Effect of positioning error on the Hilgenreiner epiphyseal angle and the head-shaft angle compared to the femoral neck-shaft angle in children with cerebral palsy.

Children with cerebral palsy (CP) often have changes in proximal femoral geometry. Neck-shaft angle (NSA), Hilgenreiner epiphyseal angle (HEA) and head-shaft angle (HSA) are used to measure these changes. The impact of femoral rotation on HEA/HSA and of ab/adduction on HEA/HSA/NSA is not well known. This study aimed to determine and compare the effect of rotation, ab/adduction and flexion/extension on HEA/HSA/NSA. Radiographic measurements from 384 patients with Gross Motor Function Classification System (GMFCS) levels I-V were utilized. NSA/HSA for affected hips were used with femoral anteversion averages to create three-dimensional models of 694 hips in children with CP. Each hip was rotated, ab/adducted and flexed/extended to simulate malpositioning. HEA/HSA/NSA of each model were measured in each joint position, and differences from correct positioning were determined. Mean HEA error at 20° of internal/external rotations were -0.60°/3.17°, respectively, with the NSA error of -6.56°/9.94° and the HSA error of -3.69°/1.21°. Each degree of ab/adduction added 1° of the HEA error, with no NSA/HSA error. NSA was most sensitive to flexion. Error for all measures increased with increasing GMFCS level. HEA/HSA were minimally impacted by rotation. NSA error was much higher than HEA/HSA in internal rotation and flexion whereas HEA was sensitive to changes in ab/adduction. Given abduction is more easily detectable on imaging than rotation, HEA may be less affected by positioning errors that are common with children with CP than NSA. HSA was least affected by position changes. HEA/HSA could be robust, complementary measures of hip deformities in children with CP.

Protective function of nicotinamide against ketamine-induced apoptotic neurodegeneration in the infant rat brain.

During development, anesthetics activate neuroapoptosis and produce damage in the central nervous system that leads to several types of neurological disorders. A single dose of ketamine (40 mg/kg) during synaptogenesis in a 7-day-old rat brain activated the apoptotic cascade and caused extensive neuronal cell death in the forebrain. In this study, we investigated the protective effect of nicotinamide against ketamine-induced apoptotic neurodegeneration. After 4 h, neuronal cell death induced by ketamine was associated with the induction of Bax, release of cytochrome c into the cytosol, and activation of caspase-3. One single dose of 1 mg/g nicotinamide was administered to a developing rat and was found to inhibit ketamine-induced neuroapoptosis by downregulating Bax, inhibiting cytochrome c release from mitochondria into cytosol, and inhibiting the expression of activated caspase-3. TUNEL and immunohistochemical analyses showed that ketamine-induced cell death occurred through apoptosis and that it was inhibited by nicotinamide. Fluoro-Jade-B staining demonstrated an increased number of dead cells in the cortex and thalamus after ketamine treatment; treatment with nicotinamide reduced the number of dead cells in these brain regions. Our findings suggest that nicotinamide attenuated ketamine-induced neuronal cell loss in the developing rat brain and is a promising therapeutic and neuroprotective agent for the treatment of neurodevelopmental disorders.