Dr D Kalpana, M.D,D.

M(Neuro)
Assoc. Professor of Pediatric Neurology,
Medical College, Trivandrum

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 Cerebral palsy (CP)

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 CP

• Definition : A non progressive disorder of

movement and posture due to an insult to
the developing brain.
• may include perceptual problems,
language deficits, seizures and intellectual
involvement.

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 Incidence

• Most common physical disability of

childhood.
• Incidence has increased since the 60’s,
maybe due to improved survival of
VLBW infants.

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 Etiology
• Variety of perinatal, prenatal, and postnatal
factors contribute, either singly or multifactorily
to CP.
• Commonly thought to be due to birth asphyxia;
now known to be due to existing prenatal brain
abnormalities.
• Premature delivery is the single most important
determinant of CP.
• In 24% of cases, no cause is found.

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 TABLE 40-1 Causes of CP
• Time (% of cases) • Causes
• Teratogens,
• Prenatal (44%) chromosomal
– First trimester abnormalities, genetic
syndromes, brain
malformations
• Intrauterine infections,
problems in
fetal/placental functioning

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 Causes of CP
• Time (% of cases) • Causes
– Second trimester • Preeclampsia,
• APH

• Labor and delivery (19%)

• complications of labor
• Perinatal (8%) and delivery
• Sepsis/CNS infection,
• Childhood (5%) asphyxia, prematurity
• Meningitis, traumatic
• Not obvious (24%) brain injury, toxins

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 Clinical Classification of CP
• Spastic-hypertonicity with poor posture control
• Dyskinetic/athetoid- abnormal involuntary
movement/slow wormlike writhing
• Ataxic- wide-based gait
• Mixed-type/dystonic- combination of spasticity
and athetosis

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 Clinical manifestations

• Delayed gross motor development

– A universal manifestation of CP
– The discrepancy between motor ability and
expected achievement tends to increase as
growth advances.

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 Clinical Manifestations
• Abnormal motor performance
– Preferential unilateral hand use may be apparent at 6
months.
– Hemiplegia, abnormal crawling or asymmetrical crawl;
spasticity may cause child to walk and stand on toes
– dyskinetic CP or uncoordinated or involuntary
movements (writhing tongue, fingers, and toes; facial
grimacing), poor sucking and feeding, persistent
tongue thrust; head staggering, tremor on reaching,
truncal ataxia.

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 Alterations in muscle tone
• Increased or decreased resistance to passive
movement (abnormal muscle tone).
• Opisthotonic postures or exaggerated back
arching, feel stiff on dressing.
• Difficulty diapering due to spastic hip adductor
muscles and lower extremities
• When pulled to a sitting position, child may
extend the entire body and be rigid at hip and
knee. This is an early sign of spasticity.

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 Abnormal postures
• Children with spastic CP have abnormal posture at rest
or when position is changed
• Infantile lying prone may have hip higher than trunk with
legs and arms drawn in.
• Persistent infantile resting and sleeping position is a sign
of spasticity.
• Hemiparetic child may rest with affected arm adducted
and held against torso, with the elbow pronated and
slightly flexed and the hand closed.

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 Reflex Abnormalities

• Persistence of primitive infantile reflexes

(one of the earliest signs of CP)
– Tonic neck reflex
– Hyperactivity or moro, plantar, palmar grasp
Hyperreflexia, ankle clonus, stretch
reflexes can be elicited from any muscle
group.

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 Associated disabilities and
problems
• Intellectual impairment
– 70% w/in normal limits; wide range
– Tests should be carried out over a period of time.
– Children with athetosis and ataxia more intelligent.
Speech difficulties (not a sign or MR)- child has motor
and sensory defects
ADHD- (may occur)-poor attention span, marked
distractibility, hyperactive behavior

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ASSOCIATED DISABILITIES
Seizures- generalized tonic-clonic;more in postnatally
acquired hemiplegia
Drooling- may occur and lead to wet clothing/skin
irritation
Feeding- alterations in muscle tone lead to difficulties
chewing, swallowing, talking, etc.
Address nutritional concerns.
Coughing, choking may lead to aspiration.
Altered respiratory patterns may lead to inadequate gas
exchange.

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 Motor Impairment
• Orthopedic complications
– Unilateral or bilateral hip dislocations, scoliosis, joint
contractures due to unbalanced muscle tone.
Decreased Mobility
– difficulties with toileting may lead to constipation
– Difficult chewing bulky foods may lead to constipation
– May need stool softeners or laxatives

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 Associated Problems
• Dental caries
– Improper dental hygiene
– congenital enamel defects (hypoplasia of primary
teeth)
– high carbohydrate intake and retention
– Dietary balance with poor nutritional intake
– Inadequate fluoride
– Difficulty in mouth closure and drooling
– Spastic or clonic movements cause gagging or biting
on toothbrush

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 Associated Problems

• Malocclusion in 90% of children

• Oral hypersensitivity causes resistance to
good hygiene
• Gingivitis is secondary to poor hygiene
• Dental health further complicated by anti-
seizure meds

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 VISION AND HEARING

• Nystagmus and amblyopia common

– May need surgery or corrective lenses
– May be due to sensoneural involvement
– Infants lying flat too long may have otitis
media which may leads to conductive hearing
loss

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 Diagnostic Studies

• Physical Assessment
• High risk babies
– LBW, preterm,
– low Apgar scores at 5 minutes.
– seizures,
– intracranial hemorrhage,
– metabolic disturbances

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 WARNING SIGNS
• Physical Signs
• poor head control after 4 months
• stiff or rigid arms/legs, arching back, floppy or
limp posture
• Cannot sit up without support by 8 months
• Uses only one side of the body or only the arms
to crawl

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 Warning Signs

• Behavioral Signs
• Extreme irritability or crying
• Failure to smile by 3 months
• Feeding difficulties
– Persistent gagging or choking when fed
– After 6 months of age, tongue pushes soft
food out of the mouth.

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 DEVELOPMENTAL
OBSERVATION CARD
• Developed by child development centre.
Trivandrum.
• Social smile - 2 months
• Head holding - 4 months
• Sitting - 8 months
• Standing - 12 months

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 Therapeutic management
• PHYSICAL THERAPY
– Most commonly used treatments.
– Goal is good skeletal alignment for the spastic child.
– For the child with athetosis, training in purposeful acts,
even in the face of involuntary motion
– Maximum development of proprioceptive sense for the
child with ataxia.
– Orthotic devices (braces, splints, casting).

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 OCCUPATIONAL THERAPY
• Training in ADL’s along developmental lines.
• Sitting to walking; feeding to cooking.
• Important to incorporate play into program
• Adaptive equipment (utensils for functional use,
i.e., eating, writing), computers, etc.

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 Speech/Language therapy

• Early speech training by speech/language

pathologist !
– Before child develops poor habits
– Advice parents to follow directions of therapist
– May need to force child to use tongue/lips in
eating

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 Special Education

• Determined by child’s needs

• Early intervention programs
• Individualized Education Program (IEP)
• Specialized learning programs and
support services in schools
• Socialization to promote self-concept
development

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 Surgical Intervention

• Reserved for child who does not respond

to conservative therapy!
– Or whose spasticity causes progressive
deformities
Orthopedic surgery
– correct contractures or spastic deformities
– provide stability for uncontrolled joint
– provide balanced muscle power

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 Surgical Therapy
• Tendon-lengthening procedures (heel-cord)
• Release of spastic wrist flexor muscles
• Correction of hip-adductor muscle spasticity or
contracture to improve locomotion
• Surgery is for improved function rather than
cosmetic reasons and is followed by PT.

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 ACUTE FLACCID PARALYSIS
ACUTE FLACCID PARALYSIS

• DEFINITION
– Acute onset of flaccid weakness in a
child less than 15 years or at any age
where polio is suspected
– ACUTE ONSET – LESS THAN 4 WEEKS
– FLACCID – LIMP OR FLOPPY
(HYPOTONIC)

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 transverse myelitis

traumatic neuritis other enteroviruses

Acute Flaccid Paralysis

Coxsackie virus Echovirus

Guillain-Barre Syndrome Poliovirus

 Differential diagnosis

• UMN – Transverse myelitis

• Anterior horn cell – Polio, enteroviruses
• Nerve roots – Guillain Barre syndrome
• Peripheral nerve – traumatic neuritis
• Neuromuscular – myasthenia gravis
• Muscle – Inflammatory myopathies

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 Paralytic poliomyelitis

• Affects anterior horn cells

• Prodrome of fever, diarrhoea, meningeal
signs, myalgia
• Asymmetric weakness of limbs
• Muscle tenderness characteristic
• Hypotonia and areflexia
• Residual paralysis

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 Guillain-barre Syndrome

• Clinical features
• Usually follows URI, diarrhoea,
• Progressive weakness(max – 2 wks) and
diminished deep tendon reflexes in a
symmetric distribution.
• Ascending progression – most common
• Proximal > distal
• Lowerlimb > upperlimb
• Hypotonia, areflexia
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 GBS

• Sensory disturbances: 40% pain or

paresthesias
• Cranial nerves
• Autonomic disturbances – infrequent but life
threatening.
• 15-20% progress to respiratory failure
• L.P, EMG, N.C.V

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 TRANSVERSE MYELITIS
• Demyelination Of Spinal Cord
• No prodromal symptoms
• Symmetrical weakness of lower limbs
• Urinary retention
• Definite sensory level
• Hypotonia, hyperreflexia hyperreflexia
• Extensor plantar response
• MRI

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• All cases of AFP should be reported and
investigated as poliomyelitis as part of the
National AFP surveillance programme.
• This is to ensure that no case of polio is
missed,
• The Background non polio AFP rate is 1
per 100000

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 VIRUS ISOLATION
• The most important aspect of this classification is
the collection of 2 adequate stool samples from all
cases. Samples are considered adequate

• if both the specimens are collected within 14 days

of paralysis onset and at least 24 Hrs apart
• are of adequate volume (8-10g)
• arrives at a WHO-accredited laboratory in good
condition (ie, no desiccation, no leakage), with
adequate documentation and evidence of cold-
chain maintenance.

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 Strategies for Polio
Eradication
• Strong routine immunization program

• National Immunization Days (NIDs)

• Acute flaccid paralysis surveillance

• "Mopping-up" immunization
Then…….

Polio-free certification

Laboratory containment of
polioviruses

Stopping polio immunization Page 47
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 GROWING PAINS
• DEFINITION

• An idiopathic symptom complex that affects 10%

to 20% of school-age children
• Pain usually occurs in shins or thigh muscles
• Joint pain is rare
• The pain is intermittent, usually occurring at
night, and lasts from 30 minutes to several hours

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 GROWING PAINS

• HISTORY

- Usually non-articular
- Calf or thighs usually involved
- Deep aching, usually worse at night
- May waken the child at night
- May be relieved with massage, rubbing

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 GROWING PAINS
• PHYSICAL FINDINGS
- No physical signs

• DIFFERENTIAL DIAGNOSIS
- Acute infection or inflammation
- Trauma

• COMPLICATIONS
- None

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 GROWING PAINS

• MANAGEMENT

- ? X-ray for reassurance if necessary

- Reassure child and family of benign nature
- Explain course of the condition and prognosis
- Counsel parents or caregiver about appropriate
home management with rest, heat and analgesia

- Heating pad or moist hot packs prn may help

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 GROWING PAINS

• MANAGEMENT

- Analgesic for pain (for children >6 years old):

- acetaminophen (Tylenol), 325 mg, 1–2 tabs
PO q6h prn
- Reassess the child if attacks become more
frequent or increase in severity
- Referral to a physician if the diagnosis is unclear
or the symptoms are worsening
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