Cerebral palsy

Dr Sujit Koirala
Lecturer, Pediatrics
MD Pediatrics
Some people with CP are brilliant
 History
• An English surgeon, Willian John Little, in 1860
coined “ Cerebral paralysis” or Little’s disease
• Disorder of
– Movement
– Posture
– Tone
– Balance
 Definition

• Non progressive injury to the immature brain - Leading to motor

dysfunction - Lesion is not progressive, but - the clinical manifestations
change over time

• The most common cause of disability in children affecting function and

development

• includes heterogenous clinical states of variable etiology and severity

ranging from minor deformity to total handicap.

• Most of the cases have multiple neurological deficits and variable mental
handicap.
 Definition

• Definition: is a permanent disorder of

movement, tone and posture causing
activity limitation attributed to developing
fetal brain accompanied by disturbances
in perception, cognition and
communication.
 Etiopathogenesis

Prenatal
• Congenital infections
• Anatomical malformation
• Metabolic factors
• Genetic factors
• Antenatal bleeding
• Maternal malnutrition
• Radiations
• Drugs
 Etiopathogenesis
Natal
•  Birth Injury
• Infections, Chorioamnionitis

Post Natal
• Head injury
• Metabolic
• Drugs & Toxins
• Birth Asphyxia
• Indirect hyperbilirubinemia
• Most infants have multiple risk factors.

• The mechanism remains unclear and primary

neurological aberrations may be unfolded in future.

• pathological lesions such as cerebral atrophy,

porencephaly ( the forebrain of embryo fails to
develop into two hemisphere), basal ganglia,
thalamic and cerebellar lesions may be observed.
 Types of CP
•  SPASTIC
• DYSKINETIC
• HYPOTONIC
• MIXED
 Spastic cerebral palsy
Commonest form

Early diagnostic feature include

-Abnormally persistent neonatal reflex- persistent Moro’s, startle, grasp
reflex
-Feeding difficulties- swallowing/coordination
-Persistent cortical thumb after 3 months of age
-Firm grasp
-Scissoring posture on vertical suspension
Fisting of the hands with the thumb adducted across the palm.
Tiptoe-walking Truncal hypertonia with head lag.
Feeding difficulties and drooling.
 Spastic cerebral palsy

Spastic diglegia:35%, pvl leukomalacia, pv cyst or scar in white

matter

Spastic hemiplegia: 25%, subcortical and cortical malformation,

focal infract

Spastic quadriplegia: 20%, pvl, multi cystic encephalomalacia,

cortical malformation

Extrapyramidal 15%, symmetry scar in putamen and thalamus

 Spastic CP: Topographically classified

1. Spastic Quadriparesis
Term babies, arching of back, feeding problems, motor deficits.
All limbs are affected. The most catastrophically disabled of the CPs.
Associated with severe intellectual disability, epilepsy, bulbar
palsy, microcephaly, growth failure, etc.

2. Spastic Diplegia
Preterm, associated with PVL
The legs are affected more than the arms. The arms may be
minimally affected where only fine motor movements may be
abnormal.
Commando crawl
3. Spastic hemiparesis:

– Recognized: 4-6mths age, early hand preference,

abnormal persistent fisting, posture.
– Affects one side of the body
– Majority should have the ability to walk
– There is strong association with prematurity, birth
asphyxia, hydrocephalus.
– Vascular insults, cerebral anomalies may be associated
Spastic CP
 Extrapyramidal CP
• 30% cases
• Athetosis, Chorea, Dystonia, tremors and
rigidity
• Arms, legs, neck and trunk may be involved.
• Intellectual defects, hearing defects +/-
• Bilirubin encephalopathy- Kernicterus is one of
the cause
 Dyskientc CP
• alternating dystonia seen over the distal
limbs, particularly the fingers and hands,
alternating slowly between extension and
flexion in a slow wreathing and sinuous
movement.
 Hypotonic/ Atonic CP
Tendon reflexes are Normal to brisk: except in cerebellar
involvement

Babinski +ve

Often severe Intellectual defect

During the first few months of life, only hypotonia may be present
but ataxia may appear when the child begins to move more.
 Mixed
Diffuse neurological involvement of mixed type
 Evaluation
• Eyes - nearly half of the patients have strabismus,
paralysis of gaze, cataracts, coloboma, retrolental
fibroplasia, perceptual and refractive errors.

• Ears - partial or complete loss of hearing is usual in

kernicterus. Brain damage due to rubella may be
followed by receptive auditory aphasia.
• Speech Aphasia, dysarthria and dyslalia ( inability to
articulate comprehensive speech) are common among
dyskinetic individuals.

• Sensory defects Astereognosis and spatial

disorientation are seen in one- third of the patients.

• Seizures Spastic patients usually have generalized or

focal tonic seizures. These patients respond poorly to
antiepileptic agents.
• Intelligence- 1/4th of the children may have
borderline intelligence (IQ 80-100); and about 1/2 of
them are severely mentally retarded.

• Miscellaneous-
– inadequate thermoregulation
– social and emotional adjustments
– dental defects
– infections.
 Diagnosis
• Diagnosing cerebral palsy takes time, and is usually not
made until the brain is fully developed when the child is
two to five years old. Exceptions exist, usually in severe
cases, when the child may be diagnosed soon after birth.

• For example the average age of diagnosis for a child with

spastic diplegia, a very common form of cerebral palsy, is
18 months.

• There is no definitive test that confirms or rules out cerebral

palsy
• Should be suspected in a child with low birth weight and
perinatal insult

• increased tone, feeding difficulties and global developmental

delay, esp motor milestones

• Disturbance of tone (Hypo/Hypertonia) Clumsiness Seizures

Irritability or decreased alertness, Persistent primitive
reflexes, asymmetries of posture

• Abnormal Gait (tip toe walking), early hand preference

• Evaluation includes perinatal history, detailed
neurological and developmental examination
and assessment of language and learning
disabilities.

• CT and MRI help delineate the extent of

cerebral damage in a case of cerebral palsy.
 Differential Diagnosis
• Neurodegerative disorders
• Hydrocephalus and subdural effusion
• Brain tumors or space occupying lesions
• Muscle disorders- Congenital myopathy and
muscular dystrophies
• Ataxia- telangiectasia
 Prevention
• Prevention of maternal infections, fetal or
perinatal insults, good maternal and neonatal
care reduces prevalence.
• Early diagnosis, prompt adequate
management plans can reduce the residual
neurological and psychosocial emotional
handicaps for the child and his family.
 Management
• The management plan should be holistic, involve the
family and be directed to severity, type of
neurological deficits and associated problems.
•  CP patients should involve a team of professionals
in the form of: Physiotherapists, Ophthalmologists
Occupational and Speech therapists Dietitians and
social workers
• Stress on improving posture, reducing tone,
preventing contractures and early stimulation is
necessary.
• Symptomatic treatment is prescribed for
seizures.
• Tranquilizers are administered for behaviour
disturbances and muscle relaxants may be
used for improving muscle functions.
• Baclofen and Tizanidine help to reduce
spasticity.
• Diazepam may ameliorate spasticity and athetosis.
• Dantrolene sodium helps in relaxation of skeletal
muscles.
• Dynamic contractures can be managed with
botulinum toxin injection or alternatively nerve
block with phenol.
• Plastic orthosis, surgical procedures for spasticity
and contractures may be required in selected
patients.
• Occupational therapy: Self help in feeding and
dressing more complex task
• Educational therapy: Special education
• Orthopedic support: Surgeries, splint for
contractures
• Social support
• Rehabilitation and vocational guidance.
THANK YOU