Cerebral Palsy Infographic- Cerebral Palsy: A Gude For Parents
7.25 Cerebral Palsy 1
Transcript of 7.25 Cerebral Palsy 1
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CEREBRAL PALSY
dr Jalila Zamzam,Sp.A
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Cerebral Palsy: Definition
Cerebral palsy is a static encephalopathy
Encephalopathy = Brain Injurythat is non-
progressivedisorder of posture and movement
Variable etiologies
Often associated with epilepsy, speech problems,
vision compromise, & cognitive dysfunction
Resulting from defect or lesion of the developingbrain
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Cerebral Palsy: Prevalence
2-4/1000; 7-10,000 new babies each yr
150 years ago described by Dr. Little anorthopedic surgeon and known as Littles
Disease During past 3 decades considerable advances
made in obstetric & neonatal care, butunfortunately there has been virtually no
change in incident of CP
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Cerebral Palsy:
Clinical Presentation
Remember that motor developmental
progression is from.
Head to Toe, (jari kaki)
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Cerebral Palsy: Classification
Various classifications of Cerebral Palsy
Physiologic
Topographic
Etiologic
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Cerebral Palsy: Physiologic
Athetoid
Ataxic
Rigid(kaku)-Spastic
Atonic
Mixed
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Cerebral Palsy: Topographic
Monoplegic
Paraplegic
Hemiplegic
Triplegic
Quadraplegic
Diplegic
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Cerebral Palsy: Etiologic
Prenatal (70%)Infection, anoxia, toxic, vascular, Rh disease,genetic, congenital malformation of brain
Natal (5-10%)Anoxia, traumatic delivery, metabolic
Post natalTrauma, infection, toxic
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The following maternal and prenatal risk
factors statistically correlate with CP:9
Long menstrual cycle (siklus mens pnjg)
Previous pregnancy loss (kehamilan sblmx)
Previous loss of newborn (kematian bayi sblmx)
Maternal mental retardation Maternal thyroid disorder, especially iodine
deficiency
Maternal seizure disorder (kejang pd ibu)
History of delivering a child weighing less than2000 g (sblmx BBLR)
History of delivering a child with a motor deficit,mental retardation, or a sensory deficit (sblmx
klhiran cacat)
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The following factors during pregnancy also
correlate statistically with CP:
Polyhydramnios
Treatment of the mother with thyroid hormone
Treatment of the mother with estrogen orprogesterone
Maternal seizure disorder Maternal severe proteinuria or high blood pressure
Maternal methyl mercury exposure (keracunanMercuri)
Congenital malformations in the fetus Male sex of fetus
Bleeding in third trimester (perdarahan)
Intrauterine growth retardation (IUGR)
Multiple gestation
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The following perinatal factors are
associated with an increased risk of CP:11
Prematurity
Chorioamnionitis
Nonvertex and face presentation of the fetus
Birth asphyxia
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The following postnatal factors may
contribute to CP:12
Infections (eg, meningitis, encephalitis)
Intracranial hemorrhage (eg, due to
prematurity, vascular malformations, or
trauma)
Periventricular leukomalacia (in premature
infants)
Hypoxia-ischemia (eg, from meconiumaspiration)
Persistent fetal circulation or persistent
pulmonary hypertension of the newborn
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Diagnosis Observation of slow motor development Abnormal muscle tone
Unusual posture (postur y tak sesuai)
Presence of persistent infantile reflexes
Ruling out of progressive hereditaryneurologic/metabolic disorder
Targeted lab tests, cerebral imaging (e.g. MRI),
ultrasound (brain lesions, abnormalities) Presence of associated disabilities: hearing &
vision impairment, seizures, perceptionproblems with touch or pain, cognitive
dysfunction
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Cerebral Palsy: Complications
Gastrointestinal and nutritional
Failure to thrive due to feeding and swallowing difficultiessecondary to poor oromotor control
Obesity, less frequently than failure to thrive
Gastroesophageal reflux and associated aspiration pneumonia
Constipation (diare)
Dental caries (karang)
Respiratory
Increased risk of aspiration pneumonia because of oromotor
dysfunction Chronic lung disease/bronchopulmonary dysplasia
Bronchiolitis/asthma
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Skin
Decubitus ulcers and sores
Orthopedic
Contractures Hip dislocation
Scoliosis
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Neurologic
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Epilepsy: Epilepsy occurs in 15-60% of childrenwith CP and is more common in patients withspastic quadriplegia or mental retardation.
Hearing loss: This occurs particularly in patientswho had acute bilirubin encephalopathy(kernicterus).
Vision: Visual acuity decreases in premature
infants because of retinopathy of prematurity withhypervascularization and possible retinaldetachment.
Visual-field abnormalities due to cortical injury
Strabismus
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Cognitive/psychological/behavioral
Mental retardation (30-50%)
Attention-deficit/hyperactivity disorder
Learning disabilities
Impact on academic performance and self-esteem
Increased prevalence of depression
Sensory integration difficulties Increased prevalence of progressive
development disorder or autism associatedwith concurrent diagnosis of CP
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Management No cure (tdk ada pengobatan)
Goals: increase functionality, improvecapabilities and sustain health in terms of
locomotion, cognitive development, socialinteraction and independence
Early, intensive, team-based management holistic approach(pendekatan), not just onesymptom (gejala)
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Treatment1. Global Strategies- Common neurodevelopmental Tx that aims to
provide immediate improvement in dynamic range ofmotion
-Conductive education: Emphasizes an integratedmodel of education & rehabilitation
2. Physical Therapy-muscle strengthening, fitness programs
3. Medications-Botulinum toxin (Botox):produces a protein that blocksthe release of acetylcholine/relaxes muscles (can alsoreduce drooling when injected into salivary glands)
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Treatment cont.)3. Medications
-Baclofen (Lioresal): can provide pain and spasm relief,improved sleep, ease of care; however, manycomplications (e.g. headache, vomiting(muntah),seizures)
4. Surgical Treatments
-Selective dorsal rhizotomy: selective cutting of dorsalrootlets from spinal cord segments; intended tominimize/eliminate spasticity; some complications
-Hip reconstruction/repair (due to muscle imbalance,incidence of hip dislocation in children with CP as highas 59%)
5. External Aids (Orthoses)
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Cerebral Palsy
What is
substantially
disablingCerebral Palsy?
Mobility
Communication
Learning
Self Care
Self Direction
Independent Living
Economic Sufficiency
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Dr.Jalila Zamzam,SpA