BackgroundThe Disability of the Arm, Shoulder and Hand (DASH) questionnaire is a region-specific self-administered questionnaire that consists of a disability/symptom (DASH-DS) scale, and two optional modules, the work (DASH-W) and the sport/music (DASH-SM) modules. The DASH was cross-culturally adapted and developed by the Impairment Evaluation Committee, Japanese Society for Surgery of the Hand. The purpose of this study was to test the reliability, validity, and responsiveness of the Japanese version of DASH (DASH-JSSH).MethodsA series of 72 patients with upper extremity disorders completed the DASH-JSSH, the medical outcomes study 36-item short-form health survey (SF-36), and the Visual Analog Scale (VAS) for pain. Thirty-eight of the patients were reassessed for test-retest reliability 1 or 2 weeks later. Reliability was investigated by reproducibility and internal consistency. To analyze the validity, a principal component analysis and correlation coefficients between the DASH-JSSH and the SF-36 were obtained. Responsiveness was examined by calculating the standardized response mean (mean change/SD) and effect size (mean change/SD of baseline value) after carpal tunnel release of the 17 patients with carpal tunnel syndrome.ResultsCronbach’s alpha coefficients in the DASH-DS and DASH-W were 0.962 and 0.967, respectively. The intraclass correlation coefficients for the same were 0.82 and 0.85, respectively. The unidimensionality of the DASH-DS and DASH-W were confirmed. The correlations between the DASH-DS score and the subscale of the SF-36 scale ranged from −0.29 to −0.73. The correlation coefficient between the DASH-DS and the DASH-W was 0.79. The standardized response mean/effect size of DASH-DS, DASH-W, and VAS for pain were −0.48/−0.26, −0.68/−0.41, and −0.40/−0.40, respectively. DASH-DS and DASH-W were as moderately sensitive as VAS for pain.ConclusionThe DASH-DS and DASH-W Japanese version have evaluation capacities equivalent to those of the original and other language versions of the DASH.

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Axonal regeneration across end-to-side neurorrhaphy has recently been reported; however, neither the mechanism by which collateral sprouting from intact axons is elicited, nor the origin of the regenerating axons are known. There has even been controversy over the presence of collateral axonal sprouting from intact axons altogether. This reported experimental study was designed to clarify these questions. A rat sciatic nerve model was used. To avoid any mechanical damage to the donor nerve during the procedure, a Y-shaped silicone chamber was employed instead of direct suture. Axonal regeneration from the intact tibial nerve across the gap into the peroneal nerve was assessed using a retrograde neurotracer and immunohistochemical staining. Axonal regeneration across the gap was observed in 66 percent of the animals. The neurotracer evaluation clearly showed that all regenerating axons were sensory axons from the dorsal root ganglia. The authors concluded that Schwann cells from the distal wallerian degeneration of nerve segments did elicit collateral axonal sprouting from intact sensory axons, but not from motor axons in end-to-side neurorrhaphy. Invasion of the Schwann cells into the epineurial layer was the crucial step for the initiation of collateral axonal sprouting from the intact axons.

Tenosynovial thickening within the confined space of the carpal tunnel is thought to be the cause of the carpal tunnel syndrome (CTS). However, little is known about the pathological mechanism of tenosynovial thickening. In this study, the role of prostaglandin E(2) (PGE(2)) and vascular endothelial growth factor (VEGF) (two representative molecules that can induce oedema by increasing vascular permeability) was analysed in CTS by using immunohistochemistry and enzyme-linked immunosorptive assay (ELISA). Expression of these molecules was compared with the patients' clinical histories and a temporary increase in production of these molecules was found in cells within the vessels and synovial lining during the intermediate phase of the syndrome when the histology of the tenosynovium changes from oedematous to fibrotic. Statistical analysis clearly demonstrated that there is a close correlation between the expression of PGE(2) and VEGF. Furthermore, immunohistochemical analysis with anti-proliferating cell nuclear antigen (PCNA) revealed that the area with distinct VEGF expression closely matched the area where endothelial cells, vascular smooth muscle cells, and synovial lining cells proliferate. In contrast, despite marked alteration in the extracellular matrix (ECM) component of the tenosynovium, the fibroblasts responsible for most ECM framework production do not proliferate during any phase of CTS. Histological analysis demonstrated that angiogenesis takes place only during the intermediate phase. Since clusters of capillaries and arterioles are often surrounded by type III collagen-rich, disorganized, degenerate connective tissue, which contains fewer fibroblasts than normal, angiogenesis appears to take place as a part of a regenerative reaction that results in fibrosis. These findings strongly indicate that both PGE(2) and VEGF are expressed in the tenosynovium in CTS during the intermediate phase and induce the histological changes seen in the tenosynovium.