Study of wrist posture, loading and repetitive motion as risk factors for developing carpal tunnel syndrome.

Occupational risk factors of carpal tunnel syndrome (CTS) are popular current research targets, with main emphasis put on wrist posture and dynamics. In this study, we do not intend to pinpoint individual occupations, but aim to identify high risk wrist postures and actions which may occur across various occupations. It is hoped that prevention can thus be instituted in a general population by directing at the particular causative wrist actions rather than exclusively targeting isolated occupations. We performed a case-control study with 166 cases and 111 controls recruited from different hospitals in Hong Kong in 2004. All cases and controls completed the survey on their general health condition, smoking status, wrist posture and motion as well as psychosocial status at the time of diagnosis of CTS. Frequent flexion OR = 4.436 (95% CI: 1.833-10.734), frequent extension OR = 2.691 (95% CI: 1.106-6.547) of the wrist were found to be associated with CTS. Frequent sustained forceful motion of the wrist OR = 2.588 (95% CI: 1.144-5.851) was also found to be associated with CTS. Neutral wrist position and repetitive wrist motion were not associated with CTS. Adjustment was made for age, sex, BMI, smoking and psychosocial stress. Our study confirms that frequent flexion, extension and sustained force of the wrist increase the risk of developing CTS.

The cholinergic stimulating effects of ciliary neurotrophic factor and leukemia inhibitory factor are mediated by protein kinase C.

The intracellular mechanisms through which two trophic factors, ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF), regulate cholinergic development were examined in sympathetic neuron cultures. Treatment with CNTF or LIF increased levels of choline acetyltransferase (ChAT) activity by 375 and 350%, respectively. However, in neuronal cultures depleted of protein kinase C (PKC) activity by chronic phorbol ester treatment, neither CNTF nor LIF elevated ChAT activity. Further, the stimulation of ChAT due to increased cell density was not observed in PKC-depleted sympathetic neurons. The inhibition of CNTF-stimulated ChAT by phorbol ester occurred in a dose-dependent manner and chronic phorbol ester treatments did not alter the levels of the catecholamine biosynthetic enzyme tyrosine hydroxylase. Moreover, increased levels of diacylglycerol, an endogenous activator of PKC, were observed in sympathetic neurons treated with CNTF. However, neither CNTF nor LIF stimulated the hydrolysis of phosphatidylinositol 4,5-bisphosphate. These observations suggest that a common PKC-dependent pathway, which is independent of phosphatidylinositol 4,5-bisphosphate hydrolysis, mediates the cholinergic stimulating effects of CNTF, LIF, and cell-cell contact in cultured sympathetic neurons.