EXTERNAL COMPRESSION AND PARTIAL ISCHEMIA ALTER FLEXOR TENDON AND SUBSYNOVIAL CONNECTIVE TISSUE MOTION

Abstract

Carpal tunnel syndrome (CTS) is a peripheral median neuropathy that is commonly characterized by thickening and fibrosis of the subsynovial connective tissue (SSCT) surrounding finger flexor tendons. The degenerative process affecting SSCT can be initiated with excessive relative motion between the tendon and SSCT that ruptures interconnecting collagen. We used colour Doppler ultrasound to evaluate flexor digitorum superficialis tendon motion at two movement speeds with palmar compression, forearm compression, and partial ischemia (via brachial blood pressure cuff). Partial ischemia decreased SSCT displacement (22.9 ± 3.3 mm vs. 22.0 ± 3.3 mm; p = 0.015) while tendon displacement did not change. There was also a trend for increased relative tendon-SSCT displacement and shear strain index (SSI – relative displacement normalized to tendon displacement), which suggested partial ischemia might increase the strain in collagen that connects tendon and SSCT. Forearm compression decreased tendon displacement (28.5 ± 4.1 mm vs. 27.0 ± 4.6 mm; p = 0.043) while SSCT displacement also trended to decrease (24.0 ± mm vs. 22.5 mm; p = 0.059). With a lack of change in relative tendon-SSCT displacement and SSI, maintaining flexion-extension range of motion may have meant that forearm compression strained the musculotendinous unit at a location where SSCT was uncompromised. Palmar compression did not significantly affect any dependent motion variables, which suggested palmar compressive forces likely do not affect tendon-SSCT shear injury risk. The fast movement speed increased relative tendon-SSCT displacement and SSI while decreasing mean velocity ratio (MVR), which suggested greater tendon-SSCT shear strain in all baseline and compression conditions. Previously, increased relative tendon-SSCT displacement with fast movement speed was only shown in cadaveric investigations, but we confirmed this effect is transferable in an in vivo model. We induced ischemia proximally and found a reduction in SSCT displacement at the distal carpal tunnel. This finding suggests that the vascular network integrated within SSCT may play a role in altering tendon-SSCT excursion, independent of other external mechanical factors previously shown to increase relative motion and potential shear injury risk. Overall, this thesis showed that external mechanical compression at the palm or forearm likely do not negatively affect relative tendon-SSCT motion and that local ischemia and carpal tunnel blood flow should be considered when evaluating tendon and SSCT motion in relation to CTS development and progression.