AN is related to chronic alcohol abuse, and the disease follows a slowly progressive course. Superficial sensory alterations are noted first and dominate the clinical picture throughout the disease [6]. Patients typically claim intense, burning pain in the lower limbs. Both hyperalgesia and allodynia have been reported. As the disease progresses, the arms become involved while sensory deficits and weakness set in [5]. Due to reduced sensations in arms and legs, AN patients are prone to injuries. Affected individuals frequently describe paresthesias, which are initially noted in hands and feet, but that subsequently progress towards proximal portions of the extremities. An unsteady gait and walking disabilities may be observed in advanced stages of the disease. In AN patients, muscle strength is largely unaltered [7].

The diagnosis of AN is based on a prior diagnosis of alcoholism which, in turn, relies on anamnestic data provided by the patient and third parties [8]. Although electrophysiological studies may be conducted to confirm a clinical diagnosis of polyneuropathy, findings such as decreased amplitudes of sensory potentials and mild to moderate reductions of nerve conduction velocities are not specific for AN [4].

Patients suffering from chronic alcoholism frequently present comorbidities such as alcoholic hepatitis, cardiomyopathy, and nutrient deficiencies. Workup should thus include studies to assess the condition of the respective organ systems and the patient's nutritional status. In this context, it should be noted that long-term alcohol abuse is associated with thiamine deficiency and possibly Wernicke-Korsakoff syndrome, a brain disorder. Even if thiamine deficiency is not a prerequisite for AN, it may modify the patient's clinical presentation [6] [9].

In detail, the following diagnostic measures may be undertaken [10]:

• Laboratory analyses of blood samples, paying particular attention to liver enzyme levels (γ-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase, ratio aspartate aminotransferase/alanine aminotransferase), carbohydrate deficient transferrin, markers of cardiac involvement (NT-proBNP, troponins, creatine kinase-MB), nutrient concentrations (thiamine, vitamin B12) and erythrocyte counts
• Assessment of fasting glucose levels and glucose tolerance to rule out diabetic neuropathy
• Imaging studies focusing on liver and brain
• Electrocardiography, echocardiography

Long-term, excessive consumption of alcoholic beverages is known to adversely affect distinct organ systems. Chronic alcoholism may cause alcoholic hepatitis and cirrhosis, arrhythmias and alcoholic cardiomyopathy, alcoholic neuropathy (AN) and epilepsy [1]. A causal relation between alcohol abuse and hypertension has repeatedly been suggested but has recently been questioned [2] [3].

AN is a neurological, potentially reversible disorder affecting the peripheral nervous system. Histopathological analyses of biopsy specimens obtained from AN patients reveal an overall reduced nerve fiber density as well as axonal degeneration with diminished axonal sprouting [4]. The clinical equivalents of these lesions are a pain, increased sensitivity to pain, dysesthesias, and weakness. Abstinence is the mainstay of treatment, but patients may benefit from supportive measures such as physical and occupational therapy as well as dietary supplementation [5].

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