Assessment of thumb positioning in the treatment of ulnar collateral ligament injuries. A laboratory study.

In the treatment of ulnar collateral ligament injuries in the metacarpophalangeal joint of the thumb, a cast or splint is often molded with the thumb and hand positioned so the patient can return quickly to a particular sport or activity. However, it is unknown whether a given position of immobilization or whether an early rehabilitation program will compromise ligament healing by causing undue tension in the ligament. To better define acceptable positions for thumb immobilization and a safe range of motion, this laboratory study measured strain in the ulnar collateral ligament at different degrees of metacarpophalangeal joint flexion. Ligament strain was found to increase with increasing joint flexion; the most significant increases in strain occurred as the joint moved from 0 degree to 25 degrees of flexion, with the dorsal portion of the ligament demonstrating greater strain than the palmar portion. Based on these results, immobilization of the metacarpophalangeal joint in excessive flexion and unrestricted early rehabilitation exercises should be done with caution and guided by the grade of injury or the quality of repair.

Internal deformations of intact and denucleated human lumbar discs subjected to compression, flexion, and extension loads.

Three rows of six evenly spaced 0.5 mm metal beads were implanted midsagittally into the discs of ten L4-5 human lumbar motion segments. The intradiscal bead displacements in response to compression, flexion, and extension loads were obtained by digitizing the bead positions from sagittal plane radiographs taken before and during the load application. Each disc was denucleated and the loading process was repeated. For the intact discs, in compression, the intradiscal bead displacements were predominantly anterior. In flexion, the beads in the center of the disc moved posteriorly whereas the beads closer to the periphery of the disc moved anteriorly. In extension, the central beads moved anteriorly and the beads closer to the periphery of the disc moved posteriorly. After denucleation, the bead displacements for compression and flexion implied an inward bulging of the inner wall of the annulus, despite outward bulging of the disc surface. We hypothesize that the inward bulging causes radial tensile stresses within the disc, leading to disruption of adjacent layers of annulus.

Hepatic triglyceride lipase in diabetic dogs.

Circulating triglyceride is cleared by a combination of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL). Although LPL has been extensively studied in diabetes, the effect of insulinization on H-TGL activity has not been well characterized. To determine whether H-TGL activity is altered in insulin-deficient diabetes, postheparin plasma was obtained from eight beagle dogs: three normal (nondiabetic) control dogs and five pancreatectomized diabetic dogs were studied acutely in poor diabetic control (underinsulinized), and again in short-term good control (well insulinized). Plasma glucose, measured at the start of the studies, was 88 +/- 10 mg/100 mL (mean +/- SD) in the normal control dogs, 434 +/- 31 mL in pancreatectomized dogs in poor diabetic control, and 87 +/- 16 in good diabetic control. Peak (five minutes) postheparin plasma H-TGL activity was increased in dogs in poor diabetic control (212 +/- 43 nmol FFA/min/mL) v the normal control dogs (135 +/- 21 nmol FFA/min/mL, P less than 0.02). When the dogs were in good diabetic control, the peak H-TGL (202 +/- 40 nmol FFA/min/mL) was also significantly increased compared with the level in normal dogs, while the sum of five and 45 minute postheparin H-TGL levels for the dogs in good diabetic control was less than when they were in poor diabetic control (P less than 0.01). Thus, insulin-deficient diabetes in dogs increases H-TGL, and short-term improvement of glycemic control with insulin partially corrects this increase.