ALCOHOLIC NEUROPATHY: THE CONCEPT OF DYING-BACK AXONAL DEGENERATION OR DYING-BACK PARANODO-AXONAL DEGENERATION?

Khodulev V.
State Institution “Republican Research and Clinical Center of Neurology and Neurosurgery” of the Ministry of Health of the Republic of Belarus, 24 F. Skoriny, 220114, Мinsk, Belarus, khodulev@tut.by

Alcoholic neuropathy is primarily an axonal degenerative neuropathy based on pathological data and the results of electrophysiological studies. The alcoholic neuropathy is characterized pathologically by degeneration beginning in the most distal portions of the longest peripheral nerve fibers. This pattern of degeneration has been called the dying-back degeneration, implying that disease in the neuron itself, rather than a disorder in the periphery, is responsible for the distal axonal degeneration. However, the exact sequence of neurophysiological and pathological events in nerve fibers, the result of which is dying back degeneration, remains unclear. Objective. To determine early neurophysiological mechanisms of development of axonal degeneration in patients with alcoholic neuropathy. Methods. Forty-six of the peroneal nerves were studied in patients with alcoholic neuropathy using nerve conduction studies. The compound muscle action potentials (CMAP) did not exceed two normal deviates. Absolute values of the indices for each patient were expressed as normal deviates. The axonal function of the nerve was evaluated by the amplitude of the CMAP from peak to peak, and the conduction function by the conduction velocity on the distal segments (ankle to knee) and the minimum F wave latency. The control group comprised 37 peroneal nerves. Results. The amplitude of the CMAP was -1.1 (-1.4, -0.2), conduction velocity -1.8 (-2.7, -1.5), the F-wave latency -1.3 (-2.1 -0.8). The change in conduction velocity (p<0.001) and F-wave latency (p=0.047) was more significant than the amplitude of the CMAP. Discussion. It was shown that axonal degeneration in alcoholic neuropathy begins with the process of mild demyelination of the fibers. However, these findings are quite distinctive and should be contrasted with electrophysiological features of a "demyelinating type of neuropathy". Subnormal conduction velocities are found distally in patients without clinical signs of neuropathy (Mawdsley and Mayer 1965). Mayer and Denny-Brown (1964) have measured reduced velocities in cat-nerves which had paranodal myelin loss. Axonal degeneration, myelin irregularity and segmental de/remyelination resulting from widening of consecutive nodes of Ranvier were also in alcoholic neuropathy (Koike et al. 2003). Continued shortage of vitamins and toxicity of alcohol affects myelin sheaths at the nodes of Ranvier, causing defects, which initially are biochemical. Later, structural alteration is seen, with retraction of myelin at the nodes. These changes occur first at the peripheral ends of the longest and largest fibers. We suggest that early, distal reductions of conduction velocity in alcoholics are due to paranodal disturbances with slow transmission in large fibers and subsequent fiber breakdown in the terminal axon. Conclusions. Thus, impairment of nerve conduction is an integral part of axonal degeneration, especially in the early subclinical stage of the disease and corresponds to the concept of the dying-back paranodo-axonal degeneration.
 

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