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Objectives: Differences in the mechanisms of subtrochanteric and diaphyseal atypical femoral fractures (AFFs) have been speculated in studies that have analyzed differences in the patients’ backgrounds. However, the etiologies of each type of AFF have not been investigated in detail. Therefore, this study aimed to investigate the nature and etiologies of the risk factors for diaphyseal AFFs. Materials and Methods: Eighty consecutive Japanese patients with 91 diaphyseal AFFs (the AFF group) and 110 age-matched female patients with osteoporosis (the non-AFF control group) were included. Their clinical data were compared and the factors affecting AFFs were investigated. Furthermore, the etiologies of the risk factors for diaphyseal AFFs were examined. Results: Multivariate analysis revealed that femoral serrated changes, bisphosphonate or denosumab usage, and lateral and anterior femoral curvatures were the risk factors for diaphyseal AFFs (p<0.0011, p=0.0137, and p<0.0001, respectively). Multivariate analyses also revealed that serrated changes and low serum 25(OH)D levels affected the lateral curvature (p=0.0088 and 0.0205, respectively), while serrated changes affected the anterior curvature (p=0.0006); each significantly affected the femoral curvature. In addition, a high serum calcium (Ca) level, lateral femoral curvature, and anterior femoral curvature were the predictors of serrated changes (p=0.0146, 0.0002, and 0.0098, respectively). Conclusion: The risk factors for diaphyseal AFFs were bone resorption inhibitor usage, a strong femoral curvature, and serrated changes. A low serum 25(OH)D level and serrated changes are the risk factors for lateral curvature, while a high serum Ca level is a risk factor for serrated changes.

The purpose of this study was to compare postcontraction hyperemia after electrical stimulation between patients with upper extremity paralysis caused by upper motor neuron diseases and healthy controls. Thirteen healthy controls and eleven patients with upper extremity paralysis were enrolled. The blood flow in the basilic vein was measured by ultrasound before the electrical stimulation of the biceps brachii muscle and 30 s after the stimulation. The stimulation was performed at 10 mA and at a frequency of 70 Hz for 20 s. The mean blood flow in the healthy control group and in upper extremity paralysis group before the electrical stimulation was 60 ± 20 mL/min (mean ± SD) and 48 ± 25 mL/min, respectively. After the stimulation, blood flow in both groups increased to 117 ± 23 mL/min and 81 ± 41 mL/min, respectively. We show that it is possible to measure postcontraction hyperemia using an ultrasound system. In addition, blood flow in both groups increased after the electrical stimulation because of postcontraction hyperemia. These findings suggest that evaluating post contraction hyperemia in patients with upper extremity paralysis can assess rehabilitation effects.Local and acute increases in blood flow, which occur just after the contraction of skeletal muscles, is related to the elevation of intramuscular pressure, and then block blood flow to the muscles. The postcontraction hyperemia, which continues for a relatively long time after each contraction, proportionally increases along with the strength and length of the contraction. This is believed to be caused by metabolic products that are generated during muscle contraction (2). Until recently, the study of postcontraction hyperemia has only been conducted in animals. Techniques for measuring blood flow in humans have been quite invasive, for example, the thermocouple inspection method, which requires a needle to be inserted into the muscle. Nowadays, the noninvasive Doppler ultrasound system is being used to evaluate blood flow. Thus, we used this system to evaluate postcontraction hyperemia in humans. It is reported that blood flow of the paretic limb is significantly reduced compared with the unaffected limb (10). Therefore, we hypothesized that this phenomenon will also decrease in upper limb paralysis patients compared with the healthy controls or the unaffected limb. Patients with upper extremity paralysis caused by upper motor neuron diseases who were admitted to the department of rehabilitation medicine, Akita University Hospital for rehabilitation from December 2013 to May 2014 and healthy controls were included in the study. A full explanation was given to the patients before taking part in this study, and informed consent was obtained. The present trials excluded patients with cardiac pacemakers; uncontrolled

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