordered motor function (evident in early infancy) - Hypoxic Ischemic Encephalopathy Irreversible Brain
o Characterized by changes in muscle tone Injury
(usually spasticity, involuntary movements, o Cord Coil may occur
ataxia, or a combination of these - Malformations & Cortical Dysgenesis r/t Neuronal
abnormalities. Migration
- Intellectual, sensory, &/or behavioral difficulties may o Brain Heterotropia (increased Brain
accompany Cerebral Palsy, however they are not Convolutions)
included in the diagnostic criteria. - Obstetrical Problems = prolonged 2nd stage, precipitate
delivery
Pathophysiology - Infections (e.g. TORCHSA [Toxoplasmosis, Others,
- main pathology in Cerebral Palsy is in the Brain. Rubella, Cytomegalovirus, Herpes, Syphilis, AIDS])
- Insults or injuries, which happen before 20 weeks AOG - Hyperbilirubinemia
result in brain malformations.
- 26-30 weeks after birth cause damage mainly to the Classification
white matter in the periventricular areas resulting to Spastic
periventricular leukomalacia in the preterm infant. o Diplegia both legs are affected
- Injury incurred towards the end of a term pregnancy o Hemiparesis lateralized of the body
results in cortical & basal ganglia damage. affected
o Quadreparesis all limbs are affected
Causes o Physical Examination to check for Spasticity:
- Cerebral Palsy may be attributed to Pre-Term Birth &
Motor Examination, Muscle Strength, & Muscle
Intrauterine Growth Retardation.
Bulk
Choreoathetotic
Low Birth Weight 35%- 40%
Ataxic
Other (maternal factors, 22.5%
etc.) Dystonic
Congenital Brain 6%-10% Ballismic
Abnormality Mixed
Infections 5%-10%
Intrauterine ischemic 5%-10% HEMIPLEGIA/HEMIPARESIS
event - Distinctive Presentation: unilateral motor disability
Intrapartum Asphyxia 9% mostly spastic.
Metabolic Errors 5% - Etiology: prenatal in 75% of cases born prematurely.
Genetic and/or 2.5% o Some brain malformations, intracerebral
Chromosomal hemorrhage, & some unspecified.
- Unilateral Paresis & Spasticity of the opposite side.
Risk Factors - Delay in passing milestones.
- Weakness usually predominates in the distal part of the
Pre-Natal Factors
limbs.
o Hyperemesis Gravidarum
- A free interval maybe observed wherein no hemiparesis
o Intrauterine Viral/Bacterial Infection
is detected, which can last up to 4-9 months of age.
o Toxemia o Substantiated by repeated normal neurological
o Chromosomal Abnormality examinations despite the presence of known
o Terratogenic Drugs extensive hemispheric lesions.
o Maternal Malnutrition - In majority of cases, the 1st manifestations become
o Placenta Previa apparent by the 4th-5th months of age where attempts
o Placenta Abruptio at reaching are always on the same side (Early Hand
o (+) Family History Preference).
Perinatal Factors - Fisting & abnormal posture of the arm with flexion at
o Prematurity the elbow are usually present.
 - Involvement of the lower limb often becomes apparent
only with ambulation.
- Growth of the affected side is usually less than that of
the opposite side.
SPASTIC DIPLEGIA
- Distinctive Presentation: increased muscle tone in the
lower extremities.
- Etiology: frequently associated with premature infants
with a relatively high frequency of perinatal factors.
o Over half of the affected children have a
history of abnormal labor/delivery but its
significance remains debated.
- r/t periventricular lesions, which are the predominant
type of brain damage in preterm babies.
- Areas involved include the external angle of the Lateral
Ventricles thus damaging the fibers from the internal
aspect of the hemisphere, which include the motor
fibers to the lower limbs.
- Clinical Features:
o Hypotonia, Lethargy, & Feeding difficulties
during the neonatal period.
o Dystonic Stage follows characterized by
involuntary mass movements & diffuse
increase in tone whenever the childs position
is altered.
o When held vertically, the legs extend &
assume a scissored position as a result of the
hips & knees become predominant.
o In the standing position, the legs are often
internally rotated.
o When independent walking is achieved, it
tends to be on tiptoes with maintained semi-
flexion of the lower limbs.
- In most cases, independent walking is not possible
because of lack of balance, truncal
hypotonia/contractures.
- The upper limbs are variable affected; the elbows tend
to be flexed when walking.
- Deep Tendon Reflexes are hyperactive.
- Strabismus is especially common.
- Intellectual function is relatively preserved in most
cases.
- Performance IQ is more affected than verbal function &
correlates with the extent of white matter lesions.
Quadrispastic Cerebral Palsy
- involves 4 extremities
- patient is unable to walk
- worst prognosis among the types of Spastic Cerebral
Palsy
- increased Risk > 50% of Seizures
- Dependent on Activities of Daily Living (ADL)
- Mental Retardation is common
ATAXIC DIPLEGIA
- Striking Feature: Incoordination, unsteady gait
- Incidence: accounts for 5-7% Cerebral Palsy
- Etiology: Prenatal causes appear to be at play in a
majority of cases (often seen in Cerebral Palsy)
- Syndrome of Infantile Hydrocephalus
- Clinical Features:
o Hypotonia is the initial presentation
o Eventually spasticity develops with increased
tendon reflexes
o Tremor & titubation in the sitting position
becomes apparent at 1 year of age.
o Staccato Speech is common
o Mental Level is normal in 70% of cases
Ataxia Cerebral Palsy
- Striking Feature: Cerebellar Signs & Symptoms
- Incidence: accounts for 7-15% of all CP cases
- Etiology: Pre-Natal factors play a dominant role
- Unknown pathology
- Clinical Features: overall clinical picture varies from
case to case
- Typical Ataxia affecting both lower & upper limbs
- Dysmetria & Intention Tremors are apparent by 2-3
years of age.
- Do not have Pyramidal Tract Signs
- Many are able to walk by 3-4 years of age
- Severe Mental Retardation is rare but many have some
degree of intellectual impairment.
DYSKINETIC/ATHETOID CEREBRAL PALSY
- Striking Feature: Abnormal Movements r/t defective
coordination
- Incidence: about 10% of all Cerebral Palsy cases
- Etiology: Prenatal factors as most common cause
- Pathology: Selective involvement with atrophy &
sclerosis of the central grey nuclei, which is a classic
lesion in Kernicterus
- CT Scan may show calcification of the Basal Ganglia
- Clinical Features:
o Persistence of Primitive Motor Patterns (e.g.
Asymmetric Tonic Neck Reflex with some
degree of Hyperkinesia)
Preterm Babies with
Hyperbilirubinemia in combination
with Hypoxia.
Among term infants of normal birth
weight with severe asphyxia
Also in SGA infants with hypoxia.
o Dystonia characterized by sudden & abnormal
shifts of general muscle tone induced by
emotional stimuli & changes in posture of
Neck Muscles on intended acts or movements
Appears between 5-10 months of age
Predictors of severity of Dystonia
(Severe Hypotonia, Persitence of
Primary Reflexes)
Deep Tendon Reflexes
(normal/increased in the lower limbs)
Speech is almost always impaired due
to involvement of the
Buccopharyngeolaryngeal muscles.
Swallowing difficulties & drooling
maybe present.
Functional Classification
Normal
Minimal Motor Quotient (MQ) = 75-100
Qualitative Abnormaliites
2/3 Normal
Mild MQ = 50-70
Walks by 24 Months
Moderate Normal
MQ = 40-50
Walks by 3 years old; may need Bracing
Usually does not require assistive
devices/surgery
Normal
Severe/Prof MQ = < 40
ound May not walk freely in the community
May need bracing, assistive devices, &
orthopedic surgery
Anatomic Location
(Disclaimer: indi ni amo ang sa slides ni doc pro dw mas bungga
ni ya. )

Diagnosis
- the diagnosis of Cerebral Palsy is generally clinical & is
highly dependent on the knowledge of normal
development & its variant.
- A history of abnormal factors in pregnancy, birth, or
neonatal period favors the diagnosis but is used only as
a support to the diagnosis.
Neuroimaging
- can have a confirmatory value in some cases
- Cranial Ultrasound has proven to be a reliable tool in
detecting extensive periventricular leukomalacia.
o Cystic/Hemorrhagic lesions predict a high
probability of neuromotor sequelae
- CT Scan seems to have a less predictive value in the
neonatal period (they are abnormal in 60-80% of cases
in Cerebral Palsy).
- MRI may prove to be more informative than CT Scan,
especially in infants with motor delay but no definitive
neurological signs.
o Predicts the development of Cerebral Palsy by
showing abnormalities of Myelination, Cortical
Malformations, & White Matter Changes
- EEG is not a predictor of normal/abnormal
development.
Management
- Intervention: Multi-disciplinary Approach
- Goals of therapy:
o To maintain function (Secondary Prevention)
o To maximize/develop function
- Rehabilitation
o Physical Therapy development of posture &
ambulation, including the use of adaptive &
seating devices.
o Occupational Therapy developing
approaches to oral motor function, visual-
perceptual problems, & ADLs.
o Speech Therapy for communication skills
both language & speech
- Neurologist/Pediatrician = for diagnosis, prescribing
Anti-Epileptic Drugs, & Drugs for Anti-Spasticity.
- Neurosurgeon = Dorsal Rhizotomy
- Nutritionist = for nutritional build-up
- Gastroenterologist = for Gastroesophageal Reflux
- Surgeon = for surgical management of
Gastroesophageal Reflux
- Developmentalis = evaluation & management of
delay in developmental milestones.
Prognosis
- Cerebral Palsy being a static condition should have no
loss of any achieved milestone.
- About 50% of Spastic Diplegic patients will walk.
- Most of those with Hemiplegia & Ataxia, oftentimes
achieve ambulation.
- Patients with persistence of Primitive Reflexes &
Protective Reflexes at 1 year of age are unlikely to walk
independently.
- > 90% of all Cerebral Palsy patients live to adulthood.
Memory Tools
A child with a history of Prenatal, Perinatal, & Postnatal
insult should be monitored on a regular basis.
To best remember the different types of Cerebral Palsy,
picture this:
o Hemiplegia/Hemiparesis half of body
affected
o Spastic Diplegia CP both legs affected
o Ataxic Diplegia CP wide based, poor
balance when walking
o Dyskinetic/Athetoid CP abnormal
movements/posture
o Ataxic CP wide based gait, poor balance,
uncoordinated hand movements, tremors
~gwapo si JHERBEN.
https://www.facebook.com/Lecitel.Candido
http://instagram.com/jherbenobishie
http://jherben.deviantart.com
https://twitter.com/JherBISHIE
V http://dissociatedlobster.tumblr.com/
V http://worldcosplay.net/member/jherBISHIE/
V http://en.curecos.com/profile/?ch=306581