Management of scoliosis with special seating for the non-ambulant spastic cerebral palsy population--a biomechanical study.

OBJECTIVE: To investigate the effects of special seating on lateral spinal curvature in the non-ambulant spastic cerebral palsy population with scoliosis. DESIGN: Prospective study with matched pairs (same subject pre- and post-intervention). BACKGROUND: It is thought that special seating can improve the sitting posture of individuals with spastic cerebral palsy. However, there is little known about how the seating can affect a scoliosis. METHOD: The shape of the spine was measured with subjects sitting in an assessment chair with a clear backrest. The measurement recorded was the "spinous process angle", an approximation to the Cobb angle. The forces exerted on the subject by the chair were measured by electrical resistance strain gauged transducers attached to the lateral support pads and seat base. Measurements were taken with three alternative arrangements of lateral support pads: upper body unsupported in configuration 1; two lateral pads at the same height in configuration 2; body supported by a 3-point force system in configuration 3. RESULTS: Configuration 3 gave a mean correction of +35% in the spinous process angle compared to configuration 1 (P=0.000) and the forces applied through the two lateral thoracic pads were, on average, of similar magnitude (mean values of 51 and 47 N). In comparison, for configuration 2 the mean correction was only +18.7% (P=0.004) and on average the pad on the concave side of the scoliosis applied a much larger force to the chest wall than the pad on the convex side (mean values of 36 and 17 N respectively). CONCLUSIONS: Significant static correction of the scoliotic spine can be achieved with an arrangement of lateral pads on a seating system that applies a 3-point force system to the sides of the body. RELEVANCE: The results suggest that the position of the lateral pads on a special seating system is important and, by the careful configuration of these supports, significant correction of a scoliosis can be obtained for a person with spastic cerebral palsy. Also the methodology and equipment from this study are potentially useful for the assessment and fitting of special seating for individuals with scoliosis.

Influence of hormones on platelet intracellular calcium.

The pathophysiology of thromboembolic disease associated with estrogen therapy is poorly understood. There are innumerable calcium-dependent activities involved in platelet function. To determine whether platelet calcium levels are affected by exogenous hormones, intracellular calcium and release were studied in platelets in various hormonal environments and findings were correlated with platelet adhesion and aggregation. Platelet intracellular calcium concentration and release was significantly decreased in women ingesting tamoxifen compared to controls and significantly increased, as was platelet adhesion, in oral contraceptive users. Platelets incubated ex vivo with estradiol had increased intracellular calcium and release but there was decreased adhesion to fibronectin. Intracellular calcium concentration and release were not affected when platelets were incubated with tamoxifen. Adhesion to collagen III was increased in tamoxifen-incubated platelets. Only oral contraceptive users had increased sensitivity to aggregating agents. This data suggests that 17 beta estradiol, progesterone, and tamoxifen likely have a nongenomic effect on platelet intracellular calcium and calcium release and that platelet calcium levels are closely related to the degree of platelet adhesion and aggregation in vivo.

Paradoxical influence of estrogenic hormones on platelet-endothelial cell interactions.

Controversies abound in the literature about the safety and efficacy of tamoxifen and estrogen. We studied the effect of these 2 hormonal agents on factors involved in in vitro thrombogenesis: platelets and endothelial cells. Endothelial cells were derived from human umbilical veins and platelets were obtained from premenopausal and postmenopausal women, women on oral contraceptives, postmenopausal women on hormone replacement therapy, men, and patients with breast cancer who had been taking adjuvant tamoxifen for more than 1 year. The interaction of platelets with endothelial cell matrix was measured in 2 systems: 1) in a flow chamber at low shear rate and, 2) with 51Cr labeled platelets in a "static" culture system. In the static system, platelets from women on tamoxifen exhibited decreased platelet adherence to endothelial cell matrix whether they were grown in tamoxifen or control conditions, when compared to platelets from premenopausal women. When flow (25 sec-1) was added these differences were negated. Neither tamoxifen nor 17 beta estradiol had an effect on endothelial cell proliferation or platelet aggregation. Adhesion of platelets at low shear was not altered when platelet rich plasma was incubated with tamoxifen nor when endothelial cells were grown in tamoxifen. In contrast, incubation of platelets in 17 beta estradiol decreased platelet adhesion at low shear rate, however, there was no effect on platelet adhesion when endothelial cells were grown in 17 beta estradiol. We conclude that in early stages of thrombus formation as measured in vitro, tamoxifen may not have a detrimental effect and estrogen may be protective.

Platelet adhesion at low shear rate: study of a normal population.

The use of oral contraceptives (OCs) has been associated with vascular complications. The mechanism(s) by which OCs predispose to thrombotic events remains unclear. Recent studies have demonstrated that postmenopausal (PM) women who take estrogen replacement therapy (ERT) have a decreased incidence of myocardial infarction compared to those who do not take ERT. This study was undertaken to determine if healthy individuals have differences in platelet adhesion depending on hormonal status. Men, PM women taking ERT, PM women not taking ERT, OC users, and premenopausal women not taking any medications were studied. Platelet studies were performed in a Hele-Shaw flow chamber at a low shear rate using platelet-rich plasma. The platelet adhesion process to subendothelial components: fibronectin, collagen I and collagen III was recorded using a 35 mm camera mounted on an inverted microscope. Photographs were taken at 30 second intervals for a total of 12 minutes and analyzed using a modified computer program which provided a numerical account of platelet adhesion. OC users had significantly higher platelet adherence to fibronectin, collagen I and collagen III compared to all other groups. All other study groups had similar platelet adhesion independent of hormonal status. These findings suggest that OCs cause increased platelet adhesion in some individuals and this may be one of the mechanisms by which OCs contribute to thrombotic events.