General Information
• Cerebral palsy; It defines a central motor deficit that limits the range of motion due to a non-progressive lesion of the immature brain and leads to deterioration of normal posture.
• The lesion may have occurred prenatally, perinatally or postnatally.
• There are many causes in etiology such as cerebral anoxia, intracranial hemorrhage, embryological malformations, infection (prenatal or postnatal) and trauma.
• The deficit is primarily in the pyramidal, extrapyramidal system and secondary motor pathways in the brain. As a result of this neurological damage, inhibition in the motor areas of the CNS is removed, and primitive reflexes become permanent. The formation of postural reflexes is abnormal.
Etiopathogenesis in Cerebral Palsy
• Etiology was not found in 1/3 of cerebral palsy cases. Prenatal factors are responsible for 50-60% of cases, perinatal factors for 30-40% and postnatal factors for 10% of cases. Recently, it has been seen that prenatal factors have come to the fore in the etiology of cerebral palsy. In one study, it was seen that most children with cerebral palsy were born term and there was no problem in their birth. Cerebral palsy is associated with 80% prenatal events. Those with cerebral palsy due to asphyxia at birth were evaluated as <10%.
• While prenatal factors are responsible in term babies, perinatal factors are often responsible in preterm babies.
• Cerebral palsy risk is around 15% in premature babies born < 1000 g.
• It is more common and more serious in men.
• The most important factor in the pathogenesis is hypoxia.
Risk factors
• Low birth weight
• Breech birth
• Birth asphyxia
• Kernicterus
• Birth trauma
• Amino acid metabolism disorders
• Maternal fever >38 °C during delivery
• Uterine bleeding in the prenatal period
• Maternal infections (urinary system infection, antibiotic use)
• TORCH infections
• Hypoglycemia
• Urea cycle defects
• Congenital hypothyroidism
• Multiple pregnancy
• Infertility treatment
• Male gender
• Functional polymorphism in the IL-6 gene
• Intrauterine ex of the twin
Clinical findings
• It is usually not possible to diagnose in the neonatal period.
• The most common initial findings; Nutritional disorder due to hypotonia or sucking-swallowing coordination disorder, trouble changing diapers due to stiffness in the adductor muscles, behavioral changes, severe colic, irritability.
• The location of the lesion in the CNS is determined by physical examination findings. Common findings; Hyperactive reflexes, abnormal movements such as chorea, athetosis or dystonia, abnormal absence or persistence of infantile reflexes. The history of delay in motor movements in the 6-18 months period forms the basis of the diagnosis.
Treatment
• Application of hypothermia treatment in hypoxic ischemic encephalopathy in term infants reduces the risk of dyskinetic or spastic quadriplegic cerebral palsy.
• Administration of magnesium sulfate to the mother before birth in premature births (<32 weeks) reduces the risk of cerebral palsy at the age of 2 years, but its benefit has not been demonstrated in term babies.
• Physical therapy is useful in the early period.
• Oral diazepam, baclofen, dantrolene can be used to treat spasticity in medical treatment.
• In patients with severe spasticity, "dorsal rhizotomy" can be applied. Again, in cases where spasticity is severe, "intrathecal baclofen" can be given.
• It is reported that botulinum toxin application gives very good results especially in spastic cerebral palsy.
