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The higher the functional impairment, the more likely patients with cerebral palsy (cP) are to develop a scoliotic deformity. This is usually long-sweeping, C-shaped, and progressive in nature, since the causes of the deformity, such as muscular weakness, imbalance, and osteoporosis, persist through adulthood. In contrast to idiopathic scoliosis, not only is the spine deformed, the patient is also sick. This multimorbidity warrants a multidisciplinary approach with close involvement of the caregivers from the beginning. Brace treatment is usually ineffective or intolerable in light of the mostly stiff and severe deformities and the poor nutritional status. The pros and cons of surgical correction need to weighed up when pelvic obliquity, subsequent loss of sitting balance, pressure sores, and pain due to impingement of the rib cage on the ileum become issues. General risks of, for example, pulmonary or urogenital infections, pulmonary failure, the need for a tracheostoma, permanent home ventilation, and death add to the particular surgery-related hazards, such as excessive bleeding, surgical site infections, pseudarthrosis, implant failure, and dural tears with leakage of cerebrospinal fluid. The overall complication rate averages around 25 %. From an orthopedic perspective, stiffness, marked deformities including sagittal profile disturbances and pelvic obliquity, as well as osteoporosis are the main challenges. In nonambulatory patients, long fusions from T2/T3 with forces distributed over all segments, low-profile anchors in areas of poor soft tissue coverage (sublaminar bands, wires), and strong lumbosacropelvic modern screw fixation in combination with meticulous fusion techniques (facetectomies, laminar decortication, use of local autologous bone) and hemostasis can be employed to keep the rate of surgical and implant-related complications at an acceptably low level. Excessive posterior release techniques, osteotomies, or even vertebrectomies in cases of very severe short-angled deformity mostly prevent anterior one- or two-stage releases. Despite improved operative techniques and implants with predictable and satisfactory deformity corrections, the comorbidities and quality-of-life related issues demand a thorough preoperative, multidisciplinary decision-making process that takes ethical and economic aspects into consideration.  相似文献   
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Acute hyperglycemia has been shown to alter gastrointestinal motility. The effects of hyperglycemia on rectal afferent neural and anal sphincter function were studied. Perception of rectal balloon distention, pressure-volume relationships, volumes necessary to induce reflex internal anal sphincter relaxation, resting anal sphincter pressure, and maximal anal sphincter squeeze pressure were measured under basal, hyperglycemic clamp, and euglycemic, hyperinsulinemic clamp conditions in 9 healthy volunteers. Hyperglycemic clamping (258 ± 14 mg/dL) significantly blunted threshold perception and the urge to defecate in response to rectal distention without altering perception of maximally tolerated distention. In contrast, euglycemic, hyperinsulinemic clamping had no effect on perception of rectal distention. Rectal pressure-volume relationships after hyperglycemic clamping were unchanged compared with basal conditions. Hyperglycemic clamping caused a significant increase in the distention necessary to induce the rectoanal inhibitory reflex. This effect was not observed under euglycemic, hyperinsulinemic clamp conditions. Hyperglycemia did not significantly affect resting internal anal sphincter pressure or maximal external anal sphincter squeeze pressure. Acute hyperglycemia but not secondary hyperinsulinemia reduces sensation of rectal distention and blunts the onset of the rectoanal inhibitory reflex, suggesting effects both on visceral afferents projecting to the cortex and intrinsic afferents mediating local reflex activity.  相似文献   
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