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  • Author or Editor: Kim J. Burchiel x
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Kim J. Burchiel and Lisa C. Russell

✓ The effect of topical glycerol application on normal and previously injured saphenous nerves was tested in 20 Sprague-Dawley rats. Anhydrous glycerol treatment of five normal nerves showed a rapid loss of C-fiber conduction within 5 minutes of application, while after 10 to 30 minutes, a complete conduction blockade in all fiber types was produced. The effect of anhydrous glycerol on both spontaneous firing from the neuroma and impulse propagation within the nerve was examined in 11 rats that had undergone saphenous neurotomy 7 days previously. In these animals, cessation of spontaneous action potential production from the neuroma was the earliest electrophysiological change noted, followed by loss first of C-fiber, then of A-fiber conduction. Graded concentrations of glycerol (25%, 50%, 75%, and 100%) were used in four rats with saphenous neuromas, which allowed selective blockade of spontaneous action potential generation and C-fiber conduction with minimal effect on A-fibers.

The neurophysiological mechanism of glycerol neurolysis appears to be a nonspecific conduction blockade of large and small fibers, which is established within minutes of its application. Spontaneous firing within damaged axons, which may play a role in a variety of cranial and peripheral nerve sensorimotor syndromes, is also exquisitely sensitive to glycerol application.

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Kim J. Burchiel and Lisa C. Russell

✓ Thirty-five Sprague-Dawley rats with saphenous neuromas underwent acute microfilament recording in the proximal nerve. The effect of the potassium channel-blocking agents, tetraethylammonium bromide (TEA) and 4-aminopyridine, on spontaneous activity in A fibers terminating in the neuroma was observed. The effects of gallamine were also tested. Of the two channel-blocking agents, TEA reliably increased spontaneous firing in active fibers and initiated spontaneous activity in some fibers with no spontaneous baseline discharge. 4-Aminopyridine had no effect on baseline activity of either spontaneously active or quiescent fibers; however, it inhibited spontaneous activity induced by prior TEA treatment. Gallamine application produced effects similar to TEA in that spontaneous activity was dramatically increased. These results imply that a tonic potassium conductance is present in regenerating fibers in the neuroma and that this conductance moderates the tendency toward hyperexcitability and spontaneous firing. Spontanous activity in nociceptive afferent fibers may represent the mechanism of chronic pain and paresthesias that often accompany peripheral nerve injury. These results suggest that agents which either increase potassium conductance or selectively inhibit the sodium current in regenerating axons might be effective in the treatment of these chronic pain syndromes.

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Kim J. Burchiel and Lisa C. Russell

✓ In 18 Sprague-Dawley rats, the left sciatic nerve was divided at the mid-femur level. Seven to 9 days later, microfilament recordings were made from the ipsilateral L-5 ventral root. Spontaneous activity in the ventral root, ranging from 0.1 to 6.1 Hz, was recorded in 12 of the 18 animals. Conduction velocity determinations showed this activity to be in A-beta and A-delta fibers. Recordings in 10 normal L-5 ventral roots from five control rats showed no spontaneous activity. In the rats with sciatic nerve division, the ongoing discharge appeared to originate in the cut end of the nerve since mechanical stimulation of the neuroma produced synchronous ventral root activity. Furthermore, cooling of the neuroma inhibited the spontaneous discharge, whereas with rewarming it returned. Spontaneous ventral root activity was also increased by systemic application of epinephrine. This activity was qualitatively similar to spontaneous activity that has been recorded in dorsal root microfilaments after peripheral nerve injury. The observation of an ongoing discharge in potentially nociceptive ventral root axons subsequent to nerve injury may be relevant to the mechanism of chronic pain of peripheral origin.