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CEREBRAL PALSY

CEREBRAL PALSY. Dr. Maninder S. Dhaliwal. Define. Is defined as a : Persistent but not unchanging Disorder of movement, tone and posture Due to non-progressive defect/lesion Of immature brain ( fetal life, infancy, childhood) ( immature brain cut off take as 5 yrs –AAP).

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CEREBRAL PALSY

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  1. CEREBRAL PALSY Dr. Maninder S. Dhaliwal

  2. Define Is defined as a : • Persistent but not unchanging • Disorder of movement, tone and posture • Due to non-progressive defect/lesion • Of immature brain ( fetal life, infancy, childhood) ( immature brain cut off take as 5 yrs –AAP)

  3. 5) Commonly associated with a spectrum of developmental disabilities such as – • Mental retardation (60%) • Epilepsy (33%) • Visual , hearing (deafness-10%) and speech defects • Strabismus(50%) • Cognitive dysfunction • Sensory problems • Emotional and behavioral problems.

  4. EXCLUDING progressive pathology and lesion of spinal cord. • INCLUDING non-progressive genetic d/s or cong malformation

  5. TOPOGRAPHIC MONO HEMI DIPLEGIA QUADRI DOUBLE HEMIPLEGIA TRIPLEGIA PHYSIOLOGY SPASTIC EXTRAPYRAMIDAL ATAXIC MIXED ATONIC CLASSIFICATIONS

  6. FUNCTIONAL • CLASS 1 – NO limitation of activity • CLASS 2 – Slight limitation • CLASS 3 – Moderate limitation • CLASS 4 – No useful physical activity

  7. Site of brain injury Cortical Sub – cortical Periventricular Basal ganglia Cerebellum Brain stem Pathological Periventricular leucomalacia –spastic diplegia Stroke in utero - hemiplegia Multifocal encephalomalacia -quadriplegia Cerebellar - ataxic Basal ganglia, thalmus, putamen - dyskinetic

  8. Severity • Motor development quotient : = motor age / chronological age × 100 >70 : minimal – deviancy without delay 50-70 : mild motor disorder <50 : classical CP

  9. Prenatal I, iron def.,poor –nut. Inf, UTI, high fever Chorioamniotis HTN, DM Teratogens Poor ANC LOW SES Twins Fetal vasculopathy Perinatal Birth asphyxia Premature / LBW IUGR Hyperbilirubenemia IVH Sepsis, pneumonia, meningitis Develop. malformation Etiological • Postnatal • CNS infections • Head injuries • Seizures • Hypoxic damage • Hyperpyrexia damage

  10. SLOW head growth Poor head control Eye – roving eyes, poor hand regard, persistent squint. Ear – lack of auditory response Irritability, seizures, poor suck, poor quality of sleep. Extreme sensitivity to light Cortical thumb beyond 8 weeks Handedness before 2 yrs Paucity of limb movements Scissoring of lower limbs Toe walking Abnormal tone Persistence of primitive reflexes or failure to acquire postural reflexes Stereotypic abnormal movements Lack of alertness Early markers of CP

  11.  Differential diagnosis • In the early infancy when the child is in hypotonic phase, neuromuscular conditions like myopathies may cause diagnostic confusion. • Children with mental retardation may have hypotonia but do not have abnormal motor patterns or postures

  12. Neurodegenerative conditions which have onset in early infancy such as Tay-Sach disease, Krabbe's disease, and Metachromatic Leucodystrophy can mimic CP. • The progressive course of these conditions can be ascertained on the basis of history, and relevant investigation can confirm the diagnosis.

  13. Dopa-responsive dystonia and organic aciduria like glutaric aciduria may look like dystonic CP.

  14. Assessment of General Health • Growth, and nutritional disorders • Frequent respiratory tract infections are common because of ineffective cough reflex. • Facial dysmorphism and other congenital anomalies should be noted. • Skin should be inspected for neurocutaneous stigmata. • Head circum­ference should be noted and plotted .

  15. Reliable measures of length may be difficult to obtain due to concomitant contractures or scoliosis. • Alternate measures to length such as segmental measures of upper arm and lower leg are sometimes used. • Skinfold thickness is a useful and a less cumbersome method of assessing nutritional status.

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