Laboratory Studies
The diagnosis is based on accurate history of prolonged and excessive alcohol intake, clinical signs and symptoms, and electrophysiologic testing. Behse and Buchtal suggested that a minimum of 100 mL of ethyl alcohol (3 L of beer or 300 mL of spirits) per day for 3 years will precipitate the neuropathy.
Other Tests
Electrophysiologic findings primarily reveal evidence of primary axonal sensory motor polyneuropathy. Electrodiagnosis might detect a subclinical peripheral neuropathy.
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Sensory conduction studies may be abnormal even before the advent of clinical symptoms.
Sural nerve sensory action potentials (SNAP) are reduced slightly to moderately in conduction velocity and SNAP amplitudes also are reduced.
As the condition worsens, the sensory potentials may become unobtainable. The median, radial, and ulnar nerves show the same response as the disease progresses.
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Motor conduction studies of the lower extremities (tibial and peroneal nerves) may reveal a slight reduction in conduction velocity (not to exceed 70-80% of the lower limit of normal), with diminution of the compound muscle action potential (CMAP) amplitude with a slight prolongation in distal latency. The upper extremity nerves follow the same pattern as time progresses.
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The tibial H reflex latency is prolonged and becomes unobtainable if the condition continues to progress. The F waves are obtained more easily but reveal slight to moderate prolongation of latency.
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Needle electromyography (EMG) examination of the distal muscles of the lower extremities shows active denervation as well as chronic changes in the form of re-innervation patterns.
Spontaneous activity (positive sharp waves and fibrillation) is seen in the tibialis anterior and gastrocnemius.
The motor unit action potentials are reduced in recruitment pattern, with high-amplitude, long-duration, and polyphasic motor units.
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Avaria et al demonstrated that prenatal alcohol exposure is associated with abnormalities in nerve electrical properties and that the pattern is different from that seen in adults, showing conduction slowing and decrease in proximal and distal amplitude. [16]
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Chronic ethanolism-associated liver involvement [17] and nutritional deficiency may be inferred by abnormal liver function test results and macrocytic anemia. Thiamine levels are not consistently reduced, but the thiamine-mediated enzyme transketolase estimation is often abnormal.
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Cerebrospinal fluid (CSF) is typically normal or might show a mildly elevated total protein level.
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Patients have an increased risk of compression neuropathy, and electrodiagnostic findings can be complicated by superimposed mononeuropathies that are present. Recent methods of demonstrating small-diameter fiber neuropathy, such as quantitative sensory testing and intraepidermal nerve fiber density, have been applied but need to be applied in large scale.
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Sural nerve biopsy often shows evidence of generalized distal axonal loss affecting both large and small fibers but without distinctive pathologic features.
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Autonomic testing of parasympathetic and sympathetic reflexes is often abnormal (25% in one study), including analysis of heart rate variability, Valsalva maneuver, handgrip, tilt table, and standing maneuvers. [18] The pattern of abnormalities often resembles the changes in diabetes and other causes of autonomic failure.
Histologic Findings
Pathologic findings of the peripheral nerve in alcoholic neuropathy generally are agreed to consist of axonal degeneration with secondary segmental demyelination.
Alcohol-related peripheral neuropathy (ALN) is associated with a small-fiber neuropathy that can be detected with skin biopsy in heavy alcohol drinking individuals with normal thiamine status. Skin biopsy is a useful, minimally invasive biomarker that could extend studies to understand the effect of alcohol on the peripheral nerves and to evaluate potential therapeutic agents in larger clinical trials. [19, 20]
