Carpal tunnel syndrome (CTS) is a common peripheral compression neuropathy which is often idiopathic in etiology. There is evidence that the development of CTS may result from circulatory disturbances. The purpose of this thesis was to improve our understanding of the vascular component to the development and progression of CTS. Ultrasound allowed for non-invasive investigation of median nerve intraneural blood flow and morphology, tissue stiffness, and mechanics of the flexor digitorum superficialis (FDS) tendon and its adjacent subsynovial connective tissue (SSCT). Nerve conduction study (NCS) allowed for investigation of median nerve function. Three studies were completed, two with patients and one involving healthy participants, to investigate the relationship between local blood flow and carpal tunnel tissue function, morphology, and mechanics. Nerve function, intraneural blood flow, individual FDS and SSCT displacements, and measures of shear strain (relative FDS-SSCT displacement and shear strain index (SSI)) were quantified in CTS patients (Chapter 2). These patients were followed-up six months later and the measures were repeated (Chapter 3), allowing me to determine the prognostic value of ultrasound measures. Results from these two studies suggested a high interdependency among intraneural blood flow velocity, nerve function, and FDS-SSCT relative displacement and SSI. Intraneural blood flow velocity, peak FDS-SSCT relative displacement, and SSI were also significant predictors of median nerve function at 6-months follow-up. To directly investigate the effects of circulatory disturbances, temporary partial ischemia of the carpal tunnel was induced in healthy participants through a 30-minute occlusion protocol (Chapter 4). Partial ischemia immediately decreased intraneural blood flow velocity. Nerve dysfunction, and increased SSI and relative displacement were observed soon after. This thesis clearly demonstrates the interrelationship among median nerve vascular dynamics, tendon-SSCT kinematics, and nerve function. Altered nerve blood flow may be a driver in the development of CTS.