Alcoholism and Nervous System Injury

, 1991, p. 376). Sosenko et al. (1991) found that vibration aesthesia impairment is highly prevalent in waterspouts. Additionally, the researchers observed that senior(a) subjects generally had a higher vibration perception threshold. Scholz et al. (1986) exhibit signs of computer circumferential neuropathy in approximately 45% of alcoholic subjects. to date another study, Victor and Adams (1953) 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 busy, the ailment tends to be detected much much frequently. Scholz et al. (1986) observed electrophysiologic abnormalities in o'er 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 fetch some degree of neural abnormality. Furthermore, in both of these studies umteen 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 rush involves some form of motor invol

vement. 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 centre disease have symptoms of paresthesia, flunk, and pain. These conditions generally develop over a period of many months. Typically, numbness and tingling firstly occur distally: the legs tend to be affected ahead 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 may become painful and penis weakness can occur. In some patients, this weakness results in gait impairment.

Additional problems may also include ulnar kernel lesions at the elbow. These can result in weakness and numbness of the hand (D'Amour & Butterworth, 1994, p. 134)." Moreover, compression of the radial nerve at the humeral groove may cause wristdrop; while peroneal nerve compression at the fibular head can cause nucleotide drop.

Laboratory studies revealed an elevation of the Mr. E.'s liver function tests: Alk. phos., 137, T. bilirubin, 1.7, SGOT, 54, LDH, 235, cholesterol, 202, triglyceride, 186, and hemoglobin electrophoresis, 13.94. Furthermore, his glucose was 516 (high) and da Gamma gt, 105 (high). The patient's differential diagnosis included diabetic neuropathy, alcohol neuropathy, and cirrhosis of the liver. Until further studies can be completed, a attainable working diagnosis was given as alcoholic neuropathy.

everyplace the last several years, various electromyographic studies have been performed on degenerative alcoholics. As anticipated, most show sensory and motor nerve lesions which tend to be more common distally. Typically, nerve conductivity velocities are found to be slowed in the lower limbs; whereas, in severely affected patients, such defects additionall
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