953) analyzed 1030 hospitalized alcoholics and reported that only 9% exhibited polyneuropathy. Forty of the 1030 subjects, however, were additionally found to be asymptomatic. It has been estimated that alcoholic neuropathy may be responsible for about 30% of all cases of peripheral neuropathy (Luft et al., 1994, p. 200).
When electrophysiologic techniques are employed, the disease tends to be detected much more frequently. Scholz et al. (1986) observed electrophysiologic abnormalities in over 50% of subjects. In addition, the electromyographic (EMG) analyses employed by both Lefebvre-D'Amour et al. (1979) and D'Amour et al. (1991) showed that 93% of ambulatory alcoholic patients have some degree of neural abnormality. Furthermore, in both of these studies many of the subjects showed few clinical signs (D'Amour & Butterworth, 1994, p. 133).
The effects of central and peripheral alcoholic neuropathy can be disabling. In fact, most patients' chief complaint involves some form of motor involvement. Regardless though, the signs and symptoms of alcoholic neuropathy are quite diverse. Obviously, in its mildest form, the disease may be completely asymptomatic. However, the majority of alcoholic patients with peripheral nerve disease have symptoms of paresthesia, weakness, and pain. These conditions generally develop over a period of many months. Typically, numbness and tingling first occur distally: the legs tend to be affected before the hands and arms. Indeed, the "hallmarks" of peripheral neuropathy in the lower limbs are paresthesia, anesthesia, hyporeflexia, and
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