CEREBRAL

PALSY
DR ARONU ANN
EBELE
 AIM
 To acquire basic and current
knowledge on Cerebral Palsy
(CP).

 Apply acquired knowledge in

the identification and
management of CP.
OBJECTIVES
Define Cerebral Palsy (CP)
Recognize a child with CP and
identify the risk factors for the
CP
Recognize comorbidities in a
child with CP
Draw a treatment plan with
reasons
OUTLINE
 Defition/introduction
 Risk factors/Causes
 Clinical
features/Classification of
motor function
 Diagnosis
 Investigations
 Management
 Prevention
DEFINITION 1

A disorder of movement and

posture resulting from a non-
progressive injury to the
developing brain.
DEFINITION 2
CP describes a group of disorders of
development of movement and
posture, causing activity limitation
that are attributed to non-
progressive disturbances that
occurred in the developing fetal or
infant brain.

The motor disorder of CP are often

accompanied by disturbances of
sensation, cognition, communication,
perception, and/or behaviour and/or
by seizure disorder” (Bax et al,2005)
INTRODUCTION
 Commonest motor disability in
childhood
 Globally occurs in 1.2-3.6 per 1000 live
births
 In Africa, accounts for 10-90% cases in
Neurology clinics in Low and Middle
Income countries(LMICs)
 CP accounted for 16.2% of new referrals
to child neurology clinic in UNTH.
 Associated with poor health related
Quality of Life
INTRODUCTION
 Increasedrisk of other
morbidities such as Epilepsy,
UTI,and malnutrition.
 Increased risk of mortality.
 Leading risk factor in High
Income countries (HICs) is
prematurity while in LMICs,
severe perinatal Asphyxia and
bilirubin encephalopathy are
dominant.
RISK FACTORS-
General
 Prematurity

 Male sex
 Black race
 Multiple pregnancies (Twins5-8x, Triplets 20-
47x)
-death of a twin in utero carries higher risk
-infertility treatments asso with increased risk
 Extremes of birth weight
 Infants of mothers with low Socio-Econ Status
RISK FACTORS-specific

 PRE-CONCEPTION (maternal health &

living conds.
 PRENATAL-maternal infections(UTI,
chorioamnionitis),IUGR, Toxin
exposure, congenital Torch infections.
- Developmental abnormality: Brain
malformations, genetic
abnormalities, metabolic
abnormality
PERINATAL brain injury:
- Perinatal Asphyxia/HIE, neonatal
stroke, traumatic brain injury,
intracranial haemorrhage.
- Brain injury related to prematurity:
Periventricular
leukomalacia,
Intraventicular haemorrhage

POSTNATAL brain injury:

Kernicterus/bilirubin encephalopathy,
CNS infections.
CLASSIFICATION
Physiologic, topographic, aetiologic, functional
characteristics are used.

[Link]:
- GMFCS (Gross Motor Function
Classification system)
- MACS—(Manual Ability Classification
system)
- CFCS (Communication function
Classification system)
- EDACS (Eating and drinking ability
Classification system)
CLASSIFICATION
Cont’d
2. Edinburgh

Spastic 60-
70%
- Spastic hemiplegia
- Spastic Diplegia
- Bilateral hemiplegia
Dyskinetic 10-20%
Ataxic 10-
15%
Mixed 10%
--
- mixture of diff types, eg spastic & dyskinetic.
CLASSIFICATION
Cont’d
3. SWEDISH
-Spastic(hemiplegia,tetraplegia,diplegia)
-Dyskinetic
-Ataxic
-Unclassified/Mixed
4. MRI Classification system
Pathophysiology

Insults resulting in neuronal loss can

be
Cortical (pyramidal), resulting in
spasticity
Basal ganglial (extrapyramidal),
resulting in abnormal movements such
as choreoathetosis
Cerebellar, resulting in hypotonia, or
Mixed
CLINICAL FEATURES-
General
 Delayedachievement of
developmental (motor)
milestones

 Abnormal/unusual
motor
movts—hand preference,
commando crawl
Pathogenesis/Clinical features
Spastic CP – most common, up to 75%.
Based on topographic distribution of
motor involvement the following
SpasticDiplegia – more of lower limb involvement;
most common; associated with prematurity

Spastic Hemiplegia – more of arm involvement

Spastic Monoplegia – result of very mild

hemiplegia

Spastic Quadriplegia – all four limbs

Bilateral hemiplegia – quadriplegia with more of

arm involvement

Triplegia – rare, results from milder and very

asymmetric double hemiplegia (sparing one leg) or
milder asymmetric diplegia (sparing one arm)
Spastic Hemiplegia – results from
stroke-like events with focal cortical
infarction(haemorrhagic infarction,
infection, thrombophilic disorders)
--↓ spontaneous activity on involved side with
hand preference,
--difficulty in hand manipulation by 1yr,
-- walking is delayed to between 18–24
months, with circumductive gait
--Growth arrest esp in hand and thumb nail
(involvement of contralateral parietal lobe)
--Spasticity of affected extremity, ↑tendon
reflexes, ankle clonus, positive Babinski
response.
--One third have seizure disorder,
--approx 25% have cognitive impairment
Spastic Diplegia – usually results
from periventricular leukomalacia
(PVL; seen in prematurity, ischaemia)
--1st noticed when infant begins to crawl
(uses arms more--commando crawl,
dragging feet along)
--Scissoring posture when suspended at
axillae
--Spasticity in legs with brisk reflexes,
ankle clonus and bilateral Babinski
reponse
--Good prognosis for normal intellect
Dyskinetic (Dystonic/Choreoathetoid) CP
 follows birth asphyxia, kernicterus;
 pathology is in basal ganglia
Less common than spastic CP
•Hypotonia initially with Head lag;
•later tone increases with rigidity and
dystonia;
• involuntary movts
•Speechis typically affected (involvement of
oropharyngeal muscles),
• also sensorineural hearing loss
•UMN signs are absent,
• seizures are uncommon,
•intellect is usually preserved
Spastic Quadriplegia –
•most severe form of CP,
• all four limbs affected;
• associated with severe PVL and cortical
encephalomalacia
•Mental retardation and seizures common
•Swallowing difficulty .
•Decreased spontaneous movements,
• increased tone and spasticity all limbs, brisk
reflexes and positive Babinski response
•Speech and Visual problems
•May have evidence of athetosis
Ataxic/Hypotonic CP
•Occurs rarely
•Results from cerebellar insult
•most children progress to other CP
subtypes.

Mixed CP
•Occurs when the child displays a
combination of features, such as
spasticity and choreoathetosis
Accompanying impairments in CP

Cognitive/intellectual impairment (Mental

retardation) – not in all CP patients.
Spastic diplegia is characterized by normal
cognition while Spastic quadriplegic CP has
greater MR

Factors associated with MR include

- severe motor deficit,
- epilepsy, and
- cortical abnormalities on neuroimaging
Epilepsy – seen in 36% of pts with 70%
manifesting in 1st yr of life (more in
quadriplegic and hemiplegic than diplegic CP).
Usually focal seizures ± secondary
generalization

Poor growth – due to difficulty in feeding from

pseudobulbar palsy/oromotor dysfunction

Bladder and Bowel dysfunctions

Bladder: urinary incontinence with UTIs
Bowel: constipation due to poor feeding, reduced
water intake and immobility
•Visual and Hearing impairment

•Secondary musculo-skeletal
abnormalities:
-Orthopaedic problems e.g. equinovarus
deformity (tip-toe walking), hip dislocation
(from severe spastic diplegia), flexion
contracture of knees and elbows

•Speech abnormalities
•Behavioural problems
Differential diagnosis
 Inheritedmetab disorders (CHO,
[Link],Lysos)
 Intellectual disability
 Metab myopathies
 Metab neuropathy
 Traumatic peripheral nerve lesions
 Vascularmalformations
(aneurysms,angioma)
MANAGEMENT OF CP

History is important
Detailed physical/neurological exam
nvestigation : EEG;FBC + Bld film; Urinalysis
& urine m/c/s; CXR, CT Scan; MRI;
Hearing & Visual Assessments
DIAGNOSIS

Diagnosis- difficult clinically in

the first year:
 Limited variety of volitional movt for evaluation
Substantial myelination takes months to evolve delaying
the clinical picture of hypertonia/hyper reflexia
TREATMENT
• Not Curable
Treatment is symptomatic and entails
multidisciplinary approach:
• Primary care physician
• Behavioural therapist
• Special education teachers
• Physical therapist
• Psychiatrist or psychologist
• Speech therapist
• Occupational therapist
• Neurologist
• Others.
 Variousforms of therapy help
affected persons function and live
more effectively
 Theearlier therapy begins the
better
 Nutritionalsupport: About 30%
are undernourished. Many show
growth delays. Early NG feeding &
later Gastrostomy tube feeding
may lead to improved growth
 Give antiepileptic drugs for seizures
e.g carbamazepine
 If there is generalized spasticity,
give baclofen, diazepam or
dantrolene and if localized give
injection botulinium toxin (Botox)
for 3 – 6 mths
 Physical therapy[Physiotherapy]
-- Aimed at encouraging the patient
to build a strength base for
improved gait & volitional movt
-- Stretching program to limit
contractures
Occupational therapy:
Helps maximize their function, and adapt to their
limitation
To live as independently as possible

Speech therapy:
Usually starts before the child begins school
Helps to control the muscles of the mouth & jaw
Helps to improve communication
Orthotic intervention using ankle-foot
orthoses aimed at prevention and/or
correction of deformities

- Provision of support & facilitation of skill

development
- Improvement of gait

 Surgery usually the last resort

- lengthening of tendons
- Rhizotomy[cutting of nerve roots]
PREVENTION
Most of the causes of CP [62%] are preventable and
the 5 levels of prevention are involved.
•Mothers should be taught to ensure optimal wellbeing
prior to conception
•Good obstetric care should be encouraged
•Anti-D immunoglobulin for Rh-ve mothers
•Vaccination against some IU infections
•Proactive treatment to minimize the effects of perinatal
brain injury.
• High risk pregnant women should be
identified early and referred for
appropriate management
• Screening children at birth for G6PD
deficiency
• Good NICU[Neonatal Intensive Care Unit]
for those children who have developed
birth asphyxia, severe jaundice and LBW
• Maintaining a good referral pediatric
service
• Physiotherapy
• Rehabilitation of pts
PROGNOSIS
•Actual
brain damage does not worsen but
symptoms can become worse overtime.
•The collaborative perinatal project found that 50%
of individuals diagnosed with CP and 66% of children
diagnosed with spastic diplegia “outgrew” findings
by 7yr of age
•The ability to sit independently at 2yrs of age is
predictive of future ambulation
•Regarding life expectancy and mortality rates, the
type and severity of disability and feeding skills are
major determinants
•Overall,the probability of reaching the age
of 20yrs in a child with severe CP is 50%
•Respiratory infections, aspirations and
epilepsy are the leading causes of death
•Newer therapeutic advances and the degree
of parental care have a strong influence on
the length of survival of these children
QUESTION
A 20 month-old male presents with inability
to sit, stand or walk compared to elder
sibling who achieved all before age 12
months. He has repeated convulsions and is
unable to speak. He was born at term
following a prolonged labour and did not cry
at birth.
1. What clinical findings are possible in this
child?
2. What is the treatment plan for this child?
THANK YOU