eMedicine Specialties > Physical Medicine and Rehabilitation > Peripheral Neuropathy

Alcoholic Neuropathy

Scott R Laker, MD, Staff Physician, Department of Rehabilitation, University of Colorado Health Sciences Center
William J Sullivan, MD, Assistant Professor, Pain Medicine Fellowship Director, Director of Medical Student Education, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver Health Sciences Center

Updated: Sep 5, 2008

Introduction

Background

The development of peripheral neuropathy, specifically, the formation of primary axonal sensorimotor peripheral polyneuropathy, is a risk for persons who have consumed large quantities of alcoholic beverages over an extended period of time. Symptoms of alcoholic neuropathy, like those of many of the other axonal mixed polyneuropathies, manifest initially in the lower extremities and feet. Sensory symptoms (eg, numbness, paresthesias, dysesthesias, loss of vibration and position sense) generally manifest prior to motor symptoms (eg, weakness). However, patients may present with motor and sensory symptoms at initial presentation.

In most cases of alcoholic neuropathy, the onset of the polyneuropathy is insidious and prolonged, but some cases have been associated with acute, rapidly progressive onset. Symptoms seem to be associated with the lifetime consumption of alcohol, although exceptions are common. Severe cases of alcoholic neuropathy can lead to the development of symptoms in the proximal lower extremities and distal upper extremities.

Related eMedicine topics:
Alcohol and Substance Abuse Evaluation
Alcohol (Ethanol) Related Neuropathy
Alcoholism
Toxicity, Alcohols

Related Medscape topic:
Resource Center Addiction

Pathophysiology

Pure alcoholic neuropathy is distinguishable from beriberi (thiamine deficiency). A histopathological review of sural nerve biopsy results revealed small-fiber axonal loss, myelin irregularities, and possibly neural regeneration in chronic cases.^{[6,7 ]}A Japanese study found an alcoholic dehydrogenase gene mutation that led to decreased alcohol metabolism and decreased sensory nerve action potentials in the affected group.^{[8 ]}

Related eMedicine topic:
Nutritional Neuropathy

Frequency

United States

The true incidence of alcoholic neuropathy in the general population is unknown, and figures vary widely, depending on the definition of chronic alcoholism and the criteria used to classify and detect neuropathy. Using the criteria for alcoholism listed in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), studies employing clinical and electrodiagnostic criteria have estimated that neuropathy is present in 25-66% of defined "chronic alcoholics." The factors most directly associated with the development of alcoholic neuropathy include the duration and amount of total lifetime alcohol consumption.

Mortality/Morbidity

Chronic consumption of alcohol has been implicated in end-organ damage to multiple systems. Damaged structures include the brain (exhibited by development of Wernicke encephalopathy, Korsakoff psychosis, and cerebellar ataxia), heart (as in cardiac myopathy and autonomic neuropathy), pancreas, gallbladder, and liver (cirrhosis), as well as the peripheral nerves. Patients with multisystem damage as a result of alcohol consumption often die of cardiac or liver failure.

Children exposed to greater than 2 oz of alcohol per day in utero exhibit nerve conduction slowing and decreased compound muscle action potential (CMAP) amplitude in comparison with children with no prenatal exposure to alcohol.^{[9 ]}

Race

Cultural and racial factors involved in the consumption of alcoholic beverages are beyond the scope of this article. The subject has not been well studied in terms of the development of alcoholic neuropathy. However, one noteworthy study suggested that the risk of developing peripheral neuropathy is higher in alcoholic patients whose parents had a history of alcoholism.^{[10 ]}

Sex

Ammendola and colleagues conducted a study to assess differences between men and women in the development of alcoholic neuropathy.^{[11 ]}This study used the sural sensory nerve action potential (SNAP) amplitude (ie, nerve conduction study) as the variable measure to detect significant neuropathy in a population of males and females with chronic alcoholism. Although the study provided control for nutritional deficiencies, the female group with chronic alcoholism had a significantly lower sural SNAP amplitude compared with the male group with similar total lifetime dose of ethanol consumption (TLDEC). This study suggested that females may demonstrate increased sensitivity to the toxic effects of alcohol on peripheral nerves.

Age

Increased incidence of alcoholism occurs within the elderly population; however, discussion of this alarming trend is beyond the scope of this article. As mentioned previously, development of alcoholic neuropathy is associated with the duration and extent of total lifetime consumption of alcohol. Elderly persons, because of the natural diminution of postural reflexes and the nerve cell degeneration that occurs with advanced age, may be more at risk for the clinical problems associated with a peripheral neuropathy, such as frequent falls and loss of balance.

Clinical

History

Ascertaining the symptomatic history of a patient with alcoholic neuropathy is not specific for diagnosis. Pure alcoholic neuropathy is characterized by a progressive, sensory-dominant symptomatology. Interestingly, concomitant thiamine deficiency creates a much more variable presentation. A detailed history of alcohol use should be obtained from any patient presenting with symptoms of general neuropathy. Additionally, nutritional history and questioning regarding other neuropathy risk factors should be documented.

• Patients with alcoholic neuropathy typically present with a history of alcoholism and an insidious onset of distal lower extremity paresthesias, dysesthesias, or weakness. The most common symptom seems to be burning dysesthesias in the feet and toes. Less commonly, patients present with a more rapid, acute onset of symptoms.
• Patients also may have a history of gait ataxia and difficulty walking or a history of frequent falls.
• In cases of more advanced presentation, patients may report upper extremity symptoms.

Physical

Classic physical examination findings associated with alcoholic neuropathy may include the following:

• Diminished sensation to vibration or pinprick stimulation in a "stocking-to-glove" distribution
• Thermal and proprioceptive sensation abnormalities
• Muscle stretch reflexes, especially of the gastrocnemius-soleus muscle complex
• Weakness of ankle/toe dorsiflexion and/or ankle plantar flexion strength
• Intrinsic atrophy of foot muscles in advanced cases
• Gait ataxia with a widened base of support or bilateral foot drop

Evidence of other alcohol-related, end-organ damage also may be observed on physical examination.

Causes

Excess alcohol consumption causes alcoholic neuropathy. As previously stated, further studies must be performed to determine genetic influences on this disorder. 

Differential Diagnoses

Other Problems to Be Considered

Age-related neuropathy
Drug-induced paraneoplastic syndromes
Heavy metal neuropathy
Heavy metal toxicity
Nutritional paraneoplastic syndromes

Workup

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).^{[12 ]}
• 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.^{[13 ]}Syphilis also should be considered as a cause of neuropathy.

Imaging Studies

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

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.^{[14 ]}
• 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.

Treatment

Rehabilitation Program

Physical Therapy

Comprehensive physical therapy for patients with alcoholic neuropathy may include the following:

• Gait and balance training, possibly with an assistive device for safety
• Range of motion (ROM) exercises and stretching, particularly for the gastrocnemius-soleus muscle, to prevent contracture and maintain normal gait mechanics
• Strength training of weakened muscles

Occupational Therapy

Occupational therapy also can be an important component of the rehabilitation process in individuals with alcoholic neuropathy. Various elements can be combined into a program to help the patient maximize function, including the following:

• Training in performance of activities of daily living (ADL), with adaptive equipment if necessary
• Compensatory strategies to accommodate for insensate or weakened limbs

Medical Issues/Complications

Home evaluations can be ordered to assess the safety, appropriateness, and functionality of the patient in the home.

Surgical Intervention

If liver damage is evident, appropriate consultation with a transplantation service is recommended. However, neuropathy is generally an exclusion criterion for transplantation.

Interestingly, there has been a case of liver transplantation resulting in resolution of alcoholic polyneuropathy, although the patient was also treated for nutritional and vitamin-deficiency polyneuropathy.^{[15 ]}

Related Medscape topic:
Resource Center Liver and Intestine Transplant

Consultations

• Consultation with a psychiatrist may be indicated to help patients with chronic alcoholism recover from the physical and emotional withdrawal associated with cessation of alcohol consumption.
• Consultation with a nutritionist may be indicated to help formulate strategies for replacement of essential nutrients in malnourished alcoholic patients.
• Referral to a substance abuse support group, such as Alcoholics Anonymous (AA), may help patients to cope with alcohol cessation.

Other Treatment

An ankle-foot orthosis (AFO) may be needed to assist patients with weak ankle dorsiflexion, eversion, and/or plantar flexion. This device also can help with ankle proprioception and can improve gait and prevent ankle sprains. Vigilant foot care and the use of shoes with an enlarged toe box are useful in preventing foot ulcers.

The use of warm or hot footbaths is a potential hazard in alcoholic neuropathy, because such treatment may cause burns to a patient with an insensate extremity.

Medication

Painful dysesthesias associated with alcoholic neuropathy can be treated using gabapentin or amitriptyline as adjunct agents with other OTC pain medications, such as aspirin or acetaminophen.

Anticonvulsants

Use of certain antiepileptic drugs, such as the gamma aminobutyric acid (GABA) analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain. These drugs have central and peripheral anticholinergic effects, as well as sedative effects, and they block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, an altered perception of pain, and an increase in the pain threshold. Rarely should these drugs be used in the treatment of acute pain, because a few weeks may be required for them to become effective.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown. Gabapentin is structurally related to GABA but does not interact with GABA receptors.

Dosing

Adult

300 mg PO tid; may increase up to 1200 mg PO tid; titration to effect can take place over several days (300 mg on day 1, 300 mg bid on day 2, and 300 mg tid on day 3)

Pediatric

Not recommended

Interactions

Antacids may significantly reduce bioavailability (administer at least 2 h following antacids); may significantly increase norethindrone levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in severe renal disease

Tricyclic antidepressants

These agents make up a complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission and block the active reuptake of norepinephrine and serotonin.

Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain.

Dosing

Adult

10-25 mg PO qhs initially; titrate to 25 mg tid if necessary

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Interactions

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Contraindications

Documented hypersensitivity; patient has taken MAOIs in past 14 d; patient has history of seizures, cardiac arrhythmias, glaucoma, and urinary retention

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances and history of hyperthyroidism, and renal or hepatic impairment; avoid using in elderly patients

Analgesic, Topical

When used topically, capsaicin works through the depletion of substance P. It causes significant burning sensations when applied, and patients must be educated about this effect. 

Capsaicin (Dolorac, Zostrix)

Natural chemical derived from plants of the Solanaceae family. Penetrates deep for temporary relief of minor aches and pains of muscles and joints associated inflammatory reactions. May render skin and joints insensitive to pain by depleting substance P in peripheral sensory neurons.

Dosing

Adult

Apply to affected area tid/qid for 3-4 consecutive wk and evaluate efficacy; not to exceed 4 applications/d; wash hands with soap and water after applying

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; broken or irritated skin

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

For external use only; avoid contact with eyes; do not use tight bandage; discontinue use if condition worsens or symptoms persist for 14-28 d

Follow-up

Further Outpatient Care

• Encourage periodic follow-up visits to monitor for neuropathic progression, as well as to assess functional deficits and the effectiveness of prior interventions (eg, alcohol cessation, gait/balance training).

Deterrence

• Cessation of alcohol consumption is necessary to improve or reverse the symptoms associated with alcoholic neuropathy. Attendance of support groups (eg, AA) or the use of pharmacologic intervention (disulfiram [Antabuse]) may be of benefit to the patient with alcoholic neuropathy. Unfortunately, disulfiram also can cause neuropathy.

Complications

• Complications of alcoholic neuropathy include morbidity associated with falls and gait ataxia, as well as the potential for thermal injuries, burns, and pressure ulcers. Multiple organ systems, including the heart and eyes, can be adversely affected by nerve damage associated with excessive alcohol consumption. Alcoholic cerebellar damage coupled with neuropathic impairment of proprioception in the legs can be devastating to a patient's gait pattern and can make independent ambulation impossible.

Prognosis

• According to Dell and Guzewicz, the prognosis for the arresting or reversal of symptoms associated with alcoholic neuropathy is fair to good following cessation of drinking.^{[16 ]}

Patient Education

• Educate patients on how to protect themselves from the deleterious effects of alcoholic neuropathy on touch, gait, balance, and general strength.
• These patients should also be counseled on the need for rigorous skin checks of the lower extremities as a means of preventing ongoing morbidity.

Miscellaneous

Medicolegal Pitfalls

• The patient must be asked whether he/she has a history of alcoholic beverage consumption; this question should not be omitted while taking the history of a patient with possible alcoholic peripheral neuropathy or any other disease. Patients may be reluctant to voluntarily admit to a history of problem drinking on an intake history form. This question should be asked directly of the patient and may help in making an accurate diagnosis of the individual's condition. It may even save the patient's life.

References

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2. Corsetti G, Rezzani R, Rodella L, et al. Ultrastructural study of the alterations in spinal ganglion cells of rats chronically fed on ethanol. Ultrastruct Pathol. Jul-Aug 1998;22(4):309-19. [Medline].

3. Narita M, Miyoshi K, Narita M, et al. Involvement of microglia in the ethanol-induced neuropathic pain-like state in the rat. Neurosci Lett. Feb 27 2007;414(1):21-5. [Medline].

4. Chen X, Levine JD. Mechanically-evoked C-fiber activity in painful alcohol and AIDS therapy neuropathy in the rat. Mol Pain. 2007;3:5. [Medline]. [Full Text].

5. Miyoshi K, Narita M, Takatsu M, et al. mGlu5 receptor and protein kinase C implicated in the development and induction of neuropathic pain following chronic ethanol consumption. Eur J Pharmacol. May 21 2007;562(3):208-11. [Medline].

6. Koike H, Iijima M, Sugiura M, et al. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann Neurol. Jul 2003;54(1):19-29. [Medline].

7. Koike H, Mori K, Misu K, et al. Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. Neurology. Jun 26 2001;56(12):1727-32. [Medline].

8. Masaki T, Mochizuki H, Matsushita S, et al. Association of aldehyde dehydrogenase-2 polymorphism with alcoholic polyneuropathy in humans. Neurosci Lett. Jun 17 2004;363(3):288-90. [Medline].

9. Avaria Mde L, Mills JL, Kleinsteuber K, et al. Peripheral nerve conduction abnormalities in children exposed to alcohol in utero. J Pediatr. Mar 2004;144(3):338-43. [Medline].

10. Pessione F, Gerchstein JL, Rueff B. Parental history of alcoholism: a risk factor for alcohol-related peripheral neuropathies. Alcohol Alcohol. Nov 1995;30(6):749-54. [Medline].

11. Ammendola A, Gemini D, Iannaccone S, et al. Gender and peripheral neuropathy in chronic alcoholism: a clinical-electroneurographic study. Alcohol Alcohol. Jul-Aug 2000;35(4):368-71. [Medline]. [Full Text].

12. Peters TJ, Kotowicz J, Nyka W, et al. Treatment of alcoholic polyneuropathy with vitamin B complex: a randomised controlled trial. Alcohol Alcohol. Nov-Dec 2006;41(6):636-42. [Medline]. [Full Text].

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14. Schott K, Schäfer G, Günthner A, et al. T-wave response: a sensitive test for latent alcoholic polyneuropathy. Addict Biol. Jul 2002;7(3):315-9. [Medline].

15. Gane E, Bergman R, Hutchinson D. Resolution of alcoholic neuropathy following liver transplantation. Liver Transpl. Dec 2004;10(12):1545-8. [Medline]. [Full Text].

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19. Hilz MJ, Zimmermann P, Rösl G, et al. Vibrameter testing facilitates the diagnosis of uremic and alcoholic polyneuropathy. Acta Neurol Scand. Dec 1995;92(6):486-90. [Medline].

20. Koike H, Sobue G. Alcoholic neuropathy. Curr Opin Neurol. Oct 2006;19(5):481-6. [Medline].

21. Monforte R, Estruch R, Valls-Sole J, et al. Autonomic and peripheral neuropathies in patients with chronic alcoholism. A dose-related toxic effect of alcohol. Arch Neurol. Jan 1995;52(1):45-51. [Medline].

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23. Oishi M, Mochizuki Y, Suzuki Y, et al. Current perception threshold and sympathetic skin response in diabetic and alcoholic polyneuropathies. Intern Med. Oct 2002;41(10):819-22. [Medline]. [Full Text].

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Keywords

alcoholic neuropathy, alcohol neuropathy, peripheral neuropathy, alcoholism-induced neuropathy, alcohol-related neuropathy, primary axonal sensorimotor peripheral polyneuropathy, neuropathy treatment, axonal neuropathy, neuropathy pain, symptoms of neuropathy, nutritional axonal sensorimotor polyneuropathy, nutritional neuropathy, toxic axonal sensorimotor polyneuropathy, alcoholism, alcohol addiction

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, Assistant Professor, Pain Medicine Fellowship 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, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Daniel D Scott, MD, MA, BS, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Colorado at Denver and Health Sciences Center
Daniel D Scott, MD, MA, BS 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Michael T Andary, MD, MS, Residency Program Director, Professor, 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

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
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.

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