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OBJECTIVEMetrics used to quantify preoperative severity and postoperative outcomes for patients with sagittal synostosis include cephalic index (CI), the well-known standard, and the recently described adjusted cephalic index (aCI), which accounts for altered euryon location. This study tracks the time course of these measures following endoscopic repair with orthotic helmet therapy. The authors hypothesize that CI and aCI show significant regression following endoscope-assisted repair.METHODSCT scans or 3D photographs of patients with nonsyndromic sagittal synostosis treated before 6 months of age by endoscope-assisted strip craniectomy and postoperative helmet therapy (n = 41) were reviewed retrospectively at three time points (preoperatively, 0–2 months after helmeting, and > 24 months postoperatively). The CI and aCI were measured at each time point.RESULTSMean CI and aCI increased from 71.8 to 78.2 and 62.7 to 72.4, respectively, during helmet treatment (p < 0.001). At final follow-up, mean CI and aCI had regressed significantly from 78.2 to 76.5 and 72.4 to 69.7, respectively (p < 0.001). The CI regressed in 33 of 41 cases (80%) and aCI in 39 of 41 cases (95%). The authors observed a mean loss of 31% of improvement in aCI achieved through treatment. A strong, positive correlation existed between CI and aCI (R = 0.88).CONCLUSIONSRegression following endoscope-assisted strip craniectomy with postoperative helmet therapy commonly occurs in patients with sagittal synostosis. Future studies are required to determine whether duration of helmet therapy or modifications in helmet design affect regression.

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Diabetic patients have a twofold to fourfold increased risk of cardiovascular disease. Despite a vast amount of research, the underlying mechanisms that predispose individuals with diabetes to the development of cardiovascular disease are unclear. To further our understanding of how diabetes promotes atherosclerosis, we have established, characterized, and manipulated a new model of hyperglycemia-induced atherosclerosis: the apolipoprotein E-deficient (ApoE(-/-)):Ins2(+/Akita) mouse. All mice were fed a standard chow diet. Male ApoE(-/-):Ins2(+/Akita) mice developed chronic hyperglycemia, which significantly accelerated atherosclerosis. Female ApoE(-/-):Ins2(+/Akita) mice presented hyperglycemia that normalized by 15 weeks of age. Despite the transient hyperglycemia, advanced atherosclerosis was observed at 15 weeks of age compared with ApoE(-/-) females. To better understand these differences, subsets of mice were castrated or ovariectomized at 5 weeks of age. Castrated ApoE(-/-):Ins2(+/Akita) mice showed a reduction in blood glucose levels that correlated with the amelioration of atherosclerosis. Interestingly, castrated normoglycemic ApoE(-/-) mice developed larger atherosclerotic lesions than sham-operated on controls. Ovariectomized ApoE(-/-):Ins2(+/Akita) mice presented chronic hyperglycemia, and atherosclerosis appeared to be advanced. We have characterized the distinctive sex-specific phenotypes exhibited by the ApoE(-/-):Ins2(+/Akita) mouse model and present evidence for the action of sex hormones on pancreatic β-cell function and the vasculature that affect the regulation of blood glucose levels and the development of atherosclerosis. This model will provide a test bed to further delineate these effects.