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cerebral palsy

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cerebral palsy by dr hardev

Publicado en: Salud y medicina
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cerebral palsy

  2. 2. CEREBRAL PALSY • A motor function disorder – caused by permanent, non-progressive brain lesion – present at birth or shortly thereafter. • Non-curable, life-long condition • Damage doesn’t worsen • May be congenital or acquired
  3. 3. A Heterogenous Group of Movement Disorders CEREBRAL PALSY Three distinctive features common to all patients with cerebral palsy : (1) Some degree of motor impairment is present, (2) An insult to the developing brain has occurred,. (3) A neurological deficit is present that is nonprogressive,
  4. 4. In CP • Muscles are unaffected • Brain is unable to send the appropriate signals necessary to instruct muscles when to contract and relax
  6. 6. An insult or injury to the brain –Fixed, static lesion(s) –In single or multiple areas of the motor centers of the brain
  7. 7. • Development Malformations – The brain fails to develop correctly. • Neurological damage – Can occur before, during or after delivery * Unknown in many instances CAUSES
  8. 8. Severe deprivation of oxygen or blood flow to the brain –Hypoxic-ischemic encephalopathy or intrapartal asphyxia CHIEF CAUSE
  9. 9. RISK FACTORS • Prenatal factors – Before birth – Maternal characteristics • Perinatal factors – at the time of birth to 1mo • Postnatal factors – In the first 5 mos of life
  10. 10. Prenatal factors 1)Risk factors inherent to the fetus (most commonly genetic disorders), 2)Factors inherent to the mother (seizure disorders, mental retardation, and previous pregnancy loss),
  11. 11. 3)Factors inherent to the pregnancy itself (Rh incompatibility, polyhydramnios, placental rupture, and drug or alcohol exposure). 4)External factors, such as TORCH (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes simplex),
  12. 12. Perinatal Factors 1)Typically is associated with asphyxia or trauma that occurs during labor. 2)Oxytocin augmentation, 3)Umbilical cord prolapse, 4)Breech presentation all have been associated with an increased occurrence of cerebral palsy. 5)Cerebral palsy often is associated with low Apgar scores during this period
  13. 13. Low-birth-weight infants (<1500 g) are at dramatically increased risk of cerebral palsy. This increased incidence is believed to be due to the fragility of the periventricular blood vessels, which are highly susceptible to physiological fluctuations during pregnancy.
  14. 14. These fluctuations, which include hypoxic episodes, placental pathology, maternal diabetes, and infection, can injure these vessels and lead to subsequent intraventricular hemorrhages. Grading of Periventricular Lesions I Bleeding confined to germinal matrix II Bleeding extends into ventricles III Bleeding into ventricles with dilation IV Bleeding into brain substance
  15. 15. Postnatal Causes Trauma, head injury Infections Lack of oxygen Stroke in the young Tumor, cyst
  17. 17. Classification of CP 1.Geographical Classification1.Geographical Classification 2. Physiological Classification2. Physiological Classification
  18. 18. One extremity involved, usually lower Monoplegia Geographical Classification
  19. 19. Hemiplegia In hemiplegia, one side of the body is involved, with the upper extremity usually more affected than the lower extremity. Patients with hemiplegia, approximately 30% of patients with cerebral palsy, typically have sensory changes in the affected extremities as well.
  20. 20. Hemiplegia limbs on only one side
  21. 21. • Hemiplegia on right side –Hip and knee contractures –Talipes equinus (“tip-toeing” - sole permanently flexed) –Asteriognosis may be present. (inability to identify objects by touch)
  22. 22. Diplegia Diplegia is the most common anatomical type of cerebral palsy, constituting approximately 50% of all cases. Patients with diplegia have motor abnormalities in all four extremities, with the lower extremities more affected than the upper.
  23. 23. The close proximity of the lower extremity tracts to the ventricles most likely explains the more frequent involvement of the lower extremities with periventricular lesions .
  24. 24. Diplegia/ Paraplegia •both legs•both legs w/ slight involvement elsewhere
  25. 25. Diplegia May also have Contractures of hips and knees and talipes equinovarus (clubfoot).
  26. 26. This type of cerebral palsy is most common in premature infants Intelligence usually is normal. Most children with diplegia walk eventually, although walking is delayed usually until around age 4 years.
  27. 27. Quadriplegia In quadriplegia, all four extremities are equally involved, and many patients have significant cognitive deficiencies that make care more difficult Head and neck control usually are present, which helps with communication, education, and seating.
  28. 28. Quadriplegia
  29. 29. Physiological Classification
  30. 30. 3 MAIN TYPES 1. PYRAMIDAL - originates from the motor areas of the cerebral cortex 2. EXTAPYRAMIDAL - basal ganglia and cerebellum 3. MIXED
  31. 31. 4 MAIN TYPES PYRAMIDAL 1. Spastic CP EXTAPYRAMIDAL 2. Athethoid CP 3. Ataxic CP MIXED 4. Spastic & Athethoid CP
  32. 32. Spastic CP • Increased muscle tone, tense and contracted muscles – Have stiff and jerky or awkward movements. – limbs are usually underdeveloped – increased deep tendon reflexes • most common form • 70-80% of all affected
  33. 33. Spastic is the most common form of cerebral palsy, constituting approximately 80% of cases, and usually is associated with injury to the pyramidal tracts in the immature brain.
  34. 34. Booth showed histologically that this altered muscle function leads to the deposition of type I collagen in the endomysium of the affected muscle, leading to thickening and fibrosis, the degree of which correlated to the severity of the spasticity. Joint contractures, subluxation, and degeneration are common in patients with spastic cerebral palsy.
  35. 35. • Spastic Quadriplegia Characteristic “scissors” positions of lower limbs due to adductor spasms.
  36. 36. Athetoid/ Dyskinetic CP • Fluctuating tone – involves abnormal involuntary movements – that disappear during sleep and increase with stress. – Interferes with speaking, feeding, reaching, grabbing, and any other skills – 20% of the CP cases,
  37. 37. Athetoid cerebral palsy is caused by an injury to the extrapyramidal tracts and is characterized by dyskinetic, purposeless movements that may be exacerbated by environmental stimulation.
  38. 38. Choreiform Choreiform cerebral palsy is characterized by continual purposeless movements of the patient's wrists, fingers, toes, and ankles. This continuous movement can make bracing and sitting difficult.
  39. 39. Rigid Patients with rigid cerebral palsy are the most hypertonic of all cerebral palsy patients. These patients have a “cogwheel” or “lead pipe” muscle stiffness that often requires surgical release.
  40. 40. Ataxic CP • Poor balance and lack of coordination – Wide-based gait – Depth perception usually affected. – Tendency to fall and stumble – Inability to walk straight line. – Least common 5-10% of cases Ataxic cerebral palsy is very rare As a result of an injury to the developing cerebellum.
  41. 41. It is important to distinguish true ataxia from spasticity because with treatment many children with ataxia are able to improve their gait function without surgery.
  42. 42. MIXED CP • A common combination is spastic and athetoid • Spastic muscle tone and involuntary movements. • 25% of CP cases, fairly common
  43. 43. Signs and Symptoms OF CEREBRAL PALSY
  44. 44. a. b. c. d. e. f. g. h.
  45. 45. Early Signs • Stiff or floppy posture • Weak suck/ tongue thrust/ tonic bite/ feeding difficulties • Poor head control • Excessive lethargy or irritability/ High pitched cry Infancy (0-3 Months)
  46. 46. • Abnormal or prolonged primitive reflexes Moro’s reflex Asymmetric tonic neck reflex Placing reflex Landau reflex Early Signs
  47. 47. Late infancy • Inability to perform motor skills as indicated: – Control hand grasp by 3 months – Rolling over by 5 months – Independent sitting by 7 months • Abnormal Developmental Patterns: – Hand preference by 12 months – Excessive arching of back – Log rolling – Abnormal or prolonged parachute response
  48. 48. Abnormal Developmental Patterns after 1 year of age: • “W sitting” – knees flexed, legs extremely rotated • “Bottom shuffling” Scoots along the floor • Walking on tip toe or hopping
  49. 49. Behavioral Symptoms • Poor ability to concentrate, • unusual tenseness, • Irritability
  51. 51. • Hearing and visual problems • Sensory integration problems • Failure-to-thrive, Feeding problems • Behavioral/emotional difficulties, • Communication disorders • Bladder and bowel control problems, digestive problems (gastroesophageal reflux) • Skeletal deformities, dental problems • Mental retardation and learning disabilities in some • Seizures/ epilepsy
  52. 52. Diagnosis OF CEREBRAL PALSY
  53. 53. History and physical examination are the primary tools in making the diagnosis of cerebral palsy. The history should include a thorough investigation of the pregnancy and delivery. Ancillary studies, such as radiographs, hematological studies, chromosomal analysis, CT, MRI, and positron emission tomography, rarely are needed to make the diagnosis, but may be helpful in determining the type and extent of cerebral palsy present.
  54. 54. Diagnosis of cerebral palsy before age 2 years can be very difficult. Nelson and Ellenberg found that 55% of children diagnosed with cerebral palsy by 1 year of age did not meet the criteria by age 7 years. Transient dystonia of prematurity is a condition characterized by increased tone in the lower extremities between 4 and 14 months old and often is confused with cerebral palsy.
  55. 55. ASSESSMENT
  56. 56. CRITERIA P osturing / Poor muscle control and strength O ropharyngeal problems S trabismus/ Squint T one (hyper-, hypotonia) E volutional maldevelopment R eflexes (e.g. increaseddeep tendon) *Abnormalities 4/6 strongly point to CP
  57. 57. Treatment OF CEREBRAL PALSY
  58. 58. - No treatment to cure cerebral palsy. - Brain damage cannot be corrected. • Crucial for children with CP: –Early Identification; –Multidisciplinary Care; and –Support
  59. 59. NON OPERATIVE TREATMENT • Commonly used as primary treatment or in conjuction with surgery  Medication  Splinting  bracing  Physical therapy
  60. 60. MEDICAL MANAGEMENT • Common agents - diazepam - baclofen - dantrolene - botulinum toxin
  61. 61. Oral agents: Dantrolene-acts at the level of skeletal muscle and decreases muscle calcium ion release. It has an affinity for fast twitch muscle fibers and selectively decreases abnormal muscle stretch reflexes and tone. Diazepam- increases inhibitory neurotransmitter activity (GABA) Baclofen -inhibit abnormal monosynaptic extensor activity and poly synaptic flexor activity and decrease substance P levels
  62. 62. Intrathecal injection of baclofen requires 1/30 the dose of oral baclofen to achieve a similar or better response. An implantable programmable pump dramatically decreases the dose required to affect spasticity and decreases some of the side effects such as sedation. This pump typically is implanted subcutaneously in the abdominal wall and requires refilling approximately every 2 to 3 months.
  63. 63. • -intrathecal baclofen injection
  64. 64.  Botulinum toxin type A (BTX-A) (Botox, Dysport) has been used to weaken muscles selectively in patients with cerebral palsy.  BTX-A injected directly into the muscle acts at the level of the motor end plate, blocking the release of the neurotransmitter acetylcholine and inhibiting muscle contraction  This effect begins approximately 24 hours after injection and lasts 2 to 6 monthsCare – Intra muscular botulinum toxin for 2-6 months – Safe maximal dose 36-50 U/kg
  65. 65. Physical therapy Physical therapy typically is used as a primary treatment modality and in conjunction with other modalities, such as casting, bracing, BTX-A, and surgery. Bracing in patients with cerebral palsy most commonly is used to prevent or slow progression of deformity. The most commonly used braces for the treatment of cerebral palsy include ankle-foot orthoses, hip abduction braces, hand and wrist splints, and spinal braces or jackets.
  66. 66. Ankle foot orthosis
  67. 67. Floor reaction AFO • Uses floor reaction force through toe aspect of foot plate to prevent forward tibial progression & subsequent knee collapse • May be articulated
  68. 68. Knee brace
  69. 69. Ankle-foot-knee orthrosis
  70. 70. Abduction spint
  71. 71. Assisted Gait Trainer
  72. 72. Walking aids • Axillary crutches • Elbow crutches • Walking sticks
  74. 74. Operative Treatment Operative treatment typically is indicated when contractures or deformities decrease function, cause pain, or interfere with activities of daily living. It is the only effective treatment when significant fixed contractures exist.
  75. 75. Selective posterior rhizotomy In some cases nerves need to be severed to decrease muscle tension of inappropriate contractions.
  76. 76. How it Works • The sensory nerve fibers in the spinal cord, usually between the bottom of the rib cage and the top of the hips are divided • The nerve fibers are then stimulated and the responses of the leg muscles are observed. • Those that have an abnormal or excessive response are severed. • Those with a normal response are left intact. • Intensive rehabilitation is required after the surgery, usually up to six weeks, followed by physical therapy on an ongoing basis
  77. 77. OPERATIVE MENAGEMENT HIP • Indications • contracture or deformities causing pain Decrease function Interfere with ADL
  78. 78. PREREQUISITES FOR EFFECTIVE SURGERY • hemiplegics / diplegics : good results quadriplegics : minimal improvement • Age : 3- 12 years • IQ : good • Good upper limb function : for walking • Underlying muscle power should be good • surgery hardly changes status in walkers/nonwalker, but improves gait
  79. 79. PROCEDURE • Neurosurgical procedures • Tendon release • Muscle tendon lengthening • Capsulotomies • Osteotomies • Resection and replacement procedures
  80. 80. DEFORMITIES • DEFORMITIES OF HIP: • Flexion deformities • adduction • Subluxation and dislocation SECODARY DEFORMITIES: • Knee Flexion • Equinus foot • Pelvic tilt • Scoliosis and lordosis
  81. 81. • Pseudoadduction deformity  Flexion internal rotation of hip  Incresed femoral anteversion  External tibial torsion  Planovalgus feet Pt sit in the ‘W’ position
  82. 82. Migration index (MI) is calculated by dividing width of uncovered femoral head A by total width of femoral head B
  83. 83. Hip flexion deformity
  84. 84. Indication for surgery • Hip flexion deformity never decrease by physiotherapy. • Hip flexion deformity > 20 needs surgery
  85. 85. Hip flexion contracture hip , knee & ankle contracture single stage 15-30 deg flexion >30 deg flexion multi level correction ilioPsoas lengthening more release of -rectus femoris -sartorius -TFL -anterior fibers of Gl.minimus Gl.medius
  86. 86. • Iliopsoas recession is most commonly used than complete tenotomy to avoid excessive flexion weakness
  88. 88. • Mild contracture severe contractures Early hip subluxation Adductor tenotomy more release of -gracilis -anterior half of adductor bevis • Leave adductor brevis ( the major hip stabilizer )
  89. 89. HIP SUBLUXATION • MI > 30 % Soft tissue release for very young Flexion adduction deformities • MI > 50% open reduction + femoral osteotomy Correction of femoral valgus and anteversion • AI > 25 deg pelvic osteotomy (Correction of acetabular deformities)
  90. 90. • Femoral varus and derotational(external rotation) osteotomy • Acetabular osteotomies: • Salter osteotomyredirection of the acetabulum anterioly and laterally • Postero-superior deficiencyshelfs osteotomy
  91. 91. HIP DISLOCATION • MI=100% Types: • Posterior dislocation (m.c) • Anterior dislocation Seen in -spastic diplegics -spastic quadriplegics
  92. 92. TRETMENT OPTIONS IN HIP DISLOCATION • Observation • Relocation procedure on femur and acetabulum • Proximal femoral resection • Hip arthrodesis • Total hip arthroplasty
  93. 93. Spastic Diplegia Spastic quadriplegia
  94. 94. hip dislocation : if detected early: surgery if detected late : no pain – leave pain – proximal resection
  95. 95. Combined one stage correction of spastic dislocated hip 1. Soft tissue release 2. Open reduction 3. femoral osteotomy 4. Pericapsular pelvic osteotomy
  96. 96. Varus derotational shortening femoral osteotomy
  97. 97. Pericapsular acetabuloplasty
  99. 99. FOOT The most common deformity is ankle equinus, with equinovarus and equinovalgus deformities being equally common.
  100. 100. Equinus Deformity Equinus deformity is the most common foot deformity in patients with cerebral palsy, affecting 70% of children. Surgical Correction of Equinus Deformity Open Lengthening of the Achilles Tendon Z-Plasty Lengthening of the Achilles Tendon Percutaneous Lengthening of the Achilles Tendon Lengthening of the Gastrocnemius-Soleus Muscle
  101. 101. Equinovarus Deformity Varus deformity, which usually is accompanied by equinus, is caused most commonly by an abnormal posterior tibial muscle that is overactive or firing out of phase. Lengthening of the Posterior Tibial Tendon Z-Plasty Lengthening of the Posterior Tibial Tendon Step-Cut Lengthening of the Posterior Tibial Tendon
  102. 102. Musculotendinous Recession of the Posterior Tibial Tendon
  103. 103. Osteotomy of the Calcaneus
  104. 104. Equinovalgus Deformity
  105. 105. Medial Displacement Calcaneal Osteotomy
  106. 106. Subtalar Arthrodesis
  107. 107. KNEE Flexion Deformity Flexion is the most common knee deformity in patients with cerebral palsy and frequently occurs in ambulatory children Spastic hamstrings, weak quadriceps, or a combination of both can cause isolated knee flexion. Fractional Lengthening of Hamstring Tendons Combined Hamstring Lengthening, Posterior Capsular Release, and Quadriceps Shortening Distal Transfer of Rectus Femoris
  108. 108. Than k you