Stasis edema and pigmentation, glossiness, and thinness of the skin of the lower legs and feet are common findings in patients with any severe form of neuropathy. Major dystrophic changes, in the form of perforating plantar ulcers and painless destruction of the bones and joints of the feet (“Charcot forefeet”), have been described but are rare. Repeated trauma to insensitive parts and superimposed infection are thought to be responsible for the neuropathic arthropathy, as discussed in Chaps. 7 and 43.
The CSF is usually normal, although a modest elevation of protein content is found in a small number. Findings of nerve conduction studies include mild to moderate degrees of slowing of motor and sensory conduction and a marked reduction in the amplitudes of sensory action potentials; the motor conduction velocities in distal segments of the nerves may be reduced, while conduction in proximal segments is normal. Denervated muscles show fibrillation potentials in a pattern that is consistent with more severe involvement peripherally.
The essential change is one of axonal degeneration, with destruction of both axon and myelin sheath. Segmental demyelination occurs only in a small proportion of fibers. The most pronounced changes are observed in the distal parts of the longest and largest myelinated fibers in the crural and, to a lesser extent, brachial nerves. In advanced cases, the changes extend into the anterior and posterior nerve roots. The vagus and phrenic nerves and paravertebral sympathetic trunks may be affected in advanced cases. Anterior horn and dorsal root ganglion cells undergo chromatolysis, indicating axonal damage. Secondary changes in the posterior columns are seen in some cases.
The nutritional factor(s) responsible for the neuropathy of alcoholism and beriberi has not been defined precisely. Because of the difficulty in producing peripheral neuropathy in mammals by means of a thiamine-deficient diet, the idea that thiamine is the antineuritic vitamin was questioned in the past. Very few of the animal experiments undertaken to settle this point were satisfactory from a nutritional and pathologic point of view. Nevertheless, several studies in birds and humans do indeed indicate that uncomplicated thiamine deficiency may result in peripheral nerve disease. The necessity of either accepting or rejecting the specific role of thiamine became less urgent when it was demonstrated, in both animals and humans; a deficiency of pyridoxine or of pantothenic acid could also result in degeneration of the peripheral nerves and therefore there were alternative reasons for nutritional polyneuropathy (Swank and Adams).
The question of whether polyneuropathy in the alcoholic patient might be a result of the direct toxic effects of alcohol and not of a nutritional deficiency has been raised from time to time (see the preceding text, and Denny-Brown, and Behse and Buchthal). The evidence for this view is not compelling, either on clinical or on experimental grounds, as already mentioned (see reference to Strauss, in introductory section on nutritional neuropathy). The data presented more recently by Koike and colleagues, ostensibly in favor of the existence of a true alcoholic neuropathy, in our view present no convincing support of a direct toxic effect of alcohol. In the end, we view alcoholic–beriberi neuropathy as a multiple B-vitamin deficiency. The interested reader will find a detailed critique of this subject in the chapters by Victor (1970) and by Windebank.
The first consideration is to supply adequate nutrition over a long period in the form of a balanced diet supplemented with B vitamins (equally important is to make certain that the patient follows the prescribed diet). If persistent vomiting or other gastrointestinal complications prevent the patient from eating, parenteral feeding becomes necessary; the vitamins may be given intramuscularly or added to intravenous fluids.