Reduced Longitudinal Excursion of the Median Nerve in Carpal Tunnel Syndrome

I read with both interest and pleasure this excellent article on the in vivo measurement of longitudinal excursion of the median nerve (or lack thereof) utilizing Doppler ultrasound in carpal tunnel syndrome (CTS).1 Hough et al,1 noting a significant reduction in the longitudinal excursion of the median nerve in patients with CTS, once again calls attention to ischemia rather than only mechanical factors, that is, compression, as a significant potential source of symptoms. Most often, neuroischemia initially induces sensory symptoms of pain and paresthesias before motor signs become evident. This phenomenon also occurs in a mixed motor and sensory nerve when compression prevails, because the sensory nerves are the largest of the 2 types and therefore more susceptible to external pressure.2

In 1985, we too recognized neuroischemia as the provocative mechanism in chronic low-grade CTS when we first described the tethered median nerve stress test (TMNST).3 In this provocative maneuver, simultaneous extension of the supinated wrist and distal interphalangeal joints of the index finger may induce thenar as well as forearm pain with proximal radiation to the pronator teres, its intensity directly related to the duration of stretch. A prolonged palmar sensory orthodromic nerve conduction delay of reduced amplitude was found to be the most sensitive test in confirming the presence of CTS. Subsequent anatomic studies4 demonstrated “tethering” of the median nerve in this instance due to the presence of either/or both a pseudoneuroma as well as celluloadipous bands adhering the nerve to the flexor tendons. The forearm discomfort induced by the TMNST has an “aching” claudicant quality not dissimilar to that of neurogenic claudication as experienced by the lumbar spinal stenotic. In both instances, the pain is primarily myalgic and is directly related to the intensity and duration of the activity that precipitates it. In each of these 2 syndromes, the motor signs may be minimal and/or absent, that is, in the stenotic even with severe radicular pain the reflexes are often normal, the straight-leg raising test unrestricted, and motor weakness absent.

As in CTS, electrophysiologic compromise of the lumbar spinal sensory root afferents can be confirmed by noting slowing of the somatosensory evoked potentials even when electroneuromyography is otherwise normal. Once again, these 2 examples call attention to the necessity of listening to the clinical history, especially in the instance of compensation medicine where the diagnosis may be disputed. Patients in their descriptions of their symptoms may relate a classic history of either CTS and/or lumbar radiculopathy. The subsequent lack of corroborative motor signs does not necessarily negate the presence of organic disease. Appropriate electrodiagnostic testing including attention to the presence of sensory nerve abnormalities in this instance may be diagnostic.