Shilla Growth Permitting Spinal Instrumentation System for Treatment of Scoliosis in the Immature Spine
The objective of this study is to retrospectively and prospectively review patients who have undergone this technique looking at age of the patient, magnitude of the curve preoperatively, postoperatively and over time, diagnosis, pulmonary function, surgical procedures, complications, and spinal growth.
The hypothesis is that Shilla growth permitting spinal instrumentation coupled with a surgical technique of aggressive correction of the apex of the scoliotic curve wil allow for natural growth of the spine in a guided fashion with a limited number of future surgeries required.
Traditional "growing rod" constructs of spinal instrumentation to treat severe scoliosis in young children require a return to the operating room every six to nine months until skeletal maturity. The Shilla system allows for more spinal growth with fewer surgical procedures necessary for lengthenings. This is a major advantage over existing growth permitting systems and allows surgery to be performed at younger ages with better deformity correction without concerns of repeated surgeries.
Time Perspective: Prospective
Arkansas Childrens Hospital
Arkansas Children's Hospital Research Institute
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00577226
- Information obtained from ClinicalTrials.gov on July 15, 2010
Medical and Biotech [MESH] Definitions
An appreciable lateral deviation in the normally straight vertical line of the spine. (Dorland, 27th ed)
Deformities of the SPINE characterized by abnormal bending or flexure in the vertebral column. They may be bending forward (KYPHOSIS), backward (LORDOSIS), or sideway (SCOLIOSIS).
Congenital or postnatal overgrowth syndrome most often in height and occipitofrontal circumference with variable delayed motor and cognitive development. Other associated features include advanced bone age, seizures, NEONATAL JAUNDICE; HYPOTONIA; and SCOLIOSIS. It is also associated with increased risk of developing neoplasms in adulthood. Mutations in the NSD1 protein and its HAPLOINSUFFICIENCY are associated with the syndrome.
A form of inherited long QT syndrome (or LQT7) that is characterized by a triad of potassium-sensitive periodic paralysis, VENTRICULAR ECTOPIC BEATS, and abnormal features such as short stature, low-set ears, and SCOLIOSIS. It results from mutations of KCNJ2 gene which encodes a channel protein (INWARD RECTIFIER POTASSIUM CHANNELS) that regulates resting membrane potential.
Autosomal recessive inborn error of methionine metabolism usually caused by a deficiency of CYSTATHIONINE BETA-SYNTHASE and associated with elevations of homocysteine in plasma and urine. Clinical features include a tall slender habitus, SCOLIOSIS, arachnodactyly, MUSCLE WEAKNESS, genu varus, thin blond hair, malar flush, lens dislocations, an increased incidence of MENTAL RETARDATION, and a tendency to develop fibrosis of arteries, frequently complicated by CEREBROVASCULAR ACCIDENTS and MYOCARDIAL INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, p979)
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