cerebral palsy

Cerebral palsyDr.Nebal waill

Definition (historical) Non progressive disorder of motion and /or posture secondary to an insult in the developing brain.


CP is a static encephalopathy . Despite the static nature , it’s peripheral manifestations can seem to progress and mimic progressive CNS pathology.


Delay in clinical expression in static brain lesion reflects changes in maturation function & distribution of various neurotransmitters

Etiology PrenatalPerinatal postnatal

Most children with CP had been born at term with uncomplicated labors and deliveries.For many decades the belief that birth complications caused most cases of cerebral palsy was widespread among physicians , families and even medical researchers less than 10% of children with CP had evidence of intrapartam asphyxia


Classification Etiologic classification Topographic classification Functional classification Physiologic classification



Physiologic classification Spastic 70%-80%Dyskinetic 10%-15% or dystonic ( extrapyramidal CP)Ataxic < 5% ( cerebellar )Hypotonic or atonic mixed


Topographic classification Spastic cases further classified according to the involvement of extremities Quadriplegic 10-15%Diaplegic 30-40%Hemiplegic 20-30%Monoplegic Double hemipleic Triplegic

Functional classification Mild Moderate Severe

Etiologic classification Congenital Acquired


Spastic Diplegic bilateral spasticity of the legs more than the arms. 1st indication (commando crawl). difficult in application of a diaper. unable to sit .increase reflexes , ankle clonus and bilateral babiniski sign Feet in equinocanus , tiptoe (some time the only manifestation in mild type )normal intellectual development , minimal seizure .causes : prematurity mainly


The ventricular margins are irregular, which is consistent with incorporation of the periventricular cysts of PVL. Mild ventriculomegaly The lateral ventricles are enlarged without hydrocephalus. The periventricular white matter is diminished


if suspended by the axillae = scissoring posture After 2 years contractures appearedDTR may difficult to be elicited because of muscle rigidity Vasomotor changes common



Spastic HemiplegicCauses C/F Focal seizure Later weakness at elbow + wrist Equinus position of the foot Increase DTR , Babiniski , Hoffmann signs Palmer or grasp reflex persists for many years 14 % 1st trimester lesion due to IU arterial ischemic lesion 45% 3rd trimester lesion 30% perinatal lesions mainly infarction of MCA

More than 50% develop seizure 50% have average IQ

Spastic quadriplegic Etiology : in the majority abnormalities in delivery particularly prolonged 2nd stage of labour Pathology : extensive cystic degeneration of brain MRI as above C/F : tone + rigidity of all limbs ( both flexion and extension )Assume decerebrate posture Vasomotor changes are common in extremities Psedobulbar signs difficulty swallowing and recurrent aspiration Optic atrophy Grandmal seizure 50% of patients Intellectual impairment all


Dyskinetic ccc by abnormal movements & posture 2˚ to defective regulation of muscle tone and coordination Spasticity frequently accompanies involuntary movements Damage of extrapyramidal system 2 types Hyperkinetic form ( choreoathetoid movement ) Dystonic form ( abnormal posture )


58% experienced perinatal asphyxia 34% LBW + SGA Evolves from hypotonia then choreoathetosis appear at the 2nd -3rd year of age Some continue manifesting hypotonia Dystonia may appear later ( 3rd decade of life ) Various involuntry movements with spasticity Delayed development of motor functions Skilled hand movement impaired Speech impaired


Impaired swallowing and saliva control Cranial nerves involvement less common Seziure 25%-40%Strabismus 1/3 Optic atrophy rare IQ underestimated ( delayed language and gross motor handicap )MRI brain = high signal intensity at ant. Thalamus , post. Thalamus , posterior Potamen Also changes in basal ganglia


Ataxicsome have signs of cerebellar disorder .mainly due to developmental anomaly of cerebellum . some due to perinatal trauma or perinatal asphyxia



Hypotonic CP Ccc by generalize muscular hypotonia that persists beyond 2-3 yr of age & not result from 1 disorder of muscle or nerve.DTR = normal or hyperactive 50% develop frank cerebellar signs My be a forruner to ECP although the majority of the latter develop involuntry movement before 3 yr Cause unknown MRI no significant anatomical changes


Mixed form minor amounts of athetotic posturing in hight % of children with spastic hemiparesis Extensor planter in patient with predominantly extrapyramidal disease Hyperreflexia , spasticity and contractures in child with frank dystonia or othere extrapyramidal movements


Ataxia Spasticity, stiff muscles and exaggerated reflexes. plegia – Hemiplegia • Impaired walk caused by asymmetrical walking gait Irritability.Variations in muscle tone, from too stiff to too floppy. Excessive drooling or difficulties swallowing, sucking or speaking. Tremors. Abnormal sensation and perception. Impairment of sight, hearing or speech. Seizures. Difficulty with precise motions. Mental retardation Clinical presentation


Diagnosis No definitive lab studies Studies to rule out other causes Brain US CT scan MRI brain DTI & FT EEG Evoked potential s


Diagnosis Other studies to rule out other causes like TFT , lactate & pyruvate level , organic and amino acid , chromosomes & CSF protein US predictive for very preterm newborn at risk of cerebral palsy CT brain : cong. Malformation , IVH , PVLMRI : location & extent of malformations DTI & FT : orientation and integrity of white matter fibers EEG: diagnosis of seizure Evoked potentials : detect abnormalities of hearing and vision

T2- MRI : no neural tract seen DTI tractographic assessment at different views

treatment Multidisciplinary team daily activities exercises physical or occupational therapy walkers , poles and standing frames motorized wheelchairs Communication skills Psyghologist psychiatrist ophthalmologist Drugs Surgical therapy



drug Dantrolene sodium benzodiazepines baclofen Botulism toxin injected into muscle Botulism toxin injected in to salivary glands Anticholinergic levo-dopa Carbamazepinetrihexyphenidyl Constipation and recurrent chest infection treatment


Surgical therapy Tenotomy of the hip adductors Hamstring lengthening Lengthening of the heel cords Lengthening of the posterior tibial tendons Usually at age of 4-8 yr. Procedures involve bone for fixed deformities Rhizotomy : selective sectioning of post. Roots of spinal cord Difficult to decide performing these procedures for mentally retarded CP child


Associated problems The likelihood and severity of associated impairments increases with the severity of motor impairment.Musculoskeletal deformities Intellectual impairment Speech impairments Visual impairment Hearing impairments Feeding and nutrition Urogenital impairment Epilepsy Spinal deformities Teeth problems

Special aids Glasses Hearing aids SplintsSpecial shoes WheelchairsCommunication aid

Causes & risk factors Maternal and prenatal 70-80%Long menstrual cycle Previous pregnancy loss Previous loss of newborn Maternal mental retardation Maternal theyroid disorder ( iodine deficiency ) Maternal seizure disorder Delivering child with weight less than 2000 gramDelivering child with motor deficit , MR or sensory deficit IU infection Abdominal trauma Blood type incomaptibility Teen ager mother Incompetent cervix Polyhydraminos Treatment of the mother with estrogen or progesterone Multiple gestation ( due to prematurity or LBW )Exposure to high level of lead during pregnancy Maternal antibiotics


Perinatal factors (10%) PrematurityChorioamnionitis BW less than 2500 gram Crowth retardation Nonvertex and face presentation of the fetus Birth asphyxia ( ≤10%)Low apgar score alone can’t be used as an indicator of birth asphyxia ICH


Postnatal factors Infection ( eg meningitis , encephalitis )ICH ( prematurity , trauma , vascular malformation )PVLHI lesion Seizure Kernicterus Neonatal pneumothorax , sepsis Brain injureis as in drowning , car accidents Coagulopathy Persistent fetal circulation or persistent pulmonary HPT of the newborn



Prevention ProvenMMR vaccination Idodine supplement Anti D for Rh –ve mother Transfer of a very preterm infant in utero to tertiary centre Probable Early routine USOvoid excessive alcohol intake in pregnancy Phototherapy for NNJVitamin K at birth to prevent brain hemorrhage Child abuse preventive strategy SIDS preventive strategy EPO has protective effect against HI injury Fetal exposure to magnesium sulfate in women at risk of preterm delivery significantly reduces the risk of CP without increasing the rate of death


Possible Zinc , folate , fish oil to prevent IUGR Operative delivery of fetal distress Rescue therapy for birth asphyxia Doubtful Electronic fetal monitoring for distress Addition of fetal scalp sample or ECG Bed rest for history of growth restriction Hospitalization for multiple pregnancy Antenatal endomethacin or thryotorpin releasing hormone


Prognosis Ultimate social adjustment depends primarily on Severity of physical and mental handicapPresence or absence of associated disabilities including seizures and visual or hearing impairment


Predictors to inability to work :IQ < 50 Non-ambulatory and without communication skills Need assistance to use their hands


All children with spastic hemiparesis became ambulatory Children with spastic diaplegia ambulatory in 86-91%ј of those with extrapyramidal CP are ultimately able to work competitively None of those with spastic quadriparesis was gainfully employed


Adult with CP New functional disabilities Extremities contracture Scoliosis Cervical pain Back pain Reduced mobility at adulthood for mobile patients Speech and self-feeding well preserved Survival rates in ambulatory adults only moderately worser than general population


Hansen got his driver's license on the third try when he was in his mid-20s. He has spastic diplegic cerebral palsy. It mostly affects his legs. He drives with his hands. He and his dad installed a $450 hand control system in his Ford Contour in just a couple of hours. Wil took David Sommerstein for a demo to the gas station and the bank. Wil Hansen in his Ford Contour



Life expectancy in CP child Mild – moderate disability 98% of them live to age of 35 years.Profound handicapped & immobile child >1/3 of them die before age of 30 years.