Cerebral palsy is defined as a group of permanent disorders of movement and posture caused by non-progressive disturbances in the developing brain before birth or in early childhood. It results in motor impairment and can be accompanied by sensory, cognitive, communication, perception, and/or behavioral and epilepsy problems. The document discusses the classification, epidemiology, risk factors, pathophysiology, etiology, clinical features, and subtypes of cerebral palsy.

1. Cerebral Palsy inCerebral Palsy in
ChildhoodChildhood
Dr /Reyad AlfakyDr /Reyad Alfaky

3. DefinitionDefinition
 It is defined as a group of disorders resulting from permanent nonIt is defined as a group of disorders resulting from permanent non
progressive cerebral dysfunction developing before maturation ofprogressive cerebral dysfunction developing before maturation of
CNS affecting the locomotor systemCNS affecting the locomotor system characterized by motor and
postural dysfunction
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4. DefinitionDefinition
 Although brain lesions that result in CP are not progressive,Although brain lesions that result in CP are not progressive,
clinical picture of CP may change with timeclinical picture of CP may change with time
 In addition to primary impairments in gross & fine motor function,In addition to primary impairments in gross & fine motor function,
there may be associated problems with cognition, seizures, vision,there may be associated problems with cognition, seizures, vision,
swallowing, speech, bowel-bladder, & orthopedic deformitiesswallowing, speech, bowel-bladder, & orthopedic deformities
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5. DefinitionDefinition
Criteria of diagnosisCriteria of diagnosis
1.1. Neuromotor control deficit that alters movement or postureNeuromotor control deficit that alters movement or posture
2.2. Static brain lesionStatic brain lesion
3.3. Acquisition of brain injury either before birth or in first 3 years of lifeAcquisition of brain injury either before birth or in first 3 years of life
(immature brain )(immature brain )
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6. Definition of Cerebral PalsyDefinition of Cerebral Palsy
•a heterogeneous group of permanent disorders of movement and posture causing motor anda heterogeneous group of permanent disorders of movement and posture causing motor and
postural dysfunction , that are attributed to nonprogressive disturbances in the in thepostural dysfunction , that are attributed to nonprogressive disturbances in the in the
developing fetal or infant braindeveloping fetal or infant brain
1.1.Group of motor disorders :-Group of motor disorders :- abnormalabnormal
1.1. ToneTone
2.2. PosturePosture
3.3. control of movementcontrol of movement
2.2. Onset before during or after birthOnset before during or after birth
 (usually before 3 years of age) (immature brain )(usually before 3 years of age) (immature brain )
3.3.Secondary to a brain injury or anomaly thatSecondary to a brain injury or anomaly that
1.1. Non-progressive andNon-progressive and
2.2. permanentpermanent
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7. EpidemiologyEpidemiology
IncidenceIncidence
• Overall, 1.5–2.5 per 1,000 live birthsOverall, 1.5–2.5 per 1,000 live births
• Incidence increases as gestational age (GA) at birth decreasesIncidence increases as gestational age (GA) at birth decreases
PrevalencePrevalence
• 3–4/1,000 of the population3–4/1,000 of the population
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8. EpidemiologyEpidemiology
•• 80% -no evidence of significant asphyxia.80% -no evidence of significant asphyxia.
•• HIE present in 16% of cases of CP.HIE present in 16% of cases of CP.
•• When prenatal factors are taken into account HIE is felt to be primary causeWhen prenatal factors are taken into account HIE is felt to be primary cause
in only 3%.in only 3%.
•• In developed countries the prevalence is 1.2 to 2.5 for every 1000 children (1In developed countries the prevalence is 1.2 to 2.5 for every 1000 children (1
in 400 children)in 400 children)
•• Prevalence is stable despite improvements in obstetrical carePrevalence is stable despite improvements in obstetrical care
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9. PathophysiologyPathophysiology
• CP results from static injury or lesions in the developing brainCP results from static injury or lesions in the developing brain
• Majority of risk factors for CP are present prior to birthMajority of risk factors for CP are present prior to birth
• may occurmay occur
1.1. PrenatallyPrenatally
2.2. PerinatallyPerinatally
3.3. postnatally.postnatally.
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10. Etiology of CP (Prenatal)Etiology of CP (Prenatal)
•• Congenital malformationsCongenital malformations
•• Congenital Infections (TORCH)Congenital Infections (TORCH)
•• Exposure to chemicals/toxins (alcohol, cocaine, crack)Exposure to chemicals/toxins (alcohol, cocaine, crack)
•• PrematurityPrematurity
•In approximately 50% of cases, the etiology is not established, and isIn approximately 50% of cases, the etiology is not established, and is
most likely multifactorialmost likely multifactorial
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11. Etiology: Prenatal (cont.)Etiology: Prenatal (cont.)
•• Low Birth WeightLow Birth Weight
•• Placental Abnormalities (small, inflammation, chorionitis)Placental Abnormalities (small, inflammation, chorionitis)
•• Multiple Births (twins 2% of population, account for 10% ofMultiple Births (twins 2% of population, account for 10% of
incidence of CP)incidence of CP)
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12. Etiology (cont.)Etiology (cont.) PerinatalPerinatal
PerinatalPerinatal
•• Placental previaPlacental previa
•• Birth AsphyxiaBirth Asphyxia
Postnatal (accounts for 10 to 15%)Postnatal (accounts for 10 to 15%)
•• Asphyxia (choking, near-drowning)Asphyxia (choking, near-drowning)
•• Head injuryHead injury
•• Meningitis and encephalitisMeningitis and encephalitis
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13. Risk FactorsRisk Factors
 Prenatal:Prenatal:
1.1. Congenital anomaliesCongenital anomalies
2.2. Multiple gestationMultiple gestation
3.3. In utero strokeIn utero stroke
4.4. Intratuterine infection (chorioamnionitis, TORCH: T –Intratuterine infection (chorioamnionitis, TORCH: T –
Toxoplasmosis/Toxoplasma gondii; O – Other infectionsToxoplasmosis/Toxoplasma gondii; O – Other infections
(see below); R – Rubella; C – Cytomegalovirus; H –(see below); R – Rubella; C – Cytomegalovirus; H –
Herpes simplex virus)Herpes simplex virus)
5.5. Antepartum bleedingAntepartum bleeding
6.6. Maternal factors (cognitive impairment, seizureMaternal factors (cognitive impairment, seizure
disorders, hyperthyroidism)disorders, hyperthyroidism)
7.7. Abnormal fetal position (e.g., breech)Abnormal fetal position (e.g., breech)
 Perinatal:Perinatal:
1.1. Preterm birthPreterm birth
2.2. Low birth weightLow birth weight
3.3. Periventricular leukomalaciaPeriventricular leukomalacia
4.4. Perinatal hypoxia/asphyxiaPerinatal hypoxia/asphyxia
5.5. StrokeStroke
6.6. IntracranialIntracranial
hemorrhage/intraventricularhemorrhage/intraventricular
hemorrhagehemorrhage
7.7. Neonatal seizureNeonatal seizure
8.8. HyperbilirubinemiaHyperbilirubinemia
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14. Classification of Cerebral PalsyClassification of Cerebral Palsy
A) Classification by number of limbs involved:A) Classification by number of limbs involved:
1) Quadriplegia- all 4 limbs1) Quadriplegia- all 4 limbs
2) Diplegia- all 4 limbs, legs more severely affected than arms2) Diplegia- all 4 limbs, legs more severely affected than arms
3) Hemiplegia- one side of the body; arm is usually more involved than the leg3) Hemiplegia- one side of the body; arm is usually more involved than the leg
4) Triplegia- three limbs are involved, usually both arms and a leg4) Triplegia- three limbs are involved, usually both arms and a leg
5) Monoplegia- only one limb is affected, usually an arm5) Monoplegia- only one limb is affected, usually an arm
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15. Types of CP (cont.)Types of CP (cont.)
B) Classification by movement disorder:B) Classification by movement disorder:
1) Spastic CP- too much muscle tone or tightness. Movements are stiff, especially in the legs, arms, and/or1) Spastic CP- too much muscle tone or tightness. Movements are stiff, especially in the legs, arms, and/or
back.back.
2) Athetoid CP (dyskinetic CP)- affect movements of the entire body. Involves slow, uncontrolled body2) Athetoid CP (dyskinetic CP)- affect movements of the entire body. Involves slow, uncontrolled body
movements and low muscle tone; hard for person to sit straight and walk.movements and low muscle tone; hard for person to sit straight and walk.
3) Ataxic CP- least common. Disturbed sense of balance and depth perception. Poor muscle tone, a staggering3) Ataxic CP- least common. Disturbed sense of balance and depth perception. Poor muscle tone, a staggering
walk and unsteady hands. Results from damage of the cerebellum.walk and unsteady hands. Results from damage of the cerebellum.
4) AtonicCP ; Affected infants usually are born at term with severe hypotonia. Many have cerebral dysgenesis,4) AtonicCP ; Affected infants usually are born at term with severe hypotonia. Many have cerebral dysgenesis,
microcephaly, and profound intellectual disability. Development is extremely delayed, and affected childrenmicrocephaly, and profound intellectual disability. Development is extremely delayed, and affected children
never stand or walk.never stand or walk.
5) Combined classifications- both movement and number of limbs involved are combined.5) Combined classifications- both movement and number of limbs involved are combined.
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16. Subtypes of CPSubtypes of CP
1.1. Spastic :-75%Spastic :-75%
2.2. Extrapyramidal :- 30%Extrapyramidal :- 30%
3.3. Atonic CP:- < 10%Atonic CP:- < 10%
4.4. Ataxic CP :-< 10%Ataxic CP :-< 10%
5.5. Mixed :-10%Mixed :-10%
6.6. Other CP (10%):Other CP (10%):
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17. Subtypes of CPSubtypes of CP
Spastic
Diplegia
Good hand funtion
Poor hand function
Asymmetric
Hemiplegia
Arm involved more than leg
Leg involved as much as or more than arm
Quadriplegia
Dyskinetic
Mainly dystonic
Mainly athetoid
Ataxia
Simple ataxia
Ataxic diplegia
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18. MOTOR
SYNDROME
NEUROPATHOLOGY/MRI MAJOR CAUSES
Spastic diplegia
(35%)
Periventricular leukomalacia
Periventricular cysts or scars in
White matter, enlargement of ventricles,
squared of posterior ventricles
Prematurity .Ischemia ,Infection
Endocrine/metabolic (e.g., thyroid)
Spastic quadriplegia
(20%)
Periventricular leukomalacia
Multicystic encephalomalacia
Cortical malformations
Ischemia, infection
Endocrine/metabolic,
genetic/developmental
Hemiplegia (25%) Stroke: in utero or neonatal
Focal infarct or cortical, subcortical damage
Cortical malformations
Thrombophilic disorders
Infection
Genetic/developmental
Periventricular hemorrhagic infarction
Extrapyramidal
(athetoid, dyskinetic)
(15%)
Asphyxia: symmetric scars in putamen and
thalamus
Kernicterus: scars in globus pallidus,
hippocampus
Mitochondrial: scaring globus pallidus,
caudate, putamen, brainstem
No lesions: ? dopa-responsive dystonia
Asphyxia
Kernicterus
Mitochondrial
Genetic/metabolic
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19. Subtypes of CPSubtypes of CP
 Spastic CP (pyramidal CP) (40%):Spastic CP (pyramidal CP) (40%): increased deepincreased deep
tendon reflexes, sustained clonus, hypertonia, andtendon reflexes, sustained clonus, hypertonia, and
the clasp-knife responsethe clasp-knife response
 Spastic diplegiaâ€Spastic diplegia—lower extremity involvement”lower extremity involvement
 Spastic hemiplegia—Spastic hemiplegia—one side of the body involvedone side of the body involved
 Spastic quadriplegia—total-body involvement.Spastic quadriplegia—total-body involvement.
 Dyskinetic CP (30%):Dyskinetic CP (30%): fluctuating tone, rigidityfluctuating tone, rigidity
total-body involvement by definition.total-body involvement by definition.
 Athetoid CPAthetoid CP: slow writhing movements (or chorea:: slow writhing movements (or chorea:
rapid, random, jerky movements),rapid, random, jerky movements),
 Dystonic CP:Dystonic CP: posturing of the head, trunk, andposturing of the head, trunk, and
extremities. Ataxic CP (< 10%): characterized byextremities. Ataxic CP (< 10%): characterized by
cerebellar signs (ataxia, dysmetria, past-pointing,cerebellar signs (ataxia, dysmetria, past-pointing,
tremor, nystagmus) and abnormalities of voluntarytremor, nystagmus) and abnormalities of voluntary
movementmovement
 Mixed CP (10%):Mixed CP (10%): two or more types codominant,two or more types codominant,
most often spastic and dyskineticmost often spastic and dyskinetic
 Other CP (10%):Other CP (10%): criteria for CP met but specific subtypecriteria for CP met but specific subtype
cannot be definedcannot be defined
 Extrapyramidal CP: sometimes applied to nonspasticExtrapyramidal CP: sometimes applied to nonspastic
types of CP as a grouptypes of CP as a group
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20.  increased deep tendon reflexesincreased deep tendon reflexes
 sustained clonussustained clonus
 HypertoniaHypertonia
 clasp-knife responseclasp-knife response
 Persistent primitive reflex patternsPersistent primitive reflex patterns
• (e.g., asymmetric tonic neck reflex [ATNR], labyrinthine)(e.g., asymmetric tonic neck reflex [ATNR], labyrinthine)
Cerebral Hypertonia: SpasticityCerebral Hypertonia: Spasticity
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21. Spastic CPSpastic CP
1.1. HemiplegiaHemiplegia
2.2. QuadriplegiaQuadriplegia
3.3. DiplegiaDiplegia
4.4. TriplegiaTriplegia
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22. Forms of Spastic Cerebral Palsy
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23. Spastic CPSpastic CP
 C/F :C/F :
1.1. clasp-knife hypertoniaclasp-knife hypertonia
2.2. hyper-reflexiahyper-reflexia
3.3. sustained clonussustained clonus
4.4. abnormal postural reflexesabnormal postural reflexes
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24. Spastic CPSpastic CP
 is an upper motor neuron syndromeis an upper motor neuron syndrome
 which includeswhich includes
1.1. spastic hypertoniaspastic hypertonia
2.2. HyperreflexiaHyperreflexia
3.3. extensor plantar responsesextensor plantar responses
4.4. ClonusClonus
 Affected patients also haveAffected patients also have
1.1. slow effortful voluntary movementsslow effortful voluntary movements
2.2. impaired fine-motor functionimpaired fine-motor function
3.3. difficulty in isolating individual movementsdifficulty in isolating individual movements
4.4. fatigabilityfatigability
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25. Hemiplegia: pathologyHemiplegia: pathology
 typically affects term infants of normal birth weighttypically affects term infants of normal birth weight
 It is usually caused by a cortical lesionIt is usually caused by a cortical lesion
 Some cases are caused by periventricular atrophy or cerebralSome cases are caused by periventricular atrophy or cerebral
dysgenesisdysgenesis
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26. Hemiplegia: pathologyHemiplegia: pathology
 MCA infarction (prenatal, perinatal)MCA infarction (prenatal, perinatal)
 Asymmetric periventricular leukomalacia in pretermAsymmetric periventricular leukomalacia in preterm
 Congenital Brain Malformations (eg.chizencephaly)Congenital Brain Malformations (eg.chizencephaly)
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27. Spasticity HemiplegiaSpasticity Hemiplegia
As the clinical features evolve, movement and tone on theAs the clinical features evolve, movement and tone on the
affected side typically decrease before tone and tendon reflexesaffected side typically decrease before tone and tendon reflexes
abnormally increaseabnormally increase
The typical posture appears when the child is approximatelyThe typical posture appears when the child is approximately
two years of agetwo years of age
arm is adducted at the shoulder and flexed at the elbow, the
forearm is pronated, and the wrist and fingers are flexed with
the hand closed
The hip is partially flexed and adducted, and the knee and
ankle are flexed because of increased tone in the hamstring and
plantar flexor muscles. The foot may remain in the equinovarus
or calcaneovalgus position.
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28. HemiplegiaHemiplegia
 Arm > legArm > leg
 SeizuresSeizures
 Normal intelligence-learning disabilities-mental retardationNormal intelligence-learning disabilities-mental retardation
 Growth retardation of affected sideGrowth retardation of affected side
 Corticosensory impairmentCorticosensory impairment
 Right hemiplegia accounts for 66% of casesRight hemiplegia accounts for 66% of cases
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29. HemiplegiaHemiplegia
 postnatal etiology :-postnatal etiology :-
 motor handicap usually is only mild or moderatemotor handicap usually is only mild or moderate
 Associated disabilities, such as intellectual impairment, hemianopsia,Associated disabilities, such as intellectual impairment, hemianopsia,
and seizures, may be worse than in cases with prenatal or perinataland seizures, may be worse than in cases with prenatal or perinatal
causes. Cognitive deficits tend to be worse in infants with seizurescauses. Cognitive deficits tend to be worse in infants with seizures
 Most children with spastic hemiplegia also have sensory deficitsMost children with spastic hemiplegia also have sensory deficits
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30. Hemiplegia/OutcomeHemiplegia/Outcome
 If no other major problem most walk by 2 years of ageIf no other major problem most walk by 2 years of age
 Can achieve independence in DLA doing one handed activitiesCan achieve independence in DLA doing one handed activities
 25% have a hemianopsia25% have a hemianopsia
 28% have cognitive disability28% have cognitive disability
 33% have seizures (highly correlated with cognitive difficulties)33% have seizures (highly correlated with cognitive difficulties)
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31. Quadriplegia: pathologyQuadriplegia: pathology
Spastic quadriplegia is the most severe form of spastic CP
It usually affects term infants who are small for gestational age,
consistent with a prenatal origin, such as cerebral dysgenesis or
infection. Other cases result from perinatal or postnatal events or a
combination of prenatal and perinatal causes
is seen in extremely low birth weight infants
Affected infants typically are severely handicapped
In addition to spasticity, they may have dystonia and feeding
and respiratory difficulties because of pseudobulbar palsy
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32. Quadriplegia: pathologyQuadriplegia: pathology
 Vascular impairment to subcortex and cortexVascular impairment to subcortex and cortex
 Diffuse neuronal injury leading to neuronal lossDiffuse neuronal injury leading to neuronal loss
 Secondary to occulusion of main arterial branches, venousSecondary to occulusion of main arterial branches, venous
thrombosisthrombosis
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33. Spastic Quadriplegia: OutcomeSpastic Quadriplegia: Outcome
 25% require total care25% require total care
 33% can learn to walk with aids33% can learn to walk with aids
 Medical Problems:Medical Problems:
1.1. visual impairmentvisual impairment
2.2. AspirationAspiration
3.3. failure to thrivefailure to thrive
4.4. seizures (50%)seizures (50%)
5.5. ConstipationConstipation
6.6. orthopedic complications (hip subluxation)orthopedic complications (hip subluxation)
 High rate of cognitive disabilityHigh rate of cognitive disability
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34. Spastic DiplegiaSpastic Diplegia
Spastic diplegia affects both term,preterm infants
Spastic diplegia in preterm infants often is associated with periventricular
leukomalacia (PVL), and the risk is greater with increasing prematurity.
The lower limbs are affected predominantly
Patients with mild PVL may have relatively good hand function and fewer
associated disabilities. In more severely affected patients, upper limb function
also may be compromised, depending upon the degree of spasticity, presence of
contractures, sensory loss, associated involuntary movements, and intelligence.
Sensory disturbances of central nervous system origin, such as poor two-point
discrimination and astereognosis, are common in all the spastic syndromes [6].
Vasomotor abnormalities also occur
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35. Spastic Diplegia: pathologySpastic Diplegia: pathology
•• Periventricular LeukomalaciaPeriventricular Leukomalacia
•• Premature infants at riskPremature infants at risk
•• Impairment of blood flow to periventricular white matterImpairment of blood flow to periventricular white matter
•• Border zone of arterial blood supply in the immature brainBorder zone of arterial blood supply in the immature brain
•• Multifactorial (arterial,venous, autoregulation, high metabolicdemands)Multifactorial (arterial,venous, autoregulation, high metabolicdemands)
•• Motor tracts for legs > armsMotor tracts for legs > arms
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36. Spastic DiplegiaSpastic Diplegia
•• Premature infants with PVLPremature infants with PVL
•• Medical Complications: strabismus (43%) contractures in lowerMedical Complications: strabismus (43%) contractures in lower
extremityextremity
•• Often ambulatoryOften ambulatory
•• Normal intelligence-can have non-verbal learning disabilitiesNormal intelligence-can have non-verbal learning disabilities
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37. Spastic Diplegia: OutcomeSpastic Diplegia: Outcome
•• >50% learn to walk often with the use of an aid such as a walker, or>50% learn to walk often with the use of an aid such as a walker, or
quad. Canesquad. Canes
•• Overflow tone to arms causing mild fine motor difficultiesOverflow tone to arms causing mild fine motor difficulties
•• Visual motor skills can be affected-learning disability, printing skillsVisual motor skills can be affected-learning disability, printing skills
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38. Dyskinetic syndromesDyskinetic syndromes
 affects term infantsaffects term infants
 it results from severe, acute perinatal asphyxiait results from severe, acute perinatal asphyxia
 The disorder is associated withThe disorder is associated with status marmoratusstatus marmoratus
 (lesions in the basal ganglia and thalamus with a marbled appearance)(lesions in the basal ganglia and thalamus with a marbled appearance)
that may appear as high-intensity areas on T2-weighted MRIthat may appear as high-intensity areas on T2-weighted MRI
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39. Dyskinetic syndromesDyskinetic syndromes
 Dyskinetic CP results fromDyskinetic CP results from
 selective neuronal necrosis in the hippocampus, thalamus, basal ganglia,selective neuronal necrosis in the hippocampus, thalamus, basal ganglia,
reticular formation, and Purkinje cells of the cerebellumreticular formation, and Purkinje cells of the cerebellum
 The neonatal presentation includesThe neonatal presentation includes
 encephalopathy characterized byencephalopathy characterized by
1.1. LethargyLethargy
2.2. decreased spontaneous movementdecreased spontaneous movement
3.3. HypotoniaHypotonia
4.4. suppressed primitive reflexessuppressed primitive reflexes
5.5. Multiple organs may be affectedMultiple organs may be affected
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40. Dyskinetic syndromesDyskinetic syndromes
 Dyskinetic syndromes are characterized byDyskinetic syndromes are characterized by
 involuntary movements of athetosis, chorea, and dystonia.involuntary movements of athetosis, chorea, and dystonia.
 They are divided into two categories, according to the predominant typeThey are divided into two categories, according to the predominant type
of abnormal movementof abnormal movement
1.1. athetoid, in which movements are athetoid, choreiform, or a combinationathetoid, in which movements are athetoid, choreiform, or a combination
of both.of both.
2.2. dystonicdystonic
Athetosis
Chorea
Dystonia
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41. ExtrapyramidalExtrapyramidal
1.1. athetoidathetoid
2.2. ataxicataxic
3.3. dystonicdystonic
 C/F :C/F :
1.1. abnormal postureabnormal posture
2.2. involuntary movementsinvoluntary movements
3.3. lead-pipe hypertonialead-pipe hypertonia
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42. Cerebral Hypertonia: DystoniaCerebral Hypertonia: Dystonia
 A movement disorder in which sustained muscle contractions causesA movement disorder in which sustained muscle contractions causes
twisting and repetitive movements, abnormal postures or bothtwisting and repetitive movements, abnormal postures or both
triggered by attempted voluntary movementtriggered by attempted voluntary movement
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43. Cerebral Hypertonia: DystoniaCerebral Hypertonia: Dystonia
 Affected patients usually are severely disabled in all four limbs, theAffected patients usually are severely disabled in all four limbs, the
trunk, and pharyngeal muscles.trunk, and pharyngeal muscles.
 The muscle tone typically is normal or hypotonic, especially in earlyThe muscle tone typically is normal or hypotonic, especially in early
childhood.childhood.
 Infants tend to have retention of primitive reflexes, involuntaryInfants tend to have retention of primitive reflexes, involuntary
grimacing, a tendency to drool, and delayed psychomotor developmentgrimacing, a tendency to drool, and delayed psychomotor development
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44. Cerebral Hypertonia: DystoniaCerebral Hypertonia: Dystonia
 The involuntary movements evolve with time and may not beThe involuntary movements evolve with time and may not be
apparent until the child is two to three years of age.apparent until the child is two to three years of age.
 Unlike spastic CP, contractures usually do not develop, unless theyUnlike spastic CP, contractures usually do not develop, unless they
are positional.are positional.
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45. Cerebral Hypertonia: DystoniaCerebral Hypertonia: Dystonia
 If hypertonus develops, it is the "tension" typeIf hypertonus develops, it is the "tension" type
 Tension is a sudden involuntary increase in tone that affects bothTension is a sudden involuntary increase in tone that affects both
flexor and extensor muscles.flexor and extensor muscles.
 The limbs become stiff during attempted movement or with emotion.The limbs become stiff during attempted movement or with emotion.
 Tendon reflexes are normal or may be difficult to elicit.Tendon reflexes are normal or may be difficult to elicit.
 Clonus and extensor plantar responses are absent, althoughClonus and extensor plantar responses are absent, although
athetoid movements of the toes may be confusing.athetoid movements of the toes may be confusing.
 Tension may be reduced with relaxation or a change in postureTension may be reduced with relaxation or a change in posture
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46. Athetoid Cerebral PalsyAthetoid Cerebral Palsy
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47. Athetoid Cerebral PalsyAthetoid Cerebral Palsy
•• Often secondary to kernicterusOften secondary to kernicterus
•• ABO incompatibility., RH, G6PD,dehydrationABO incompatibility., RH, G6PD,dehydration
•• Excess bilirubin pigmentExcess bilirubin pigment
•• Deposits in basal ganglia, cerebellum, and brainstem nuclei (8th nerve)Deposits in basal ganglia, cerebellum, and brainstem nuclei (8th nerve)
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48. Athetoid Cerebral PalsyAthetoid Cerebral Palsy
 Slow writhing involuntary movements of distal extremitiesSlow writhing involuntary movements of distal extremities
 DysarthriaDysarthria
 Difficult motor controlDifficult motor control
 Sensorineural hearing lossSensorineural hearing loss
 Paresis of upward gazeParesis of upward gaze
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49. Athetoid Cerebral PalsyAthetoid Cerebral Palsy
 There is dyssynergia (antagonistic action) of opposing muscleThere is dyssynergia (antagonistic action) of opposing muscle
groups, such as flexion and extension or pronation and supination.groups, such as flexion and extension or pronation and supination.
 Emotion, change in posture, or intended movement mayEmotion, change in posture, or intended movement may
accentuate or induce the abnormal movements.accentuate or induce the abnormal movements.
 Athetosis is most apparent during reaching, as the fingers extendAthetosis is most apparent during reaching, as the fingers extend
and abduct. Primitive reflexes often are retained.and abduct. Primitive reflexes often are retained.
 Oropharyngeal difficulties may result from facial grimacing.Oropharyngeal difficulties may result from facial grimacing.
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50. ChoreaChorea
 Chorea consists of rapid, irregular, unpredictable contractions ofChorea consists of rapid, irregular, unpredictable contractions of
individual muscles or small muscle groups that involve the face,individual muscles or small muscle groups that involve the face,
bulbar muscles, proximal extremities, and fingers and toes.bulbar muscles, proximal extremities, and fingers and toes.
 the chorea may be exacerbate bythe chorea may be exacerbate by
1.1. StressStress
2.2. ExcitementExcitement
3.3. FeverFever
 In some cases, fever may result in ballismus, a form of severe,In some cases, fever may result in ballismus, a form of severe,
coarse choreacoarse chorea
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51. Ataxic Cerebral PalsyAtaxic Cerebral Palsy
 ataxia indicates an incoordination of cerebellar or sensory origin,ataxia indicates an incoordination of cerebellar or sensory origin,
ataxic CP represents a widespread disorder of motor function.ataxic CP represents a widespread disorder of motor function.
 Affected patients usually are born at term.Affected patients usually are born at term.
 Most cases are caused byMost cases are caused by
 early prenatal events.early prenatal events.
 Some cases have genetic causes.Some cases have genetic causes.
 Autosomal recessive conditions include cerebellar hypoplasia, granule cellAutosomal recessive conditions include cerebellar hypoplasia, granule cell
deficiency, and Joubert syndromedeficiency, and Joubert syndrome
 An autosomal dominant form of nonprogressive ataxia has been describedAn autosomal dominant form of nonprogressive ataxia has been described
 Congenital hypoplasia of the cerebellum and pure ataxia occur rarelyCongenital hypoplasia of the cerebellum and pure ataxia occur rarely
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52. Ataxic Cerebral PalsyAtaxic Cerebral Palsy
 The clinical presentation of ataxic CP is variableThe clinical presentation of ataxic CP is variable
 Most patients haveMost patients have
 congenital hypotoniacongenital hypotonia
 Motor milestones and language skills typically are delayed.Motor milestones and language skills typically are delayed.
 Ataxia usually improves with time.Ataxia usually improves with time.
 In general, associated disabilities are worse with increasing severity ofIn general, associated disabilities are worse with increasing severity of
motor impairment.motor impairment.
 Speech, which is related to intellectual ability, typically is slow, jerky, andSpeech, which is related to intellectual ability, typically is slow, jerky, and
explosive.explosive.
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53. Ataxic Cerebral PalsyAtaxic Cerebral Palsy
 The diagnosis of ataxic CP is madeThe diagnosis of ataxic CP is made
 by exclusion, as all patients with CP have incoordination and disturbedby exclusion, as all patients with CP have incoordination and disturbed
posture.posture.
 Other causes of weakness, spasticity, dystonia, or choreoathetosis shouldOther causes of weakness, spasticity, dystonia, or choreoathetosis should
be ruled out.be ruled out.
 Ataxic CP also should be distinguished from progressiveAtaxic CP also should be distinguished from progressive
neurodegenerative disorders, which may present with some of the sameneurodegenerative disorders, which may present with some of the same
featuresfeatures
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54. Atonic Cerebral PalsyAtonic Cerebral Palsy
 Affected infants usually are born at term with severe hypotonia.Affected infants usually are born at term with severe hypotonia.
 Many have cerebral dysgenesis, microcephaly, and profound intellectual disability.Many have cerebral dysgenesis, microcephaly, and profound intellectual disability.
Development is extremely delayed, and affected children never stand or walk.Development is extremely delayed, and affected children never stand or walk.
 Typical findings that characterize other CP syndromes are absent in this disorder.Typical findings that characterize other CP syndromes are absent in this disorder.
 Tone often remains decreased for approximately 12 to 18 months and then becomesTone often remains decreased for approximately 12 to 18 months and then becomes
variable and paratonic (ie, with passive movement of a joint, resistance increasesvariable and paratonic (ie, with passive movement of a joint, resistance increases
proportionally to the amount of pressure applied)proportionally to the amount of pressure applied)
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55. Mixed CPMixed CP
•• Features of spasticity and extrapyramidal findingsFeatures of spasticity and extrapyramidal findings
•• Commonly found in children with spastic quadriplegiaCommonly found in children with spastic quadriplegia
•• Obstetrical history often reveals an acute emergency (e.g.. placentalObstetrical history often reveals an acute emergency (e.g.. placental
abruption) with a rescueabruption) with a rescue
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56. Classification according toClassification according to
Severity (Palisano, Rosenbaum)Severity (Palisano, Rosenbaum)
 Class 1:No limitation of activity.Class 1:No limitation of activity.
 Class 2: Slight to moderate limitation.Class 2: Slight to moderate limitation.
 Class 3: Moderate to great limitationClass 3: Moderate to great limitation
 Class 4: No useful physical activity.Class 4: No useful physical activity.
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57. ASSOCIATEDASSOCIATED
IMPAIRMENTSIMPAIRMENTS
SensorySensory
1.1. Sensorineural and conductive hearingSensorineural and conductive hearing
lossloss
2.2. Impairments of visual acuityImpairments of visual acuity
3.3. Oculomotor dysfunctionOculomotor dysfunction
4.4. StrabismusStrabismus
5.5. Somatosensory impairmentsSomatosensory impairments
CognitiveCognitive
1.1. Mental retardation (MR) in about 50%,Mental retardation (MR) in about 50%,
especially in spastic quadriparesisespecially in spastic quadriparesis
2.2. High incidence of learning disabilitiesHigh incidence of learning disabilities
3.3. Attention deficit/hyperactivity disorderAttention deficit/hyperactivity disorder
4.4. Sleep and behavioral disturbancesSleep and behavioral disturbances
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58. ASSOCIATEDASSOCIATED
IMPAIRMENTSIMPAIRMENTS
 NeurologicNeurologic
 SeizuresSeizures
 HydrocephalusHydrocephalus
 SkinSkin
 Decubitus ulcersDecubitus ulcers
 MusculoskeletalMusculoskeletal
 ContracturesContractures
 Hip subluxation/dislocationHip subluxation/dislocation
 ScoliosisScoliosis
 DentalDental
 CariesCaries
 Gingival hyperplasiaGingival hyperplasia
 Abnormalities of enamelAbnormalities of enamel
(congenital)(congenital)
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59. ASSOCIATEDASSOCIATED
IMPAIRMENTSIMPAIRMENTS
 CardiorespiratoryCardiorespiratory
 Upper airway obstructionUpper airway obstruction
 Aspiration pneumonitisAspiration pneumonitis
 Restrictive lung diseaseRestrictive lung disease
 Secondary to thoracic deformitySecondary to thoracic deformity
 Reactive airway diseaseReactive airway disease
 Gastrointestinal tract/nutritionGastrointestinal tract/nutrition
 Failure to thriveFailure to thrive
 Gastroesophageal refluxGastroesophageal reflux
 ConstipationConstipation
 Oral motor dysfunction/dysphagiaOral motor dysfunction/dysphagia
 Gastrourinary tractGastrourinary tract
 Neurogenic bladderNeurogenic bladder
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60. Commonly Associated ConditionsCommonly Associated Conditions
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61. Differential DiagnosisDifferential Diagnosis
 Cerebral palsy (CP) is a diagnosis of exclusion.
1.1. Benign congenital hypotoniaBenign congenital hypotonia
2. neurodegenerative diseases
3. inborn errors of metabolism
4. developmental or traumatic lesions of the brain or spinal cord
5. neuromuscular or movement disorders
6. neoplasm
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62. Differential DiagnosisDifferential Diagnosis
 following features raise the possibility of a diagnosis other than CP,
such as a neurodegenerative disease or metabolic disorder:
1. Family history of the neurologic condition
2. Loss of developmental milestones
3. Ataxia, involuntary movements, oculomotor abnormalities, muscle atrophy,
or sensory loss
4. Hypotonia associated with weakness
5. Rapid deterioration of neurologic signs
6. Marked worsening during periods of catabolism (fasting or illness)
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63. Differential DiagnosisDifferential Diagnosis
1.1. Brachial plexus injuryBrachial plexus injury
2.2. Familial spastic paraplegiaFamilial spastic paraplegia
3.3. Dopa-responsive dystoniaDopa-responsive dystonia
4.4. Transient toe-walkingTransient toe-walking
5.5. Muscular dystrophyMuscular dystrophy
6.6. Metabolic disorders (e.g., glutaric aciduria type 1)Metabolic disorders (e.g., glutaric aciduria type 1)
7.7. Mitochondrial disordersMitochondrial disorders
8.8. Genetic disorders (e.g., Rett syndrome)Genetic disorders (e.g., Rett syndrome)
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64. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
1.1. Etiology (from history and thorough clinical examination). CPEtiology (from history and thorough clinical examination). CP
may be post-encephalitic, post-kernicteric, post-anoxic,...etc.may be post-encephalitic, post-kernicteric, post-anoxic,...etc.
2.2. Topography.Topography.
3.3. Physiology.Physiology.
4.4. Functional classification.Functional classification.
5.5. Associated deficits deficits.Associated deficits deficits.
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65. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
•• HistoryHistory
1.1. delayed motor milestonesdelayed motor milestones
2.2. assessment of risk factorsassessment of risk factors
3.3. no regressionno regression
•• Neurological ExamNeurological Exam
1.1. abnormal toneabnormal tone
2.2. PosturePosture
3.3. MovementMovement
•• Can be supported by central imaging (MRI, CAT Scan)Can be supported by central imaging (MRI, CAT Scan)
•• Usually by 2 -3 years of ageUsually by 2 -3 years of age
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66. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
 The diagnosis of CP depends upon a combination of findings,The diagnosis of CP depends upon a combination of findings,
includingincluding
1.1. motor delaymotor delay
2.2. neurologic signsneurologic signs
3.3. persistence of primitive reflexespersistence of primitive reflexes
4.4. abnormal postural reactions.abnormal postural reactions.
 A diagnosis rarely is made on the basis of an isolated abnormality.A diagnosis rarely is made on the basis of an isolated abnormality.
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67. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
 Infants with normal functional development and behavior whoInfants with normal functional development and behavior who
have mild hypertonia or hyperreflexia should be observed→ Ifhave mild hypertonia or hyperreflexia should be observed→ If
these abnormalities remain isolated, they will resolve progressivelythese abnormalities remain isolated, they will resolve progressively
after the child reaches nine months of age in most casesafter the child reaches nine months of age in most cases
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68. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
 Clues to an early diagnosis includeClues to an early diagnosis include
1.1. abnormal behaviorabnormal behavior
2.2. psychomotor delaypsychomotor delay
3.3. abnormal oromotor or oculomotor patternsabnormal oromotor or oculomotor patterns
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69. Making a Diagnosis of Cerebral PalsyMaking a Diagnosis of Cerebral Palsy
 Although the lesion in CP is static, clinical signs evolve as theAlthough the lesion in CP is static, clinical signs evolve as the
nervous system matures.nervous system matures.
 infants at high risk for CP who had serial examinations for twoinfants at high risk for CP who had serial examinations for two
yearsyears
 The presence of three or more abnormal signs at eight months ofThe presence of three or more abnormal signs at eight months of
age was highly predictive of CP.age was highly predictive of CP. However, CP often was missed atHowever, CP often was missed at
one month and sometimes overdiagnosed at four months.one month and sometimes overdiagnosed at four months.
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70. Levine (POSTER) criteria for the diagnosis of CPLevine (POSTER) criteria for the diagnosis of CP
1.1. P :- Posturing/abnormal movementsP :- Posturing/abnormal movements
2.2. O :- Oropharyngeal problemsO :- Oropharyngeal problems
 (e.g., tongue thrusts, swallowing abnormalities)(e.g., tongue thrusts, swallowing abnormalities)
1.1. S :- StrabismusS :- Strabismus
2.2. T :- Tone (hyper- or hypotonia)T :- Tone (hyper- or hypotonia)
3.3. E :- Evolutional maldevelopmentE :- Evolutional maldevelopment
 (primitive reflexes persist or protective/equilibrium reflexes fail to develop [e.g., lateral prop, parachute reflex])(primitive reflexes persist or protective/equilibrium reflexes fail to develop [e.g., lateral prop, parachute reflex])
1.1. R :- Reflexes (increased deep tendon reflexes/persistent Babinski's reflex)R :- Reflexes (increased deep tendon reflexes/persistent Babinski's reflex)
 Abnormalities in four of these six categories strongly point to the diagnosis of CPAbnormalities in four of these six categories strongly point to the diagnosis of CP
Abnormalities in four of these six categories strongly point to the diagnosis of
CP
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71. Clinical features of cerebral palsy
 Neurobehavioral signsNeurobehavioral signs
 Motor abnormalitiesMotor abnormalities
 Developmental reflexesDevelopmental reflexes
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72. Neurobehavioral signsNeurobehavioral signs
1.1. IrritableIrritable
2.2. Sleeps PoorlySleeps Poorly
3.3. Vomits FrequentlyVomits Frequently
4.4. Is Difficult To Handle And CuddleIs Difficult To Handle And Cuddle
5.5. Poor Visual AttentionPoor Visual Attention
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73. Motor abnormalitiesMotor abnormalities

Tone in theTone in the extremities may be normal or increased.extremities may be normal or increased.
 Persistent or asymmetric fisting may be present.Persistent or asymmetric fisting may be present.
 Abnormal oromotor patterns includeAbnormal oromotor patterns include
 tongue retraction and thrust, tonic bite, oral hypersensitivity, and grimacing.tongue retraction and thrust, tonic bite, oral hypersensitivity, and grimacing.
 Poor head control may be an early motor sign.Poor head control may be an early motor sign.
 However, increased neck extensor and axial tone may make head control appear betterHowever, increased neck extensor and axial tone may make head control appear better
than it actually is.than it actually is.
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74. Motor abnormalitiesMotor abnormalities
 In addition to the neurologic examinationIn addition to the neurologic examination
 achievement of motor milestones should be evaluated.achievement of motor milestones should be evaluated.
 The infant should be observed in the prone and supine positions.The infant should be observed in the prone and supine positions.
 Posture and tone are assessed on pulling to sit, supported sitting, and vertical and ventralPosture and tone are assessed on pulling to sit, supported sitting, and vertical and ventral
suspension.suspension.
 The infant should be able to support himself or herself on arms and hands and rotateThe infant should be able to support himself or herself on arms and hands and rotate
within the body axis at the appropriate ages.within the body axis at the appropriate ages.
 The emergence and quality of protective postural reactions should be noted.The emergence and quality of protective postural reactions should be noted.
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75. Motor abnormalitiesMotor abnormalities
 Serial examination using motor milestones can be an effective screening process for CP.Serial examination using motor milestones can be an effective screening process for CP.
 six motor milestonessix motor milestones (roll prone to supine, roll supine to prone, sit with support, sit(roll prone to supine, roll supine to prone, sit with support, sit
without support, crawl, and cruise)without support, crawl, and cruise)
 Serial screening of these milestones predicted the development of CP better than did any individualSerial screening of these milestones predicted the development of CP better than did any individual
milestone.milestone.
 Delays in more than four milestones were especially worrisome.Delays in more than four milestones were especially worrisome.
 In another report, signs present at four months of age that indicated increased risk of CPIn another report, signs present at four months of age that indicated increased risk of CP
were failure to support weight on the forearms in a prone position, sit supported withwere failure to support weight on the forearms in a prone position, sit supported with
head erect, or show interest in surroundings or respond sociallyhead erect, or show interest in surroundings or respond socially
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76. Developmental reflexesDevelopmental reflexes
 In normal infants, most developmental reflexes related to postureIn normal infants, most developmental reflexes related to posture
(tonic labyrinthine, tonic neck, and neck-righting and body-righting(tonic labyrinthine, tonic neck, and neck-righting and body-righting
reflexes) disappear when the infants are between three and six monthsreflexes) disappear when the infants are between three and six months
of age.of age.
 These reflexes often are not appropriately integrated or inhibited inThese reflexes often are not appropriately integrated or inhibited in
children with CPchildren with CP
 Thus, delay in the disappearance or exaggeration of a developmentalThus, delay in the disappearance or exaggeration of a developmental
reflex may be an early indication of motor disabilityreflex may be an early indication of motor disability
 An obligatory developmental reflex (a response that persists for asAn obligatory developmental reflex (a response that persists for as
long as the stimulus is applied) is abnormal at any agelong as the stimulus is applied) is abnormal at any age
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77. Developmental reflexesDevelopmental reflexes
 The tonic labyrinthine response is tested in the supine position.The tonic labyrinthine response is tested in the supine position.
1.1. Extension of the neck results in shoulder retraction, leg extension, and eitherExtension of the neck results in shoulder retraction, leg extension, and either
elbow flexion or extension and pronation of the arms.elbow flexion or extension and pronation of the arms.
2.2. Flexion of the neck results in flexion of the extremities.Flexion of the neck results in flexion of the extremities.
 Infants with an exaggerated tonic labyrinthine response may haveInfants with an exaggerated tonic labyrinthine response may have
opisthotonic posturing or roll over at an age that is earlier thanopisthotonic posturing or roll over at an age that is earlier than
appropriate.appropriate.
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78. Developmental reflexesDevelopmental reflexes
 Other abnormal signs can be elicited when the infant is held in vertical suspension.Other abnormal signs can be elicited when the infant is held in vertical suspension.
 During the first few months, the appropriate response is for the baby to assume aDuring the first few months, the appropriate response is for the baby to assume a
sitting position ("sit in the air").sitting position ("sit in the air").
 An abnormal response is persistent extension of the legs.An abnormal response is persistent extension of the legs.
 This may be followed by or associated with an abnormal positive support reaction. TheThis may be followed by or associated with an abnormal positive support reaction. The
latter is tested by placing the anteromedial areas of the soles on a firm surface, whichlatter is tested by placing the anteromedial areas of the soles on a firm surface, which
should result in a few seconds of plantar flexion, then return of the feet to a neutralshould result in a few seconds of plantar flexion, then return of the feet to a neutral
position.position.
 An abnormal response is plantar flexion that is obligate or maintained for more than 30An abnormal response is plantar flexion that is obligate or maintained for more than 30
seconds, especially if accompanied by equinus posturingseconds, especially if accompanied by equinus posturing
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79. Algorithm for the
evaluation of the
child with cerebral
palsy (CP)
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80. Priorities of managementPriorities of management
Communication
Social and emotional development
Education
Maximal independence in activities of daily living
As near-normal appearance as possible
Nutrition
Mobility
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81. TREATMENT GOALS
 Interventions for CP should be directed at maximizing the quality ofInterventions for CP should be directed at maximizing the quality of
life by improvement in daily function and reduction of the extent oflife by improvement in daily function and reduction of the extent of
disability.disability.
 Initially, the parents and other caregivers should learn how to seat,Initially, the parents and other caregivers should learn how to seat,
dress, feed, communicate with, transfer, transport, and toilet the childdress, feed, communicate with, transfer, transport, and toilet the child
 With growth and development, the child should achieve maximalWith growth and development, the child should achieve maximal
independence in these activitiesindependence in these activities
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82. TREATMENT GOALSTREATMENT GOALS
 Psychological development, communication, and education are priorities inPsychological development, communication, and education are priorities in
the management of CP.the management of CP.
 Longitudinal social, language, and psychometric assessment provides aLongitudinal social, language, and psychometric assessment provides a
rational basis for training in communication and activities of daily livingrational basis for training in communication and activities of daily living
and allows the child to derive the maximum benefit from schooland allows the child to derive the maximum benefit from school
 As the child becomes older, assessment and training for a potentialAs the child becomes older, assessment and training for a potential
occupation become importantoccupation become important
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83. Multidisciplinary teamMultidisciplinary team
 Management should be directed at promoting the child's:Management should be directed at promoting the child's:
1.1. Social and emotional developmentSocial and emotional development
2.2. CommunicationCommunication
3.3. EducationEducation
4.4. NutritionNutrition
5.5. MobilityMobility
6.6. Maximal independence in activities of daily livingMaximal independence in activities of daily living
7.7. Appearance as nearly normal as possibleAppearance as nearly normal as possible
 The team should set functional goals for the child that are realistic andThe team should set functional goals for the child that are realistic and
periodically reevaluated.periodically reevaluated.
 The aim of these goals is for the child to achieve maximal potential inThe aim of these goals is for the child to achieve maximal potential in
all areas of development and promote independence.all areas of development and promote independence.
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84. Treatment Options forTreatment Options for
Children with HypertoniaChildren with Hypertonia
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85. SpasticitySpasticity
Lancet 1980Lancet 1980
 A motor disorder characterized by aA motor disorder characterized by a velocity-dependentvelocity-dependent
increase in tonic stretch reflexesincrease in tonic stretch reflexes (muscle tone) with(muscle tone) with
exaggerated tendon jerks, resulting from hyper excitability ofexaggerated tendon jerks, resulting from hyper excitability of
the stretch reflex which is as one component of the upper motorthe stretch reflex which is as one component of the upper motor
neuron syndrome.neuron syndrome.
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86. AdvantagesAdvantages
 It may substitutes for strength, thus facilitating transfer,It may substitutes for strength, thus facilitating transfer,
standing and ambulation.standing and ambulation.
 May help prevent muscle atrophy, decrease edema as well asMay help prevent muscle atrophy, decrease edema as well as
reduce the risk of osteoporosisreduce the risk of osteoporosis
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87. DisadvantagesDisadvantages
 Interference with functional mobility and activities of daily living.Interference with functional mobility and activities of daily living.
 It may cause painful spasms, result in fractures, interfere with sleep orIt may cause painful spasms, result in fractures, interfere with sleep or
increase the risk of bed ulcers.increase the risk of bed ulcers.
 do not improve weakness and incoordination
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88. SpasticitySpasticity
Why to treatWhy to treat
 Improve functionImprove function
 Prevent complicationsPrevent complications
 Alleviate painAlleviate pain
 Ease nursingEase nursing
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89. Spasticity ManagementSpasticity Management
 NoneNone
 Reduce external factorsReduce external factors
 Seating/PositioningSeating/Positioning
 PhysiotherapyPhysiotherapy
 Oral medicationOral medication
 Nerve blocksNerve blocks
 Botulinium toxinBotulinium toxin
 Intrathecal TechniqueIntrathecal Technique
 SurgerySurgery
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90. Treatment of SpasticityTreatment of Spasticity
 First LineFirst Line
 Baclofen (10)[C]:Baclofen (10)[C]:
 γ-γ-aminobutyric acid B (GABAaminobutyric acid B (GABABB) agonist, facilitates presynaptic inhibition of mono- and polysynaptic reflexes) agonist, facilitates presynaptic inhibition of mono- and polysynaptic reflexes
 Adults: Initial dose is 5 mg t.i.d. and increase dosage every 3 days to an average maintenance dose of 20 mg t.i.d. 80 mg/24-hrAdults: Initial dose is 5 mg t.i.d. and increase dosage every 3 days to an average maintenance dose of 20 mg t.i.d. 80 mg/24-hr
maximummaximum
 Pediatric dose (>2 y/o): Initial 10–15 mg/24 hrs. Titrate to effective dose. <8 y/o = 40 mg/24 hrs. maximum. >8 y/o 60 mg/24Pediatric dose (>2 y/o): Initial 10–15 mg/24 hrs. Titrate to effective dose. <8 y/o = 40 mg/24 hrs. maximum. >8 y/o 60 mg/24
hrs. maximumhrs. maximum
 Intrathecal Baclofen (Baclofen Pump) :Intrathecal Baclofen (Baclofen Pump) :
 Continuous intrathecal route allows greater maximal response with smaller dosageContinuous intrathecal route allows greater maximal response with smaller dosage
 Significantly reduces spasticity in children with cerebral palsySignificantly reduces spasticity in children with cerebral palsy
 Multiple adverse effects due to catheter placement and medication side effectsMultiple adverse effects due to catheter placement and medication side effects
 Diazepam (10)[C]:Diazepam (10)[C]:
 A GABAA GABAAA agonist, facilitating CNS inhibition at spinal and supraspinal levels to reduce spasticityagonist, facilitating CNS inhibition at spinal and supraspinal levels to reduce spasticity
 Adult dose: 2–12 mg/dose p.o. q. 6–12 hrs.Adult dose: 2–12 mg/dose p.o. q. 6–12 hrs.
 Pediatric dose (<12 yrs): 0.12–0.8 mg/kg/24 h. p.o., divided q.6–8h.Pediatric dose (<12 yrs): 0.12–0.8 mg/kg/24 h. p.o., divided q.6–8h.
 Botulinum toxin type A:Botulinum toxin type A:
 Injected directly into muscles of interestInjected directly into muscles of interest
 Acts at neuromuscular junction to inhibit the release of acetylcholineActs at neuromuscular junction to inhibit the release of acetylcholine
 Chemically denervates muscles, reducing toneChemically denervates muscles, reducing tone
 Lasts for 12–16 weeks following injectionLasts for 12–16 weeks following injection
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91. Treatment of SpasticityTreatment of Spasticity
 Second LineSecond Line
 The following medications are used far less frequently:The following medications are used far less frequently:
 Dantrolene:Dantrolene:
 Limits calcium release from muscles, reducing spasticityLimits calcium release from muscles, reducing spasticity
 Adult dosing: 25 mg p.o. daily titrated to effective dose, maximum 100 mg p.o. q.i.d.Adult dosing: 25 mg p.o. daily titrated to effective dose, maximum 100 mg p.o. q.i.d.
 Pediatric dosing: 0.5 mg/kg p.o. daily titrated to effective dose, maximum 12 mg/kg/24 hrs.Pediatric dosing: 0.5 mg/kg p.o. daily titrated to effective dose, maximum 12 mg/kg/24 hrs.
 Tizanidine and otherTizanidine and other α-α-adrenergic agents:adrenergic agents:
 α-α-adrenergic agonist, presynaptically inhibits motor activation, reducing spasticityadrenergic agonist, presynaptically inhibits motor activation, reducing spasticity
 Adult dosing: 4 mg/day p.o., titrate to effective dose, up to 8 mg p.o. q.4–6h., 36 mg/24 hrs. maximumAdult dosing: 4 mg/day p.o., titrate to effective dose, up to 8 mg p.o. q.4–6h., 36 mg/24 hrs. maximum
 Pediatric dosing: Not specificedPediatric dosing: Not specificed
 Gabapentin:Gabapentin:
 Anticonvulsant structurally similar to GABA, increases levels of GABA in brain and reduces spasticityAnticonvulsant structurally similar to GABA, increases levels of GABA in brain and reduces spasticity
 Adult dosing: Titrate to starting dose 100 mg t.i.d. starting dosage, maximum dose 3600 mg/day inAdult dosing: Titrate to starting dose 100 mg t.i.d. starting dosage, maximum dose 3600 mg/day in
divided dosingdivided dosing
 Pediatric dosing: Not specifiedPediatric dosing: Not specified
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92. Treatment of SpasticityTreatment of Spasticity
 For medical therapy of spasticity, there is stronger evidence to support the use ofFor medical therapy of spasticity, there is stronger evidence to support the use of
botulinum toxin than there is for oral antispastic drugsbotulinum toxin than there is for oral antispastic drugs
 TizanidineTizanidine
 BaclofenBaclofen
 DiazepamDiazepam
 Dantrolene SodiumDantrolene Sodium
 ClonidineClonidine
 GabapentinGabapentin
 Botulinum ToxinBotulinum Toxin
 RhizotomyRhizotomy
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93. Oral antispastic drugsOral antispastic drugs
When to use?When to use?
 Mild spasticity – need any medicationMild spasticity – need any medication
 Sever spasticity – medication likely to be unhelpful – consider focalSever spasticity – medication likely to be unhelpful – consider focal
treatmentstreatments
 Moderate spasticity – most likely scenarioModerate spasticity – most likely scenario
 Balance between benefit and side effectBalance between benefit and side effect
 Dantrolene, benzodiazepines, and baclofenDantrolene, benzodiazepines, and baclofen
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94. Nerve BlocksNerve Blocks
 Phenol or alcoholPhenol or alcohol
 2-6 mls of 3-6% phenol2-6 mls of 3-6% phenol
 Any accessible nerve but good result from obturator andAny accessible nerve but good result from obturator and
posterior tibial nerve injectionposterior tibial nerve injection
 Dysaesthesia can be a problemDysaesthesia can be a problem
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95. Intrathecal MedicationsIntrathecal Medications
 Spasticity is not adequately controlled by oral medication inSpasticity is not adequately controlled by oral medication in
one third of patients.one third of patients.
 Baclofen, do not cross the blood brain barrier effectively andBaclofen, do not cross the blood brain barrier effectively and
the need to use higher doses to achieve desired efficacy canthe need to use higher doses to achieve desired efficacy can
result in serious side effects.result in serious side effects.
 Intrathecal baclofen pump.Intrathecal baclofen pump.
 Botulinum toxin injectionsBotulinum toxin injections
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96. Intrathecal baclofen pumpIntrathecal baclofen pump
 Should undergo a screening trial of a test dose administered intrathecally throughShould undergo a screening trial of a test dose administered intrathecally through
LPLP
 If the trial dose is effective, implantation of the intrathecal pump can then beIf the trial dose is effective, implantation of the intrathecal pump can then be
performed and the pump dose adjusted according to the clinical response.performed and the pump dose adjusted according to the clinical response.
 Side effects include orthostatic hypotension, sedation, loss of erection,Side effects include orthostatic hypotension, sedation, loss of erection,
 Local infection, CSF leak and the cost.Local infection, CSF leak and the cost.
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97. Intrathecal BaclofenIntrathecal Baclofen
 Subcutaneous implantable pump connected to intrathecalSubcutaneous implantable pump connected to intrathecal
cathetercatheter
 Pump is programmablePump is programmable
 Effective in resistant spasticityEffective in resistant spasticity
 Potentially serious side effects include overdosage, pumpPotentially serious side effects include overdosage, pump
failure, infection, catheter movement, tolerancefailure, infection, catheter movement, tolerance
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98. Botulinum Toxin InjectionsBotulinum Toxin Injections
 Is a neurotoxin derived from bacteria.Is a neurotoxin derived from bacteria.
 Act on the neuromuscular junction at the presynaptic site by inhibitingAct on the neuromuscular junction at the presynaptic site by inhibiting
the release of acetylcholine, thus leading to muscle weakness andthe release of acetylcholine, thus leading to muscle weakness and
reduce muscle tone.reduce muscle tone.
 Local effect within2-3 days and last for 3-6 months.Local effect within2-3 days and last for 3-6 months.
 Skin reaction and spread of weakness.Skin reaction and spread of weakness.
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99. TechniqueTechnique
 Clinically identify overactive muscleClinically identify overactive muscle
 Inject into muscleInject into muscle
 Some spread possible to nearby musclesSome spread possible to nearby muscles
 Combine with other treatments, especially physiotherapyCombine with other treatments, especially physiotherapy
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100. Botulinum toxin ABotulinum toxin A
AdvantagesAdvantages
1.1. Focal, selective, graded effectsFocal, selective, graded effects
2.2. No CNS side effectsNo CNS side effects
3.3. Works independently of pathophysiologyWorks independently of pathophysiology
mechanism of motor over activitymechanism of motor over activity
4.4. No sensory disturbanceNo sensory disturbance
5.5. Non-destructiveNon-destructive
6.6. Weakness resolves spontaneouslyWeakness resolves spontaneously
7.7. Safe & well toleratedSafe & well tolerated
DisadvantagesDisadvantages
1.1. BBiological effects last only 3-4 monthsiological effects last only 3-4 months
- require repeated injections- require repeated injections
2.2. Effects non-reversible during period ofEffects non-reversible during period of
actionaction
3.3. Injection (painful)Injection (painful)
4.4. Limited maximal doseLimited maximal dose
5.5. May require EMG guidanceMay require EMG guidance
6.6. Secondary failure/antibodiesSecondary failure/antibodies
7.7. CostCost
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101. Botulinum toxin ABotulinum toxin A
Mechanism of Action:Mechanism of Action:
 Produces neuromuscular junction blockade:Produces neuromuscular junction blockade:
taken up at the presynaptic nerve terminaltaken up at the presynaptic nerve terminal
BtxA binds irreversibly to an ACh vesicle binding proteinBtxA binds irreversibly to an ACh vesicle binding protein
(SNAP-25)(SNAP-25)
prevents binding of acetylcholine (ACh) vesicles to the presynaptic membrane inhibiting their releaseprevents binding of acetylcholine (ACh) vesicles to the presynaptic membrane inhibiting their release
muscle becomes functionally ‘denervated’muscle becomes functionally ‘denervated’
 Full clinical effect: expected within 2-3 weeksFull clinical effect: expected within 2-3 weeks
 Recovery: sprouting of new axons from adjacent nerves as well as from pre-terminal portions ofRecovery: sprouting of new axons from adjacent nerves as well as from pre-terminal portions of
affected nerves (~3months)affected nerves (~3months)
 Injection may be repeated at 16-week intervals:Injection may be repeated at 16-week intervals:
 as required to maintain response, not more frequently than 8 weeksas required to maintain response, not more frequently than 8 weeks
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102. Botulinum toxin ABotulinum toxin A
Adverse EffectsAdverse Effects
 Excessive weakness with reduced functionExcessive weakness with reduced function
 Unintentional weakness of adjacent musclesUnintentional weakness of adjacent muscles
 Local pain or haematomaLocal pain or haematoma
 Flu-like illnessFlu-like illness
 Neuralgic amyotrophy-like illnessNeuralgic amyotrophy-like illness
 Long-term-secondary clinical resistanceLong-term-secondary clinical resistance
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103. Botulinum injection:Botulinum injection:
locating injection sitelocating injection site
 Determine which specific muscle/s to be selectedDetermine which specific muscle/s to be selected
 Electrical stimulationElectrical stimulation oror EMG may be useful to locate smaller or deeper or multi-EMG may be useful to locate smaller or deeper or multi-
fasciculated muscles eg FDSfasciculated muscles eg FDS
 Palpation using anatomical landmarks is usually adequate for larger muscles:Palpation using anatomical landmarks is usually adequate for larger muscles:
 Correct placement of the needle can be confirmed by moving the joint through its full range of movementsCorrect placement of the needle can be confirmed by moving the joint through its full range of movements
in the appropriate plane and observing the resultant movement of the needlein the appropriate plane and observing the resultant movement of the needle
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104. IndicationsIndications
 BTX A is indicated in patients who have increased muscle tone thatBTX A is indicated in patients who have increased muscle tone that
interferes with function or is likely to lead to joint contracture withinterferes with function or is likely to lead to joint contracture with
growth; the best evidence is for equinus varusgrowth; the best evidence is for equinus varus
 Patients younger than four years old and without fixed contractures arePatients younger than four years old and without fixed contractures are
expected to have the most favorable response. Ideally, only two or threeexpected to have the most favorable response. Ideally, only two or three
muscles will require treatment at one time.muscles will require treatment at one time.
 In general, BTX A should NOT be used in children younger than 18In general, BTX A should NOT be used in children younger than 18
months old because no data are available on the long-term use of thismonths old because no data are available on the long-term use of this
therapytherapy
 BTX A is not appropriate for patients with diffuse hypertonia, althoughBTX A is not appropriate for patients with diffuse hypertonia, although
it might be used to treat focal aspects of generalized spasticity. Fixedit might be used to treat focal aspects of generalized spasticity. Fixed
contractures are not amenable to BTX therapy, although BTX Acontractures are not amenable to BTX therapy, although BTX A
injections may facilitate serial castinginjections may facilitate serial casting
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105. CRITICAL post-injection managementCRITICAL post-injection management
 Physical managementPhysical management
 Stretching, facilitation of activity in opposing muscle groups, electricalStretching, facilitation of activity in opposing muscle groups, electrical
stimulationstimulation
 SplintingSplinting
 Aim: to correctAim: to correct and prevent flexion contracturesand prevent flexion contractures
 Medical follow-upMedical follow-up
 Assessment at 4–6 weeks to determine if treatment goals have been achievedAssessment at 4–6 weeks to determine if treatment goals have been achieved
 Review at 3–4 months to evaluate need for further injectionsReview at 3–4 months to evaluate need for further injections
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106. Surgical treatmentSurgical treatment
 selective dorsal rhizotomy and stereotactic encephalotomyselective dorsal rhizotomy and stereotactic encephalotomy
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107. ORTHOPEDIC INTERVENTIONSORTHOPEDIC INTERVENTIONS
 Orthopedic interventions are directed at relief and prevention ofOrthopedic interventions are directed at relief and prevention of
deformity and maximizing functiondeformity and maximizing function
 Gait analysis, using physical examination, electromyography, andGait analysis, using physical examination, electromyography, and
videotaping of limb motion, is often used to identify which musclesvideotaping of limb motion, is often used to identify which muscles
might benefit from lengthening procedures and to evaluate the effectsmight benefit from lengthening procedures and to evaluate the effects
of surgeryof surgery
 This should be performed when the gait is mature, usually between sixThis should be performed when the gait is mature, usually between six
and ten years of ageand ten years of age
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108. Muscle-tendon surgeryMuscle-tendon surgery
 Release or recession of limb muscles and tendons (muscle-tendonRelease or recession of limb muscles and tendons (muscle-tendon
surgery) is sometimes performed to reduce restricted joint motion orsurgery) is sometimes performed to reduce restricted joint motion or
malalignment.malalignment.
 They are recommended when fixed contractures interfere with possibleThey are recommended when fixed contractures interfere with possible
function or carefunction or care
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109. Hip disordersHip disorders
 Disorders of the hip, including subluxation, dislocation, and dislocation with degeneration and pain are commonDisorders of the hip, including subluxation, dislocation, and dislocation with degeneration and pain are common
complications of spastic CPcomplications of spastic CP
 lthough the hip is initially normal, progressive dysplasia results from a combination of bony deformity and musclelthough the hip is initially normal, progressive dysplasia results from a combination of bony deformity and muscle
imbalance, usually involving the adductor and iliopsoas musclesimbalance, usually involving the adductor and iliopsoas muscles
 Because earlier surgical intervention is associated with better outcomes, some clinicians recommend screeningBecause earlier surgical intervention is associated with better outcomes, some clinicians recommend screening
radiographic examination in all nonambulatory children with bilateral CP, beginning at 18 months of age andradiographic examination in all nonambulatory children with bilateral CP, beginning at 18 months of age and
repeated every six to 12 monthsrepeated every six to 12 months
 Postural management may have a role in prevention of hip dysplasia.Postural management may have a role in prevention of hip dysplasia.
 When hip subluxation is detected, soft-tissue lengthening is performedWhen hip subluxation is detected, soft-tissue lengthening is performed
 Comprehensive hip reconstruction can be performed in children younger than four years old who are moreComprehensive hip reconstruction can be performed in children younger than four years old who are more
severely affected but have not developed advanced degenerative changes of the femoral headseverely affected but have not developed advanced degenerative changes of the femoral head
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110. PHYSICAL THERAPYPHYSICAL THERAPY
 Physical therapy is typically started early and continued by the parentsPhysical therapy is typically started early and continued by the parents
at homeat home
 Interventions attempt to reduce muscle toneInterventions attempt to reduce muscle tone
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111.  Family-centered care is directed toward optimizing function/minimizing handicapFamily-centered care is directed toward optimizing function/minimizing handicap
(habilitation).(habilitation).
 Interdisciplinary clinics: to provide multiple services (medical, surgical, therapy,Interdisciplinary clinics: to provide multiple services (medical, surgical, therapy,
etc.) coordinated with primary care physicianetc.) coordinated with primary care physician
 Education services: recent emphasis on inclusion/mainstreaming; for manyEducation services: recent emphasis on inclusion/mainstreaming; for many
children, special education services are still required and appropriatechildren, special education services are still required and appropriate
 Physical, occupational, speech/language therapy, other allied health professionals:Physical, occupational, speech/language therapy, other allied health professionals:
therapy provided in home, school, and hospital settings, directed primarily attherapy provided in home, school, and hospital settings, directed primarily at
improved functioning in the areas of mobility, self-care, and communication;improved functioning in the areas of mobility, self-care, and communication;
orthodontists for braces.orthodontists for braces.
 Social services: provided in a variety of contexts to aid in the coordination of careSocial services: provided in a variety of contexts to aid in the coordination of care
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112. CONSTRAINT THERAPYCONSTRAINT THERAPY
 Constraint-induced movement therapy (CIMT) has been used as aConstraint-induced movement therapy (CIMT) has been used as a
treatment for children with hemiplegic cerebral palsytreatment for children with hemiplegic cerebral palsy
 Children with hemiplegia avoid using the affected limb, in a processChildren with hemiplegia avoid using the affected limb, in a process
termed "developmental disregard“termed "developmental disregard“
 CIMT aims to promote function of the affected limb by encouragingCIMT aims to promote function of the affected limb by encouraging
its use through intermittent restraint of the unaffected limb duringits use through intermittent restraint of the unaffected limb during
therapeutic taskstherapeutic tasks
 The method of restraint varies from holding a child's hand to casting,The method of restraint varies from holding a child's hand to casting,
and the length of time in the restraint varies from 1 to 24 hours a dayand the length of time in the restraint varies from 1 to 24 hours a day
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113. ELECTRICAL STIMULATIONELECTRICAL STIMULATION
 Electrical stimulation has been used in an effort to increase muscleElectrical stimulation has been used in an effort to increase muscle
strength in children with cerebral palsy.strength in children with cerebral palsy.
 In neuromuscular electrical stimulation (NMES), electrical impulsesIn neuromuscular electrical stimulation (NMES), electrical impulses
of high intensity and short duration generate muscle contractionof high intensity and short duration generate muscle contraction
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114. FEEDING DISORDERSFEEDING DISORDERS
 Problems with sucking and swallowing are common in children withProblems with sucking and swallowing are common in children with
CP, and can interfere with nutrition and quality of life, and causeCP, and can interfere with nutrition and quality of life, and cause
complications such as aspiration pneumonia.complications such as aspiration pneumonia.
 Gastrostomy feeding may improve nutrition in severely affectedGastrostomy feeding may improve nutrition in severely affected
children, and it reduces, but does not eliminate, aspirationchildren, and it reduces, but does not eliminate, aspiration
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115. DROOLINGDROOLING
 Oromotor dysfunction in children with CP often leads to drooling, which is aOromotor dysfunction in children with CP often leads to drooling, which is a
significant impediment to social acceptancesignificant impediment to social acceptance
 Approaches to improve drooling include medication, behavior therapy, and surgery.Approaches to improve drooling include medication, behavior therapy, and surgery.
Anticholinergic agents, such as benzhexol hydrochlorideAnticholinergic agents, such as benzhexol hydrochloride
(trihexyphenidyl hydrochloride), scopolamine, or glycopyrrolate may be effective(trihexyphenidyl hydrochloride), scopolamine, or glycopyrrolate may be effective
by decreasing the flow of salivaby decreasing the flow of saliva
 Another approach is injection of botulinum toxin A (BTX) into the salivary glandsAnother approach is injection of botulinum toxin A (BTX) into the salivary glands
 Surgical treatment of drooling is directed at reducing salivary productionSurgical treatment of drooling is directed at reducing salivary production
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116. Additional TreatmentAdditional Treatment
 Comorbid conditions must be identified and appropriately managed.Comorbid conditions must be identified and appropriately managed.
 General MeasuresGeneral Measures
 Referral to early intervention for children ages 0–3 is essential.Referral to early intervention for children ages 0–3 is essential.
 Various therapy modalities enhance functioning:Various therapy modalities enhance functioning:
 Physical therapy: Posture stability and gait, motor strength and control, contracture preventionPhysical therapy: Posture stability and gait, motor strength and control, contracture prevention
 Occupational therapy: Functional activities of daily living and other fine motor skillsOccupational therapy: Functional activities of daily living and other fine motor skills
 Speech therapy:Speech therapy:
 Verbal and nonverbal speechVerbal and nonverbal speech
 Aid in feeding and other oromotor skillsAid in feeding and other oromotor skills
 Equipment optimizes participation in activities:Equipment optimizes participation in activities:
 Orthotic splinting: Maintains functional positioning and prevents contractruresOrthotic splinting: Maintains functional positioning and prevents contractrures
 AFOs (ankle-foot orthosis)AFOs (ankle-foot orthosis)
 DAFOs (dynamic ankle-foot orthosis)DAFOs (dynamic ankle-foot orthosis)
 Spinal bracing (body jacket) may slow scoliosisSpinal bracing (body jacket) may slow scoliosis
 Augmentative communication: Pictures, switches, or computer systems for nonverbal individualsAugmentative communication: Pictures, switches, or computer systems for nonverbal individuals
 Electrical stimulation: Therapeutic and functionalElectrical stimulation: Therapeutic and functional
 Use of adaptive equipment such as standers to allow weight bearingUse of adaptive equipment such as standers to allow weight bearing
 Mobility: Crutches, walkers, wheelchairsMobility: Crutches, walkers, wheelchairs
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117. SOCIALAND PSYCHOLOGICALSOCIALAND PSYCHOLOGICAL
SUPPORTSUPPORT
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118. Follow-UpFollow-Up
 Requirements for follow-up vary greatly with the degree of disabilityRequirements for follow-up vary greatly with the degree of disability
and the scope of impairments. An interdisciplinary clinic setting mayand the scope of impairments. An interdisciplinary clinic setting may
be more appropriate for a child with severe CP.be more appropriate for a child with severe CP.
 Early referral to a pediatric orthopedist is indicated, especially forEarly referral to a pediatric orthopedist is indicated, especially for
monitoring of early hip subluxation, which is best managed beforemonitoring of early hip subluxation, which is best managed before
progression to frank dislocation.progression to frank dislocation.
 Early referral for developmental assessment to establish need for earlyEarly referral for developmental assessment to establish need for early
intervention, to optimize development, and to promote family copingintervention, to optimize development, and to promote family coping
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119. PITFALLSPITFALLS
 Overdiagnosis of CP in infants with spastic hypertonia (especiallyOverdiagnosis of CP in infants with spastic hypertonia (especially
those born prematurely); normalization of tone/function may take up tothose born prematurely); normalization of tone/function may take up to
2 years.2 years.
 Slowly progressive neurogenerative disease may masquerade as CP.Slowly progressive neurogenerative disease may masquerade as CP.
 Cervical cord lesions may masquerade as quadriparetic spastic CP.Cervical cord lesions may masquerade as quadriparetic spastic CP.
Swallowing reflexes may be preserved; cognitive development isSwallowing reflexes may be preserved; cognitive development is
normal.normal.
 Determination of ideal body weight may be complex in CP; growthDetermination of ideal body weight may be complex in CP; growth
standards according to CP type are under developmentstandards according to CP type are under development
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120. The prognosisThe prognosis
 The prognosis for survival and motor function in children with CP isThe prognosis for survival and motor function in children with CP is
highly variable, and depends on the severity and type of the CPhighly variable, and depends on the severity and type of the CP
syndrome. Nearly all children with hemiplegic CP will walk. Thesyndrome. Nearly all children with hemiplegic CP will walk. The
prognosis for walking is poor in children who do not achieve headprognosis for walking is poor in children who do not achieve head
balance by 20 months, retain primitive reflexes, or have no posturalbalance by 20 months, retain primitive reflexes, or have no postural
reactions by 24 monthsreactions by 24 months
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121. Return to index