Alcoholic Neuropathy Workup

  • Author: Scott R Laker, MD; Chief Editor: Robert H Meier III, MD   more...
 
Updated: Dec 5, 2011
 

Laboratory Studies

  • Chemistry profile - Chronic alcohol consumption may cause an increase in liver enzyme levels (eg, aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase).
  • Diabetes testing - Peripheral neuropathy may be among the first presenting symptoms associated with diabetes mellitus (DM); however, patients who present with diabetes-related polyneuropathy have been diagnosed with DM several years previously. Hemoglobin A1C can be used to estimate average blood glucose levels over the course of previous months.
  • Creatinine level - Renal insufficiency indicated by elevated blood creatinine levels also may be a cause for peripheral neuropathy.
  • Thiamine, vitamin B-12, and folic acid levels - These essential vitamins play an important role in the proper functioning of the peripheral and central nervous systems and should be the among the first laboratory tests ordered on a patient with polyneuropathy. Nutritional deficiencies associated with alcoholism are common and may contribute to the development of neuropathy in alcoholic patients (see Pathophysiology).[14]
  • The following laboratory tests are ordered once more common diagnoses are essentially excluded:
    • Screen for heavy metal toxicity. The toxicity of lead and other heavy metals is a well-known cause of neuropathy.
    • Determine the erythrocyte sedimentation rate. It may be elevated in patients with symptoms of a peripheral polyneuropathy, owing to an inflammatory condition (eg, paraneoplastic syndrome).
    • Test for human immunodeficiency virus (HIV) infection and venereal disease. Symptoms of peripheral neuropathy can be an early manifestation of HIV.[15] Syphilis also should be considered as a cause of neuropathy.
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Imaging Studies

In the appropriate presentation of alcoholic neuropathy, imaging may be required to evaluate the etiology of nerve dysfunction.

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Other Tests

  • Nerve conduction studies (NCSs) - Although not specific for alcoholic neuropathy, NCSs can help to clarify the diagnosis and can to some extent quantify the amount of peripheral neuropathy present, when comparisons are made with age-adjusted normal values. However, nerve conduction velocities (NCVs) are generally normal or mildly slowed in patients with alcoholic neuropathy. Some fast-conducting axons can be spared, preserving measured velocity until axon loss has severely progressed. Demyelinating neuropathies show a greater loss of conduction velocity.
    • Sural/superficial peroneal SNAP - In ethanol (ETOH) neuropathy, the response may be absent or the amplitude may be significantly reduced. The superficial peroneal SNAP generally is more difficult to obtain than is the sural in average patients, including elderly individuals; therefore, it is less specific for pathology. The sural SNAP should be readily obtainable in most patients, including those of advanced age.
    • Tibial/peroneal compound motor action potential (CMAP) and NCV to intrinsic foot muscle - In ETOH neuropathy, test results may show significantly reduced amplitude. Results may demonstrate slowing of NCV below the reference range.
    • Ulnar/median SNAP - Consider performing this test to evaluate the extent of neuropathy if lower extremity sensory studies suggest abnormalities.
    • Ulnar/median CMAP - Consider performing this test to evaluate the extent of neuropathy if lower extremity motor studies suggest abnormalities.
    • Tibial H-reflex - In ETOH neuropathy, the patient may have an absent response or may have symmetrically reduced amplitude or increased latency. Typically, this is thought to be the most sensitive of electrophysiologic tests, with some studies quoting rates as high as 50%.
    • T-wave - One study found that the T-wave is somewhat more sensitive for alcoholic neuropathy.[16]
  • Needle electromyography (EMG)
    • Needle EMG is based on presentation. A typical peripheral neuropathy screen will involve a proximal muscle and a distal one in the lower and upper extremities.
    • A more extensive screen also may be useful in evaluating for the presence of a concomitant lumbosacral radiculopathy.
    • Significant abnormalities seen in patients with ETOH neuropathy include the presence of positive sharp waves and/or fibrillation potentials. Complex, repetitive discharges also may be observed. However, if the NCSs are normal, the presence of positive sharp waves in 1 intrinsic foot muscle is not necessarily indicative of neuropathic pathology. Occasionally, intrinsic foot muscles display abnormal electromyographic potentials in asymptomatic people.
    • If lower extremity muscle abnormalities are detected, a sampling of upper extremity muscles is indicated to estimate extent of disease.
  • Vibrometer testing - Results may be useful in detecting early signs of subclinical neuropathic disease.
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Contributor Information and Disclosures
Author

Scott R Laker, MD  Staff Physician, Department of Rehabilitation, University of Colorado Health Sciences Center

Scott R Laker, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Coauthor(s)

William J Sullivan, MD  Associate Professor, Pain Medicine Fellowship Site Director, Director of Medical Student Education, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center

William J Sullivan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, International Spine Intervention Society, and North American Spine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel D Scott, MD, MA  Associate Professor, Department of Physical Medicine and Rehabilitation, University of Colorado School of Medicine; Attending Physician, Department of Physical Medicine and Rehabilitation, Denver Veterans Affairs Medical Center, Eastern Colorado Health Care System

Daniel D Scott, MD, MA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, National Multiple Sclerosis Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Michael T Andary, MD, MS  Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine

Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists

Disclosure: Allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD  Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

References
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