The clinical symptoms of alcoholic peripheral neuropathy were described more than 200 years ago. The descriptions by Lettsom (1787)1 and Jackson (1822)2 have led to the recognition and association of peripheral nerve disease with excessive ethanol use. Several terms connote alcohol neuropathy, including neuritic beriberi, neuropathic beriberi, and alcoholic neuritis. In patients with alcoholic neuropathy, nutritional deficiency goes hand in hand with alcohol abuse.

The similarity between beriberi, which is caused by deficiency of thiamine (vitamin B 1 ), and alcoholic neuropathy had long been noted, but in 1928, Shattuck was the first to seriously discuss the relationship.3 He suggested that polyneuritis of chronic alcoholism was caused chiefly by failure to take or assimilate food containing a sufficient quantity of vitamin B complex and might properly be regarded as true beriberi. However, this theory may be only partially true. Independently of thiamine deficiency, ethanol now appears to have a direct toxic effect on peripheral nerves.


The precise pathogenesis of alcohol neuropathy remains unclear. Separating ethanol use from nutritional and vitamin deficiencies, especially thiamine, has always been difficult and a source of long-standing debate. Nutritional deficiency (frequently associated with alcohol neuropathy) and/or the direct toxic effect of alcohol or both have been implicated and studied. In Wernicke-Korsakoff syndrome, a clear association between reduction of thiamine levels or thiamine-mediated enzyme activity (transketolase) has been established, though this has not been conclusively established in the case of peripheral neuropathy.

  • In their comparison of patient with alcoholism and nonalcoholic control subjects, Behse and Buchthal concluded that nutritional deficiencies alone did not produce the neuropathy.4
  • Monforte et al concluded that alcohol appears to be toxic to autonomic and peripheral nerves in a dose-dependent manner, based on heart rate, blood pressure, and electrophysiologic examination.5
  • In a study of macaque monkeys, Hallett et al failed to produce clinical and electrophysiologic signs of neuropathy in monkeys that were given a certain amount of alcohol for 3-5 years.6
  • Studies in rats also failed to demonstrate a direct toxic effect of alcohol on the peripheral nerves.
  • Most studies of peripheral neuropathy in humans and animals implicate nutritional deficiency as an etiology as opposed to the direct toxic effect of alcohol.
  • Independent of thiamine deficiency, ethanol now appears to have a direct toxic effect on the peripheral nerves. Dina et al suggest that catecholamines in nociceptors are metabolized to neurotoxic products by monoamine oxidase-A (MAO-A). This can cause neuronal dysfunction, which leads to neuropathic pain.7
  • Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status is well known. The clinicopathologic features of painful symptoms and small axon loss are distinct from those of beriberi neuropathy. This supports the view of direct neurotoxic effect by alcohol or its metabolites.8
  • Axonal transport and cytoskeletal properties are impaired by ethanol exposure. Protein kinase A and protein kinase C may also play a role in the pathogenesis, especially in association with painful symptoms.9



Depending on criteria and patient selection, incidence of peripheral neuropathy ranging from 10-50% has been reported. These studies included alcoholics hospitalized for other reasons or for detoxification. Neuropathy is more prevalent in frequent, heavy, and continuous drinkers compared to more episodic drinkers.5


Johnson and Robinson studied the mortality rate of individuals with alcoholism who had autonomic neuropathy. 10

  • Their findings suggested that evidence of vagal neuropathy in long-term alcoholics is associated with a significantly higher mortality rate than in the general population (a reported 88% survival rate at 7 years in alcoholics with autonomic neuropathy as compared to 94% in the general population).
  • Deaths due to cardiovascular disease are a major factor.
  • Many deaths were attributed to strokes, since heavy alcohol consumption is a significant risk factor for stroke.


A high incidence of alcoholic polyneuropathy has been observed in women and men. Women, when compared to men, are more predisposed to alcohol-induced damage, and the susceptibility extends to hepatic, cardiac, cerebral, and muscular changes. Also, there appears to be a greater sensitivity of females to the toxic effects of alcohol on peripheral nerve fibers unrelated to malnutrition.



Clinical manifestations of alcoholic neuropathy can be summarized as slowly progressive (over months) abnormalities in sensory, motor, autonomic, and gait function. Patients might ignore early symptoms, and seek help only when significant complications develop. Symptoms are often indistinguishable from other forms of sensory motor axonal neuropathy.

  • Sensory symptoms include early numbness of the soles, followed by dysesthesias of feet and legs, especially at night. "Pins and needles" sensation, which is reported commonly, progresses to severe pain that is described as burning or lancinating. Symptoms typically start distally and progress slowly to proximal involvement (dying-back neuropathy). When symptoms extend above the ankle level, the fingertips often get similarly affected, giving rise to the well-known stocking and glove pattern. Paresthesia might become unpleasant, even painful.
  • Motor manifestations include distal weakness and muscle wasting.
  • When proprioception becomes involved, sensory ataxia will occur giving rise to gait difficulty, independent of alcoholic cerebellar degeneration.
  • Autonomic disturbances are seen less commonly than in other neuropathic conditions (eg, diabetes).
    • Dysphagia and dysphonia are prominent secondary to degeneration of the vagus nerve. Other parasympathetic abnormalities include depressed reflex heart rate responses, abnormal pupillary function, sexual impotence, and sleep apnea.
    • Sympathetic dysfunction is rare but if present can produce orthostatic hypotension and hypothermia.
  • Frequent falls and accidents are common. These are secondary to gait unsteadiness and ataxia that are caused by cerebellar degeneration, sensory ataxia, or distal weakness.


  • Examination shows distal sensory loss in the lower extremities. In severe cases, the hands may be involved.
  • In addition to distal atrophy and weakness, deep tendon reflexes usually are decreased or absent.
  • Stasis dermatitis, glossiness, and thinness of skin of the lower legs are common findings.
  • Hyperesthesia and hyperalgesia may be seen along with hyperpathia.
  • Excessive sweating of the soles and dorsal aspects of the feet and of the palms and fingers is a common manifestation of alcoholic neuropathy and is indicative of involvement of the peripheral (postganglionic) sympathetic nerve fibers.
  • Occurrence of trophic ulcers is rare.
  • Charcot arthropathy, also known as neuroarthropathy, is most commonly associated with diabetes mellitus, despite a variety of other etiologies. It has also been associated with chronic alcoholism in nondiabetic individuals.
  • Rare cases have been reported of severe acute or subacute neuropathy mimicking Guillain-Barré syndrome.
  • Pressure palsies include radial neuropathy (Saturday night palsy), which is radial nerve compression at the spiral groove that yields wrist drop, in addition to compression neuropathy at many additional sites. Ulnar neuropathy at the elbow, radial or axillary nerve injury in the axilla (crutch-type compression), peroneal neuropathy at the fibular head, and superficial radial nerve are just a few of the potential sites of nerve injury.


  • Variants
    • Rare cases of acute or subacute alcoholic peripheral neuropathy have been described. They mimic Guillain-Barré syndrome, although biopsy and electrodiagnostic studies have revealed an axonal neuropathy, with normal CSF parameters. A causal association with ethanol has been proposed.
    • Pressure palsies: Alcoholics with generalized axonal peripheral neuropathy are prone to pressure palsies at multiple sites. Associated nutritional deficiency and weight loss might potentiate the same. Neurapraxia is more common than axonotmesis, and recovery is often the rule, although elderly patients do poorly.
Source: Medscape

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Parag said... @ March 22, 2011 at 2:41 AM

Eliminate alcohol completely from your diet.Peripheral neuropathy symptoms

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