y 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. Using the methods, Scholz et al. (1986) observed 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, it was additionally found that, among this group of patients, many 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 weakness (Gonzalez-Reimers et al., 1991, pp. 219-222). As the disease progresses, the paresthesias can become painful. Finally, in more advanced cases of alcoholic peripheral neuropath
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