Computer keyboarding biomechanics and acute changes in median nerve indicative of carpal tunnel syndrome.

BACKGROUND: Carpal tunnel syndrome is a common and costly peripheral neuropathy. Occupations requiring repetitive, forceful motions of the hand and wrist may play a role in the development of carpal tunnel syndrome. Computer keyboarding is one such task, and has been associated with upper-extremity musculoskeletal disorder development. The purpose of this study was to determine whether continuous keyboarding can cause acute changes in the median nerve and whether these changes correlate with wrist biomechanics during keyboarding. METHODS: A convenience sample of 37 healthy individuals performed a 60-minute typing task. Ultrasound images were collected at baseline, after 30 and 60 min of typing, then after 30 min of rest. Kinematic data were collected during the typing task. Variables of interest were median nerve cross-sectional area, flattening ratio, and swelling ratio at the pisiform; subject characteristics (age, gender, BMI, wrist circumference, typing speed) and wrist joint angles. FINDINGS: Cross-sectional area and swelling ratio increased after 30 and 60 min of typing, and then decreased to baseline after 30 min of rest. Peak ulnar deviation contributed to changes in cross-sectional area after 30 min of typing. INTERPRETATION: Results from this study confirmed a typing task causes changes in the median nerve, and changes are influenced by level of ulnar deviation. Furthermore, changes in the median nerve are present until cessation of the activity. While it is unclear if these changes lead to long-term symptoms or nerve injury, their existence adds to the evidence of a possible link between carpal tunnel syndrome and keyboarding.

Effects of computer keyboarding on ultrasonographic measures of the median nerve.

BACKGROUND: Keyboarding is a highly repetitive daily task and has been linked to musculoskeletal disorders of the upper extremity. However, the effect of keyboarding on median nerve injuries is not well understood. The purpose of this study was to use ultrasonographic measurements to determine whether continuous keyboarding can cause acute changes in the median nerve. METHODS: Ultrasound images of the median nerve from 21 volunteers were captured at the levels of the pisiform and distal radius prior to and following a prolonged keyboarding task (i.e., 1 hr of continuous keyboarding). Images were analyzed by a blinded investigator to quantify the median nerve characteristics. Changes in the median nerve ultrasonographic measures as a result of continuous keyboarding task were evaluated. RESULTS: Cross-sectional areas at the pisiform level were significantly larger in both dominant (P = 0.004) and non-dominant (P = 0.001) hands following the keyboarding task. Swelling ratio was significantly greater in the dominant hand (P = 0.020) after 60 min of keyboarding when compared to the baseline measures. Flattening ratios were not significantly different in either hand as a result of keyboarding. CONCLUSION: We were able to detect an acute increase in the area of the median nerve following 1 hr of keyboarding with a computer keyboard. This suggests that keyboarding has an impact on the median nerve. Further studies are required to understand this relationship, which would provide insight into the pathophysiology of median neuropathies such as carpal tunnel syndrome.

The effects of long-term spinal cord injury on mechanical properties of the rat urinary bladder.

We have demonstrated that bladder wall tissue in spinal cord injury (SCI) rats at 10 days post-injury is more compliant and accompanied by changes in material class from orthotropic to isotropic as compared to normal tissue. The present study examined the long-term effects (3-, 6-, and 10-weeks) post-SCI on the mechanical properties of bladder wall tissues, along with quantitative changes in smooth muscle orientation and collagen and elastin content. Bladder wall compliance (defined as det(F) - 1 under an equi-biaxial stress state of 100 kPa, where F is the deformation gradient tensor) was found to be significantly greater at 3- and 6-weeks (0.873 +/- 0.092 and 0.864 +/- 0.112, respectively) when compared to the normal bladders (0.260 +/- 0.028), but at 10 weeks the compliance reduced (0.389 +/- 0.061) to near that of normal bladders. This trend in mechanical compliance closely paralleled the collagen/elastin ratio. Moreover, changes in material class, assessed using a graphical technique, correlated closely with quantitative changes in smooth muscle fiber orientation. The results of the present study provide the first evidence that, while similarities exist between acute and chronic responses of the urinary bladder wall tissue to SCI, the overall alterations are distinct, result in profound and complex time dependent changes in bladder wall structure, and will lay the basis for simulations of the bladder wall disease process.

Contribution of the extracellular matrix to the viscoelastic behavior of the urinary bladder wall.

We previously reported that when the stress relaxation response of urinary bladder wall (UBW) tissue was analyzed using a single continuous reduced relaxation function (RRF), we observed non-uniformly distributed, time-dependent residuals (Ann Biomed Eng 32(10):1409-1419, 2004). We concluded that the single relaxation spectrum was inadequate and that a new viscoelastic model for bladder wall was necessary. In the present study, we report a new approach composed of independent RRFs for smooth muscle and the extracellular matrix components (ECM), connected through a stress-dependent recruitment function. In order to determine the RRF for the ECM component, biaxial stress relaxation experiments were first performed on decellularized extracellular matrix network of the bladder obtained from normal and spinal cord injured rats. While it was assumed that smooth muscle followed a single spectrum RRF, modeling the UBW ECM required a dual-Gaussian spectrum. Experimental results revealed that the ECM stress relaxation response was insensitive to the initial stress level. Thus, the average ECM RRF parameters were determined by fitting the average stress relaxation data. The resulting stress relaxation behavior of whole bladder tissue was modeled by combining the ECM RRF with the RRF for the smooth muscle component using an exponential recruitment function representing the recruitment of collagen fibers at higher stress levels. In summary, the present study demonstrated, for the first time, that stress relaxation response of bladder tissue can be better modeled when divided into the contributions of the extracellular matrix and smooth muscle components. This modeling approach is suitable for prediction of mechanical behaviors of the urinary bladder and other organs that exhibit rapid tissue remodeling (i.e., smooth muscle hypertrophy and altered ECM synthesis) under various pathological conditions.