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DEFINITION. A group of chronic disorders impairing control of movement that appear in the first few years of life and generally do not worsen over time.. Epidemiology . Incidence : 2 per 1000 live births.90% cases : No intrapartum cause found.Remaining 10% cases: Hypoxia may have had antena

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2. DEFINITION A group of chronic disorders impairing control of movement that appear in the first few years of life and generally do not worsen over time.

3. Epidemiology Incidence : 2 per 1000 live births. 90% cases : No intrapartum cause found. Remaining 10% cases: Hypoxia may have had antenatal/intrapartum origins.

4. ETIOLOGY Congenital : 85% Acquired : 15% Genetic : small % age

5. PRENATAL FACTORS Maternal pathology : Systemic diseases. Prenatal nutrition. Infections (TORCH). Trauma. CO poisoning.

6. Contd. FETAL CONDITIONS - twinning - arterial occlusion in utero - blood dyscrasias

7. Contd. PLACENTAL & CORD ABNORMALITIEs chronic placental insufficiency true knots/tight cord around neck abruptio placentae. chorioamnoinitis.

8. Perinatal factors Prematurity/LBW ICH/skull # Breech Neryous system malformations.

9. POSTNATAL FACTORS CNS infections Head injury ICH/Thrombosis Late onset/mistreated hydrocephalous Toxic poisoning

10. TYPES OF LESIONS Pre/Sub/Ependymal . Encepholopathy. Neuropathy.

11. CLASSIFICATION BY GEOGRAPHIC INVOLVEMENT Quadriplegia: basal nuclei,brain stem,cortical lesions. Hemiplegia:periventricular Diplegia: periventricular (commonest)

12. CLASSIFICATION(Contd.) By physiologic type: SPASTIC: Cortex ATHETIOD: Basal ganglion ATAXIC: Cerebellum HYPOTONIC: Cerebellum MIXED

13. Problems in defining the cause & timing of neuropathology of CP. CP not diagnosed until mths./yrs. after birth. Retrospective review. Signs of fetal compromise neither sensitive nor specific to a cause/timing of the cause. Proven metabolic acidemia can be due to a chronic/acute hypoxic event.

14. CRITERIA TO DEFINE ACUTE INTRAPARTUM HYPOXIC EVENT Essential criteria : Intrapartum umbilical arterial cord blood pH < 7 and base deficit = > 12 mmol/ l. Early onset severe or mod. neonatal encephalopathy in infants >34 wks. Spastic quadriplegic or dyskinetic CP

15. Contd. Non specific additional criteria: Sentinel hypoxic event occuring just before or during labour. Sudden deterioration of FHR following the above event AS 0-6 > 5 mins. Early evidence of multisystem involvement Early imaging evidence of acute cerebral abnormality

16. Predicting CP in Neonatal Nursery Term babies: Clinical staging by Sarnat(76) . Preterm babies:(Lacey et al,97) Coarse jitters. Asymmetrical neck reflex. Stereotypical repetive movements. Hypertonia.

17. DIAGNOSIS Test motor skills Check infants medical history Reflexes Hand preference Rule out other disorders causing movement problems

18. INVESTIGATIONS CT Scan MRI / Magnetic resonance spectroscopy Ultrasound

19. PATHOPHYSIOLOGY Dec. C.B.F. hypoxia / ischemia of brain Opening of calcium channels Inc. in lactate due to anaerobic glycolysis Dec high energy phosphates

20. Contd. Redistibution of CO,inc. CBF at the cost of autoregulation leads to cerebral edema Inc. glutamate conc. causes rapid and delayed cell death by osmotic lysis & free radical activation

21. Management Preventive mgt. Neuroprotection: Mag.Sulf. Steroids. Excitatory amino acid inhibitors. Conventional therapy for CP.

22. Malpractice Claims Is cerebral palsy preventable?

23. MALPRACTICE CLAIMS Find out , if possible, the reasons behind the decision for claim Offer to meet parents and to go thru clinical history Evaluate the childs current condition Study neonatal records Review obst. care

24. Conclusion Large majority of pathologies are multifactorial & mostly unpreventable reasons during fetal development and neonatal period.

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