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The pain mechanisms underlying radiculopathy due to disc herniation are still incompletely understood. This study assessed changes in brain-derived neurotrophic factor (BDNF) expression, a modulator of nociceptive information, in the dorsal root ganglion (DRG) and spinal cord dorsal horn following experimental disc herniation. Immunohistochemical analysis revealed an increase in percentage of BDNF-immunoreactive (IR) neurons profiles in the affected DRG and marked elevation in the BDNF-IR regions within both the superficial and deep layers at the corresponding spinal level with a peak at 3 days after nucleus pulposus (NP) application. These results thus show that herniated NP increases the BDNF production in the pain-processing neurons. Such changes can contribute to the development of inflammatory hyperalgesia.

This study determines the change in tension after an acute nerve lengthening, as would occur in peripheral nerve repair. Stress relaxation, a viscoelastic property, was studied with the use of 24 rabbit tibial nerves. The nerves were divided into three groups and were stretched 6%, 9%, or 12% beyond their original resting length. The mean 1-hour stress relaxations for the three groups were 48%, 34%, and 34%, respectively. Nerve stress relaxation was significantly greater at 6% strain than at 9% or 12% strain. These biomechanical findings have important clinical implications for nerve-stretch injury and for nerve repair.

The exact pathophysiologic mechanisms behind sciatica are incompletely known; however, compression of spinal nerve roots is known to be correlated to both pain and neural dysfunction in a segmental distribution of that specific nerve root. Compression per se may impair the transport of nutrients to the nerve tissue in such a way that affects the nerve root function. There also might be a local affect on nerve roots or root sleeves by substances leaking from the degenerated intervertebral discs.

We describe the morphologic changes that follow division of the transverse carpal ligament in patients with carpal tunnel syndrome. Fifteen hands in 12 patients with carpal tunnel syndrome were studied with magnetic resonance imaging before operation and for 6 weeks after operation. Eight hands were studied at 8 months after operation. Carpal arch width, anterior displacement of the carpal canal contents, and carpal canal volume were measured by use of multiplanar reformation and three-dimensional reconstruction of magnetic resonance images. There was a 24.2 +/- 11.6% increase in carpal canal volume 6 weeks after carpal tunnel release (p less than 0.001). This difference persisted at 8-month follow-up. There was an anterior displacement of carpal canal contents 3.5 +/- 1.9 mm from its original position 6 weeks after operation (p less than 0.001). This palmar displacement persisted at the 8-month follow-up. There was no statistically significant increase in carpal arch width 8 months after carpal tunnel release. We believe that division of the transverse carpal ligament restores median nerve function by increasing the volume of the carpal canal. This volumetric increase results from an anterior displacement of the newly formed transverse carpal ligament and not from a widening of the bony carpal arch.

Compression applied to a peripheral nerve may easily interfere with intraneural blood flow. In the present experimental study, a vital microscopic technique was used to observe changes in intraneural microcirculation (intrafascicularly and extrafascicularly) when graded compression was applied to a rabbit's tibial nerve by a specially designed minicompression device. Interference with venular flow was observed already at a pressure of 20 to 30 mm Hg while arteriolar and intrafascicular capillary flow was impaired at about 40 to 50 mm Hg. At 60 to 80 mm Hg no blood flow could be observed in the nerve. Nerves observed 3 or 7 days after 2 hours of compression at 400 mm Hg showed no or very slow stagnant blood flow within the previously compressed segment. It is concluded that acute compression of nerve may cause persistent impairment of intraneural microcirculation due to mechanical injury to blood vessels.

The minimal pressure for impairment of fast anterograde axonal transport was determined in rabbit vagus nerve. Proteins, transported by fast anterograde axonal transport, were labeled by a microinjection of [3H]leucine into the nodose ganglion, and a small compression chamber was applied around the cervical vagus nerve. In this way the nerve was subjected to acute, graded compression. Compression at 20 mm Hg for 2 h as well as sham compression did not induce accumulation of axonally transported proteins at the level of compression. However, a pressure of 30 mm Hg for 2 h induced a block of axonal transport at the site of compression. The causes of the axonal transport block are discussed as well as the minimal pressure level in relation to pressures found in clinical nerve compression lesions.

Severed and subsequently sutured rabbit flexor tendons were kept free and isolated in the synovial cavity of the knee joint. In one series the tendon specimens were surrounded by a dialyzing membrane to avoid cell seeding from the synovial fluid. At different intervals of time over a period of 3 weeks, the tendons were studied morphologically with special reference to scanning electron microscopy. Adhesions were not observed and, with synovial fluid as the nutrient medium, the tendons showed an intrinsic ability to repair in the superficial layers, also bridging the suture gap. Moreover, cell seeding, mainly of macrophages, from the synovial fluid could be demonstrated on the very surface of the tendon. When this cell seeding was prevented, the fibroplasia in the superficial layer of the tendon did decrease slightly, but tendon cell morphology was that of active fibroblasts. The results support the concept that flexor tendons may show intrinsic fibroplasia when nourished by synovial fluid, while macrophages, mainly, of extrinsic origin, contribute to restoration of the tendon surface.

Endoneurial fluid pressure measurements were made in the interstitial space of rat L5 dorsal root ganglia and in the corresponding sciatic nerves. Endoneurial fluid pressure was always higher in the ganglia than in the paired distal nerve. This proximodistal gradient in endoneurial fluid pressure may be the driving force responsible for the proximodistal convection of endoneurial fluid.