Browsing by Author "Terrill, Tyler A."
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Item Assessing Complications of Epiphysiodesis for Leg Length Discrepancy(2014-02-04) Terrill, Tyler A.; Dunn, Samuel H.; Birch, John; Makarov, MarinaINTRODUCTION: Leg length discrepancy in children and adolescents is a serious orthopedic problem that can cause leg and back problems due to abnormal gait. This condition may be congenital or caused by disease or trauma. One method to correct leg length discrepancies in children is to perform an epiphysiodesis. This surgical procedure removes one or more growth plates from the femur, tibia, or fibula. This operation slows down the growth of the long leg to allow the shorter leg to catch up, or at least prevent the discrepancy from increasing. As there has been no large study of epiphysiodesis patients in the literature, the rates for surgical complications and errors associated with this surgery are not well known. These complications may include infections, nerve damage, and incomplete epiphysiodesis, which often results in an angular deformity. Because of the lack of understanding for rate of complications and characteristics associated with these, we studied a large patient population to gain insight into these aspects of the procedure. METHODS: The patient population at Texas Scottish Rite Hospital for Children undergoing epiphysiodesis for the treatment of leg length discrepancy from 1980 to 2008 was examined by a retrospective review of both charts and radiographs, with a total of 755 patients included in the study. The information recorded in the study included the extent of leg length discrepancy, angular measurements of the joints, method of epiphysiodesis, postoperative development of angular deformities, underlying etiology, length correction prediction, and other clinical features. RESULTS: Of the 755 patients examined, 38 had surgical complications, (5%). Of these patients, 27 had incomplete epiphysiodesis, 6 had neurological problems, 3 had overcorrection of the leg length discrepancy, and 2 had other complications not specific to this procedure. Patients incurring complications had statistically significant risk factors that include greater leg length discrepancies at the time of epiphysiodesis, congenital defects instead of acquired ones, and younger age. There were also trends towards open curettage method, epiphysiodesis involving the femoral growth plate, and male gender as risk factors, though these did not achieve statistical significance. DISCUSSION: It is important that surgeons understand which populations of patients are at greater risk for complications during this procedure, so that extra caution may be taken to prevent harm. Also, parents should be aware that there is a 5% risk of surgical complication, so that they may be fully informed before committing to the procedure.Item In Vivo Sensory Cortex Dysfunction in Pyruvate Dehydrogenase Deficient Mice(2015-01-26) Terrill, Tyler A.; Jakkamsetti, Vikram; Good, Levi; Pascual, Juan M.BACKGROUND: Pyruvate Dehydrogenase (PDH) is a critical enzyme in all organisms, providing pyruvate for the Krebs cycle to generate ATP. As a result, PDH-deficient patients develop lactic acidosis and intellectual disability. Processing of sensory information in the cerebral cortex is crucial for intellectual function. We hypothesize that cortical thinning in these patients contributes to aberrant sensory processing and resulting intellectual disability. Specifically, we hypothesize that there exists a deficit in neurotransmission between cortical layers of the primary somatosensory cortex that can be tested in a novel mouse model of PDH deficiency that replicates the cardinal features of the human disorder. METHODS: Wild-type (WT, n=11), GFAP-CrePDHflox/+ heterozygous (GFAPhet, n=7), GFAP-CrePDHflox/flox knockout (GFAPKO, n=10), and Nestin-CrePDHflox/+ heterozygous mice (NChet, n=14) were anesthetized and their cortex exposed. A vertical linear electrode array was modified to stimulate in layer IV and record in layers IV and II. Synaptic activation and neuronal output were reflected on the recorded local field potentials (LFP) and action potentials. In each mouse, we examined spontaneous activity in layer II and IV, evoked response in layer II from stimulation in layer IV, and synchronized spontaneous activity between the two layers. RESULTS: Spontaneous oscillations of synaptic activation in layer II were significantly reduced in amplitude in both the GFAPKO and NChet mice (p=.02, p=.01). Thus, spontaneous synaptic input into a processing unit of the sensory cortex is severely impaired. Evoked LFPs in layer II were decreased in the GFAPhet, GFAPKO, and NChet mice (p<.001, p=.002, p=.02). Hence, neurotransmission from layer IV to layer II is significantly decreased. Synaptic oscillations in layer IV and II were less synchronized in NChet mice (p<.001) indicating a lack of normal cortical network activity. Additionally, there was electrophysiological evidence of paroxysmal, seizure-like activity in layer 2 of the GFAPKO mice (42% of animals, similar to the EEG of human patients. CONCLUSION: We have observed a significant loss of spontaneous electrophysiological activity, evoked response, and synchronization of LFP oscillations in the PDH mutant mice. This implies cortical dysfunction in sensory processing that could contribute to intellectual disability. Treatments targeting this aspect of the phenotype could be beneficial to PDH-deficient patients.