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Cerebral palsy summary


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Cerebral palsy summary

  1. 1. Cerebral Palsy  Dr Surya Kumar
  2. 2. Cerebral Palsy = Brain Paralysis Definition Prevalence Etiology Classifications Clinical Presentation Treatments Substantially Disabling
  3. 3. Cerebral Palsy: Definition Cerebral palsy is a static encephalopathy Encephalopathy = Brain Injury that is non- progressive disorder of posture and movement Variable etiologies Often associated with epilepsy, speech problems, vision compromise, & cognitive dysfunction
  4. 4. LATEST DEFINITION OF CEREBRAL PALSY “Cerebral palsy describes a group of permanent disorders of the development of movement and posture causing activity limitation that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication and behavior, by epilepsy, and by secondary musculoskeletal disorders” Rosenbaum P et al: Dev Med Child Neurol (Suppl.) 2007;109:8-14
  5. 5. Cerebral Palsy: Classification Various classifications of Cerebral Palsy Physiologic Topographic Etiologic
  6. 6. Cerebral Palsy: Physiologic Athetoid Ataxic Rigid-Spastic Atonic Mixed
  7. 7. Cerebral palsy Classification According to Pattern of involvement Monoplegia : one limb / rare Diplegia : both LL >> UL / good intelligence / prematurity Hemiplegia : unilateral usually UL > LL / 33 % seizures 50 % mentally retarded Triplegia : rare / usually both LL + one UL Quadriplegia : total body / often mentally retarded / with seizures / severe hypoxia Double hemiplegia : bilateral UL > LL
  8. 8. Cerebral palsy Classification According to Type of motor dysfunction Spastic 65 % Athetoid 10 % Ataxic 5 % Mixed 12 % Hypo tonic 1 %
  9. 9. Gross motor functional classification system Level Function I Ambulatory in all settings II Walks without aides but has limitations in community settings III Walks with aides IV Mobility requires wheelchair or adult assist V Dependent for mobility
  10. 10. Etiology Prenatal – 70 to 80 % Natal - Upto 10 % Rest postnatal Upto 5 year ? ( Veena kalra AIIMS)
  11. 11. “ASPHYXIA” AND CP IN THE NCPP STUDY 2 3 C H IL D R E N W IT H O T H E R R E A S O N S F O R C P 1 2 < 2 K G , 1 4 N O N -C N S A N O M A L Y 1 M IC R O C E P H A L Y , 7 P R E N A T A L R IS K 1 7 C H IL D R E N "P U R E " A S P H Y X IA L D A M A G E < 1 0 % O F A L L C P 1 P E R 2 ,7 0 0 B IR T H S 4 0 C H IL D R E N W IT H A N Y A S P H Y X IA IN D IC A T O R 1 4 9 C H IL D R E N W IT H N O A S P H Y X IA IN D IC A T O R 1 8 9 C H IL D R E N W IT H C P 4 5 , 4 4 9 C H IL D R E N
  12. 12. All four criteria must be met: Evidence of metabolic acidosis: umbilical artery pH<7 and base deficit ≥12 mmol/L at delivery Early onset of severe or moderate neonatal encephalopathy in infants ≥34 weeks of gestation Cerebral palsy of the spastic quadriplegic or dyskinetic type Exclusion of other identifiable etiologies (eg, trauma, coagulation disorders, infection, genetic disorders) Task force on neonatal encephalopathy and cerebral palsy criteria for Adapted from: Neonatal Encephalopathy and Cerebral Palsy: Executive Summ
  13. 13. A sentinel hypoxic event occurring immediately before or during labor A sudden and sustained fetal bradycardia or absence of fetal heart rate variability in the presence of persistent late or variable decelerations. This usually occurs after a hypoxic sentinel event with a normal fetal heart rate pattern prior to the event. Apgar score of 0 to 5 after five minutes Onset of multisystem involvement within 72 hours of birth Early imaging studies showing evidence of an acute nonfocal cerebral abnormality Peripartum events that may be related to development of cerebral palsy but which are not specifically asphyxial insults Adapted from: Neonatal Encephalopathy and Cerebral Palsy: Executive Summary. Obstet Gynecol 2004; 103:780.
  14. 14. Table 1 Mimics of cerebral palsy disorder Clue Familial spastic paraplegia Family history Transient toe walking Normal deep tendon reflexes Muscular dystrophy Calf hypertrophy, positive Gower’s sign Metabolic disorders Regression, lethargy, unusual vomiting Sjogren-Larrson Ichthyosis Lesch-Nyhan Severe self- mutilation Mitochondrial disorders Recurrent stroke, cardiomyopathy,
  15. 15. Impaired movements • 65% speech defects • 50% are mentally retarded • 50% ocular defects • 25% hearing impairment • 40% seizure disorders • 20% seriously disabled • 1.5 to 2.5 per 1,000 births will result in severe to moderately severe
  16. 16. Static Vs slowly progressive neurological disorder Global devlopmental delay/ differential devlopmental delay
  17. 17. Disorder Gross motor Fine motor Social language Mental retardation Delay + + to + + + ++ t+++ +++ Cerebral palsy Delay +++ ++ + + CP with MR +++ +++ +++ +++ Hearing impairment No No No +++ Impaired vision ++ + Spinal muscular atrophy ++ + + to ++ No Expressive may be delayed
  18. 18. Levine ( poster) criteria P- Posturing/ abnormal movement O- oropharyngeal problems (normality tongue thrust and swallowing abnormality S- strabismus T – tone ( hyper to hypo) E- Evolutional maldevlopment ( persistent primitive reflexex or protective / equilibrium reflexes fail to devlop ( parachute reflex) R – reflexes ( increased deep tendon/ persistent babinski
  19. 19. Difficulty to diagnose CP during the 1st year of life 1. Hypotonia more common then hypertonia in 1st yr 2. early abundance of primitive reflexes may confuse 3. limited variety of volitional movement for evolution 4 subtantioal myelination takes months to evovle 5 most instace of CP doesn’t have substancial risk fac
  20. 20. What behaviour symptoms during 1st year arouse suspicion of CP 1. excessive irritablity, crying , sleep difficulties 2. early feeding difficulties ( Co-ordination of sucking and swallowing) 3. Jitter or jerky behavoiur 4. easily startle behaviour 5. Stiffness during dressing , diaper, hand washimg 6. paradoxical precocious devlopment  a , early rolling ( actually sudden reflex roll rathe then volitional Stiff leg standing
  21. 21. Feature suggestive of progressive rather then CP 1. Abnorma increase in heaad circumference Eye abnormalities Skin abnormalty Hepatomegaly and / or spleenomegaly Decrease or absent deep tendon reflex Sensory abnormalities Devlopmental regression ( Rett syndrome )
  22. 22. Head and Neck Findings • 24% inability to chew • 20% inability to swallow easily • 20% frequent dental caries • High rate of temporo-mandibular disorders
  23. 23. Positive signs of spastic CP include: Spastic hypertonia Hyperreflexia caused by hyperexcitability of the stretch reflex Extensor plantar responses Clonus
  24. 24. Negative signs of spastic CP include: Slow effortful voluntary movements Impaired fine-motor function Difficulty in isolating individual movements Fatiguability
  25. 25. Athetoid CP Findings (con’t) • Grimacing • Drooling • Speech defects • Continuous mouth breathers • Excessive head movements • Tongue protrusion • Primitive reflexes of varying severity
  26. 26. ASSOCIATED DISORDERS Intellectual disability Children with spastic quadriplegia are typically the most severely affected, while cognitive function usually is better with dyskinetic CP that is mainly athetoid Psychiatric disorders including emotional lability, poor attention and vigilance, and obsessive-compulsive traits Epilepsy most common in patients with spastic quadriplegia and acquired hemiplegia, and less common in mild symmetric spastic diplegia and CP that is mainly athetoid
  27. 27. Visual disorders strabismus and clinically significant refractive errors each occurred in 50 percent, and amblyopia and visual field defects each Speech impairment including aphasia and dysarthria, occur in about 38 percent of children with CP Hearing impairment most common in those with very low birthweight or severe hypoxic-ischemic insults Pulmonary disease a leading cause of death among patients with severe CP Growth failure Urinary disorders Orthopedic disorders Osteopenia
  28. 28. DIAGNOSIS The diagnosis of CP depends upon a combination of findings, including motor delay, neurologic signs, persistence of primitive reflexes, and abnormal postural reactions Neurobehavioral signs Motor abnormalities Developmental reflexes Laboratory studies serum concentrations of glucose, thyroid, ammonia, lactate and pyruvate, plasma amino acid analysis, urine organic acid analysis, and arterial acid-base status, should be obtained to exclude a metabolic disorder
  29. 29. NEUROIMAGING FOR CP [Bax et al JAMA 2006;296:1602] Emerging imaging modalities will likely provide further insight into the etiology of CP by making imaging easier in children (PROPELLAR) and by mapping white matter tracts (DTI). The American Academy of Neurology now recommends that all cases of cerebral palsy of unknown origin undergo neuroimaging Most children with cerebral palsy have abnormal neuroradiological findings, white matter damage being the most common.
  30. 30. lgorithm for the evaluation of the child with cerebral palsy (CP)
  31. 31. Cerebral palsy Clinical Assessment Goals of Physical Examination Determine grades of muscle strength and selective control. Evaluate muscle tone and determine type. Evaluate degree of deformity / contracture at each joint. Assess linear, angular and torsional deformities of spine, long bones, hands and feet. Appraise balance, equilibrium and standing / walking posture.
  32. 32. Cerebral palsy Goals of Management (Treatment) Turn focus of parents from the disease to the goal- oriented approach needs time and a lot of discussion Physician and Physiotherapist must have the same perspective
  33. 33. Cerebral palsy Types of Management (Treatment) Physical therapy Orthotics Control of spasticity Orthopedic surgery
  34. 34. Cerebral palsy Spasticity Approaches : Selective dorsal rhizotomy Intrathecal baclofen Botulinum-A toxin
  35. 35. Cerebral palsy Selective Dorsal Rhizotomy Cut 30 – 50 % of abnormal dorsal rootlets L2 - S1 Followed by intensive physiotherapy Results encouraging May cause hyperlordosis / hip subluxation Best for : spastic diplegia, 4-8 yrs, no previous surgery, no contractures, no extra pyramidal signs ? Not enough alone Orthopedic procedures obtain similar results
  36. 36. Cerebral palsy Baclofen GABA agonist – inhibits release of excitatory neurotransmitter at level of spinal cord Oral : mixed reports/ side effects/ not selective Continuous intrathecal – implantable pump Good results in releasing spasticity, and improving function Complications of pump and catheter Needs specialized centers
  37. 37. Cerebral palsy Botulinum-A toxin Acts at myo-neural junctions Inhibits exocytosis of Acetylcholine Inject selected muscles at multiple sites Spasticity reduction may last up to 6 months Reversible , painless , minimal side effects Most patients still require lengthening for permanent correction Role : - Facilitates physiotherapy and mobilization - Delays surgical management - Trial to determine effects of specific proposed surgical treatment
  38. 38. Cerebral palsy Physical Therapy Involve parents as much as possible (even if they resist) Do not raise false hopes which could increase frustration
  39. 39. Cerebral palsy Physical Therapy There is no evidence that any type of physical therapy can have a beneficial lasting effect on motor function beyond early to middle childhood (age 4-8 years). Thomas S. Renshaw ( Lovell & Winter’s Pediatric Orthop.)
  40. 40. Cerebral palsy Orthotics Immobilization may cause atrophy Night splints : - Do not prevent nor reduce deformity - may cause irritation, pain or stimulate reflexes in spastic muscles and relaxes the weaker apponents – thus may increase deformity rather than reduce it ! May be useful only in Athetoid
  41. 41. Cerebral palsy Prerequisites foreffective surgery Type : spastic Extent : hemiplegics / diplegics : good results quadriplegics : minimal improvement Age : 3- 12 years IQ : good Good upper limb function : for walking Underlying muscle power : not weak Walker / non-walker : surgery hardly changes state but improves gait
  42. 42. Cerebral palsy Prerequisites foreffective surgery Type : spastic Extent : hemiplegics / diplegics : good results quadriplegics : minimal improvement Age : 3- 12 years IQ : good Good upper limb function : for walking Underlying muscle power : not weak Walker / non-walker : surgery hardly changes state but improves gait
  43. 43. Cerebral palsy Timing For Orthop Surgery For structural changes : Early e.g. Hip subluxation , usually <5 years To improve function ( gait ) : defer until walking ( independently / with aids ) until gait pattern develops and could be assessed walking : 18 – 21 months in hemiplegia 3 – 4 years in spastic diplegia Optimum time of lower extremity surgery 5 – 7 years: can analyze and observe gait pattern
  44. 44. The ‘‘Birthday Syndrome’’ One group of complications related to a chain of operations over the years is social isolation, loss of motivation, frustration, and psychosocial problems termed the birthday syndrome.31
  45. 45. SEMLARASS Single Event Multilevel Lever Arm Restoration Anti Spasticity surgery
  46. 46.  Thanks