Median Nerve Trunk Research Articles

Carpal Tunnel Neuropathy Caused by Injury: Reconstruction of the Transverse Carpal Ligament for the Complex Carpal Tunnel Syndromes

A comprehensive surgical and therapy program for the management of carpal tunnel neuropathy caused by injury has been proposed. The program is based on the restoration of the gliding interface between the median nerve trunk, the flexor tendons of the fingers, and the inner gliding surface of the transverse carpal ligament. The development of these new gliding surfaces is achieved by a surgery program of circumferential mesoepineurolysis of the median nerve in the hand and wrist followed by an anatomic reconstruction of the transverse carpal ligament. This biologic process is completed by a postoperative program of immediate hand function and median nerve gliding. Three hundred consecutive surgical patients were studied to confirm that the elastic mobilization of the median nerve actually doubled after a comprehensive nerve mobilization, thus supporting the ligament closure and early nerve gliding. Patients who have been available for repeat electromyographic (EMG) study at four to six months show EMG improvement that supports the clinical improvement. Finally, mobilization of the median nerve as described in the study has shown nerve revascularization within 30 seconds after tourniquet release and biologic recovery signals in the postoperative nerve gliding period and has proven to be, from the nerve nutrition standpoint, a safe procedure. The reliability that has been achieved in median nerve recovery is due to the anatomic reconstruction of the entire transverse carpal ligament. This surgical technique has proven to be the step necessary to produce a symbiotic alignment of the median nerve and the flexor tendon gliding anatomy. It has resulted in a consistent improvement in comfortable postoperative hand function in the complex class II and the complicated class III median neuropathies.

The oviduct musculature of the stable fly Stomoxys calcitrans: Properties of its spontaneous motility and neural regulation

AbstractThe muscles of the stable fly oviduct were striated and in the common oviduct both circular and longitudinal fiber layers were present. Although two muscle layers were evident in the lateral oviducts, both consisted of an irregular lattice of longitudinal fibers with extensive branching. This branching between fibers seemed to provide a pathway for the spread of excitation because semi‐isolated preparations of the oviduct severed from their connections to the central nervous system continued to contract in a spontaneous and rhythmic manner. Compression or shortening of the longitudinal muscles of the oviduct was the predominant mode of activity. Both phasic contractions (1–2 s in duration) and tonic events (15–30 s in duration) were observed. Innervation of the oviduct arises from the four major branches of the median abdominal nerve trunk that enter the ovipositor. Five to seven peripheral nerve cells were found along these four branches. Electrical stimulation of the severed median abdominal nerve trunk caused the oviduct to respond to a single pulse. However, these individual responses approached a fusion at 6 pulses per second (pps). Two of five preparations showed an inhibition of spontaneous phasic concentrations and a noticeable drop in baseline tonus during and after a 10–20 s interval of stimulation at a frequency of 0.5–2 pps. Endogeneous electrical activity was recorded from branch nerves in the ovipositor after connections to the central nervous system were cut. Potentials of two distinct durations were evident in this recorded activity. The significance of this and other findings are discussed.

Nerve compression as an essential factor in causing ischaemic and post-ischaemic paraesthesiae

In order to explain why ischaemia produced by compression at the proximal part of the forearm or at the wrist, does not cause sensory disturbances identical to those observed in compression at the upper arm, several experiments were made on ourselves and other subjects. The method used was essentially that of Lewis and Pochin. Circulation was blocked at different levels of the limb by applying the pressure of 200 mm/Hg with a sphygmomanometer cuff; compression of the median, ulnar and tibial nerve trunks was made with the aid of a small cushion under the cuff. We observed always that the nerve compression is an essential factor in causing ischaemic and post-ischaemic paraesthesiae.