Alcoholic_Neuropathy by ajizai


									                             Alcoholic Nneuropathy
Synonyms and related keywords: nutritional axonal sensorimotor polyneuropathy, toxic axonal sensorimotor

Background: Persons who have consumed large quantities of alcoholic beverages over an extended period of
time are at risk for developing a primary axonal sensorimotor peripheral polyneuropathy. Symptoms of
alcoholic neuropathy, like those of many of the other axonal mixed polyneuropathies, typically manifest
initially in the lower extremities and feet. Sensory symptoms (e.g., numbness, paresthesias, loss of vibration
and position sense) may present prior to or at the same time as motor symptoms (e.g., weakness). In most
cases, onset is insidious and prolonged, but some cases have been associated with acute and rapidly
progressive onset. Severe cases of alcoholic neuropathy can lead to the development of symptoms in the
proximal lower extremities and distal upper extremities.

Pathophysiology: Alcoholic neuropathy is a primary axonal neuropathy characterized by Wallerian
degeneration of the axons and reduction in the myelination of neural fibers. Controversy surrounds the
pathogenic role of alcohol in development of this neuropathy. The literature implicates nutritional deficiencies
that are common in alcoholic patients as the primary causative factor in development of this neuropathy.
Persons with alcoholism may consume smaller amounts of essential nutrients and vitamins and/or exhibit
impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol.

Thiamine, also known as the antiberiberi or antineuritic factor, is an essential vitamin in metabolism of
pyruvate and has a role in the health of the peripheral nervous system. Thiamine deficiency commonly is found
in alcoholic patients. Other studies have linked the direct toxic effects of alcohol on peripheral n erves with
development of neuropathy. A combination of nutritional deficiency and direct toxicity probably is involved in
the pathogenesis of alcoholic neuropathy, and these effects may be additive. Alcohol also has been implicated
in the development of cardiac autonomic neuropathy (CAN) and various cranial neuropathies, including optic
neuropathy and vagus neuropathy.

 In the US: True incidence of alcoholic neuropathy in the general population is unknown, and figures vary         Formatted: Bullets and Numbering
   widely, depending upon the definition of chronic alcoholism and the criteria used to classify and detect
   neuropathy. Studies using both clinical and electrodiagnostic criteria have estimated that neuropathy is
   present in 25–66% of defined “chronic alcoholics” using DSM-IV criteria for alcoholism. 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); the heart (as in cardiac myopathy and autonomic neuropathy);
pancreas; gallbladder; liver (cirrhosis); and peripheral nerves. Patients with multisystem damage as a result of
alcohol consumption often die of cardiac or liver failure.

Race: Cultural or racial factors involved in the consumption of alcoholic beverages are beyond the scope of
this article. The subject has not been studied well in terms of the development of alcoholic neuropathy. One

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noteworthy study, however, suggested that the risk of developing peripheral neuropathy is higher in alcoholic
patients with a history of parental alcoholism.

Sex: Ammendola et al recently conducted a study to assess differences between men and women in
development of alcoholic neuropathy This study used the sural sensory nerve action potential (SNAP)
amplitude (i.e., nerve conduction study) as the variable measure to detect significant neuropathy in a
population of males and females with chronic alcoholism. While 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

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 with advanced age, may be more at risk with the clinical
problems associated with peripheral neuropathies, such as frequent falls and loss of balance.

History: Ascertaining the symptomatic history of the patient with alcoholic neuropathy is not specific for
diagnosis. A detailed history of alcohol use should be obtained from any patient presenting with symptoms of
general neuropathy.
 Patients with alcoholic neuropathy typically present with a history of alcoholism and an insidious or rapid      Formatted: Bullets and Numbering
    onset of distal lower extremity paresthesias, dysesthesias, or weakness.
 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 complain of upper extremity symptoms.

Physical: Classic physical examination findings associated with alcoholic neuropathy may include the
 Diminished sensation to vibration or pinprick stimulation in a “stocking glove” distribution may be noted.       Formatted: Bullets and Numbering
 Thermal and proprioceptive sensation also may be reduced.
 Muscle stretch reflexes, especially of the gastroc-soleus muscle, may be diminished or absent.
 Weakness of ankle/toe dorsiflexion and/or ankle plantar flexion strength may be noted.
 Intrinsic atrophy of foot muscles may be observed in advanced cases.
 Gait ataxia with a widened base of support or bilateral foot drop may be observed.
 Evidence of other alcohol-related end-organ damage also may be observed on physical examination.

Causes: Excess alcohol consumption causes alcoholic neuropathy.

Charcot-Marie-Tooth Disease
Diabetic Neuropathy
Mononeuritis Multiplex

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Other Problems to Be Considered:

Heavy metal toxicity
Nutritional paraneoplastic syndromes
Drug-induced paraneoplastic syndromes

Lab Studies:
 Chemistry profile                                                                                                 Formatted: Bullets and Numbering
   o In alcoholic neuropathy, as in alcoholic liver disease, chronic alcohol consumption may cause an
       increase in liver enzyme levels (measured by aspartate aminotransferase [AST] and alanine
       aminotransferase [ALT] tests).
        Peripheral neuropathy may be among the first presenting symptoms associated with diabetes
           mellitus (DM); however, typically patients who present with diabetic-related polyneuropathy have
           had known DM for several years.
        Renal insufficiency indicated by elevated blood creatinine levels also may be a cause for
           peripheral neuropathy.
 Thiamine, vitamin B-12, and folic acid levels
   o These essential vitamins play an important role in the proper functioning of the peripheral and central
       nervous system.
   o Nutritional deficiencies associated with alcoholism are common and may contribute to the
       development of neuropathy in alcoholics (see Pathophysiology for discussion).
 Sedimentation rate: Erythrocyte sedimentation rate (ESR) may be elevated in patients with symptoms of a
   peripheral polyneuropathy due to an inflammatory condition (e.g., paraneoplastic syndrome).
 Screen for heavy metal toxicity: Lead and other heavy metal toxicities may be a cause for neuropathy.
 Test for human immunodeficiency virus (HIV) and venereal disease
   o Symptoms of peripheral neuropathy can be an early manifestation of HIV disease.
   o Syphilis also should be considered as a cause for neuropathy.

Other Tests:
 Nerve conduction studies                                                                                          Formatted: Bullets and Numbering
   o Sural / superficial peroneal sensory nerve action potential (SNAP): In ethanol (ETOH) neuropathy,
       response may be absent or amplitude may be reduced significantly.
   o Tibial / peroneal compound motor action potential (CMAP) and nerve conduction velocity (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.
   o Tibial H-Reflex: In ETOH neuropathy, the patient may have an absent response or may have
       symmetrically reduced amplitude or increased latency.
   o Ulnar / median SNAP: Consider performing this test to evaluate the extent of neuropathy if lower
       extremity sensory studies suggest abnormalities.
   o Ulnar / median CMAP: Consider performing this test to evaluate the extent of neuropathy if lower
       extremity motor studies suggest abnormalities.
 Needle electromyography
   o A thorough sampling of bilateral lower extremity muscles for testing includes intrinsic foot muscles,
       medial and lateral gastroc-soleus, tibialis anterior and posterior, short head of biceps femoris, adductor
       longus, rectus femoris, vastus medialis, tensor fascia latae, and lumbar paraspinals. This extensive
       screen also may be useful in evaluating for the presence of a concomitant lumbosacral radiculopathy.

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    o  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.
    o 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                                                                                                        Formatted

Rehabilitation Program:

   Physical Therapy: Comprehensive physical therapy for patients with alcoholic neuropathy may include          Formatted: Bullets and Numbering
    the following:
    o Gait and balance training, possibly with an assistive device for safety
    o Range of motion (ROM) exercises and stretching, particularly for the gastroc-soleus muscle, to prevent
         contracture and maintain normal gait mechanics
    o 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:
    o Training in performance of activities of daily living (ADL), with adaptive equipment if necessary
    o Compensatory strategies to accommodate for insensate or weakened limbs

 Psychiatric consultation may be indicated to help patients with chronic alcoholism recover from the            Formatted: Bullets and Numbering
   physical and emotional withdrawal associated with cessation of alcohol consumption.
 Nutrition consultation 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 cope
   with alcohol cessation.

Other Treatment (injection, manipulation, etc.): 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.

Painful dysesthesias associated with alcoholic neuropathy can be treated with gabapentin or amitriptyline as
adjunct agents with other over-the-counter pain medications, such as aspirin or acetaminophen.

Drug Category: Anticonvulsants
Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in
some cases of neuropathic pain. They 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, altered perception of pain, and increase in the pain threshold. Rarely
should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become
Drug Name

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Gabapentin (Neurontin) — Has anticonvulsant properties and antineuralgic effects; however, exact mechanism
of action is unknown. Structurally related to GABA but does not interact with GABA receptors.
Adult Dose
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 Dose
Not recommended
Documented hypersensitivity
Antacids may reduce bioavailability of gabapentin significantly (administer at least 2 h following antacids);
may increase norethindrone levels significantly
C - Safety for use during pregnancy has not been established.
Caution in severe renal disease

Drug Category: Tricyclic antidepressants
These agents are a complex group of drugs that have central and peripheral anticholinergic effects, as well as
sedative effects. They have central effects on pain transmission. They block the active reuptake of
norepinephrine and serotonin.
Drug Name
Amitriptyline (Elavil) — Analgesic for certain chronic and neuropathic pain.
Adult Dose
10-25 mg qhs initially; titrate to 25 mg tid if necessary
Pediatric Dose
<12 years: Not recommended
 >12 years: Administer as in adults
Documented hypersensitivity; patient has taken MAO inhibitors in past 14 d; has history of seizures, cardiac
arrhythmias, glaucoma, and urinary retention
Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (e.g.,
cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with
thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
D - Unsafe in pregnancy
Caution in cardiac conduction disturbances and history of hyperthyroidism, and renal or hepatic impairment;
avoid using in elderly patients

Further Outpatient Care:
 Encourage periodic follow-up visits to monitor for neuropathic progression and to assess functional            Formatted: Bullets and Numbering
   deficits and the effectiveness of prior interventions (e.g., alcohol cessation, gait/balance training).

 Cessation of alcohol consumption is necessary to improve or reverse the symptoms associated with               Formatted: Bullets and Numbering

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    alcoholic neuropathy. Support groups (e.g., AA) or pharmacologic intervention (Antabuse) may be of
    benefit to the patient with alcoholic neuropathy. Unfortunately, Antabuse also can cause neuropathy.

 Complications of alcoholic neuropathy include morbidity associated with falls and gait ataxia, as well as       Formatted: Bullets and Numbering
   the potential for thermal injuries, burns, and pressure ulcers. Multiple organ systems, including the heart
   and eyes, can be affected adversely by nerve damage associated with excessive alcohol consumption. The
   combination of alcoholic cerebellar damage coupled with impaired proprioception in the legs from
   neuropathy can be devastating to one's gait pattern and can make independent ambulation impossible.

 According to Dell et al, prognosis for arrest or reversal of symptoms associated with alcoholic neu ropathy     Formatted: Bullets and Numbering
   is fair to good following cessation of drinking.

Patient Education:
 Educate patients on how to protect themselves from the deleterious effects of alcoholic neuropathy on           Formatted: Bullets and Numbering
    touch, gait, balance, and general strength.

Medical/Legal Pitfalls:
 The question “Do you have a history of alcoholic beverage consumption?” should not be omitted while             Formatted: Bullets and Numbering
  taking the history of a patient with suggested alcoholic peripheral neuropathy, or any other disease for that
  matter. Patients may be reluctant to admit voluntarily to a history of problem drinking on an intake history
  form. This question should be asked directly to patients and may help with accurate diagnosis of their
  condition. It may even save their lives!

   Agelink MW, Malessa R, Weisser U, et al: Alcoholism, peripheral neuropathy (PNP) and cardiovascular           Formatted: Bullets and Numbering
    autonomic neuropathy (CAN). J Neurol Sci 1998 Dec 11; 161(2): 135-42[Medline].
   Ammendola A, Gemini D, Iannaccone S, et al: Gender and peripheral neuropathy in chronic alcoholism: a
    clinical- electroneurographic study. Alcohol Alcohol 2000 Jul-Aug; 35(4): 368-71[Medline].
   Bushbacher L: Rehabilitation of patients with peripheral neuropathies. In: Braddom RL, ed. Physical
    Medicine and Rehabilitation. WB Saunders Co; 1995:984.
   Dell PC, Guzewicz RM: Atypical peripheral neuropathies. Hand Clin 1992 May; 8(2): 275-83[Medline].
   Dumitru D: Axonal Loss: Mixed Sensorimotor Polyneuropathy. Vol 1. 1995:799-801.
   Hilz MJ, Zimmermann P, Rosl G, et al: Vibrometer testing facilitates the diagnosis of uremic and alcoholic
    polyneuropathy. Acta Neurol Scand 1995 Dec; 92(6): 486-90[Medline].
   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 1995 Jan; 52(1): 45-51[Medline].
   Nishiyama K, Sakuta M: Mexiletine for painful alcoholic neuropathy. Internal Medicine 1995, June; 34(6):
   Pessione F, Gerchstein JL, Rueff B: Parental history of alcoholism: a risk factor for alcohol-related
    peripheral neuropathies. Alcohol Alcohol 1995 Nov; 30(6): 749-54[Medline].

            By Mail: The Neuropathy Association 60 E. 42nd Street, Suite 942, New York, NY 10165 Online:
             Scholz E, Diener HC, Dichgans J, et al: Incidence of peripheral neuropathy and cerebellar ataxia in chronic
              alcoholics. J Neurol 1986 Aug; 233(4): 212-7[Medline].
             Victor M: Polyneuropathy due to nutritional deficiency and alcoholism. 1984; 2: 1899-1940.
         Alternative names:
neuropathy - alcoholic; alcoholic polyneuropathy
         A disorder involving decreased nave functioning because of damage that results from habitual use of
         Causes, incidence, and risk factors:
         Alcoholic neuropathy may be caused by the toxic effect of alcohol on nerve tissue. It is usually also
         associated with nutritional deficiencies and may be indistinguishable from nutritional-related
         neuropalhies such as beriberi. It can affect autonoinic nerves (those that regulate internal body
         functions) and nerves that control movement and sensation. Habitual alcohol use, prolonged heny use
         of alcohol, or alcoholism that is present for 10 years or more indicate high risk for alcoholic
         Avoid or minimize alcohol use. Total abstinence from alcohol may be necessary for persons with
         -- abnormal sensations (~anesthesia)
         painful sensations
         muscle weakness
         muscle cramps or muscle aches
         heat intolerance, especially after exercise
         impotence (in men)
         difficulty urinating
         incontinence (leaking urine)
         feeling of incomplete bladder emptying . .
         difficulty begining to urinate
         nausea vomiting
         Additional symptoms that may be associated with this disease:

          each impairment
          muscle function feeling loss
          muscle contractions
          muscle atrophy
          movement, dysfunctional
          eyelid drooping
          Note: Changes in muscle strength and/or sensation usually occur on both sides of the body and are
          more common in the legs than in the arms. Symptoms may develop gradually and progressively
          over weeks to years.

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Signs and tests:
Neuromuscular examination may indicate neive dysfuntion. Reflexes may be abnormal. and focal
neurological deficits (localized nerve abnormalities) may be present. Neurologic deficits that usually
symmetrical. Signs of autonomic dysfunction may be present. Eye inspection may show decreased
pupil response or other abnormality. Blood pressure may show orthostatic changes (a fall in blood
pressure when the person rises to a standing position).
Lab tests may be performed as indicated by the history, signs, and symptoms to rule out other
causes of neuropathy.
Nutritional studies may show deficiencies of thiamine (vitamin B l), pyidoxine ( vitamin B6)?
pantothenic acid and biotic vitamin Bl2, folic acid, niacin (vitamin B3), vitamin A, or other
Serum chemistries may show abnormalities (see chem-20).
Nerve conduction tests and EMG (a test of electrical activity in muscles) may be used to
determine the extent of neurological damage. - Nerve biopsy may be used to rule out other possible
causes of the signs and symptoms.
An upper GI and small bowel series may show decreased motility, delayed emptying of the
stomach, or other abnormalities. This series may be used to rule out physical obstruction as a
cause of vomiting or other GI (gastrointestinal) symptoms.
EGD (esophagogastroduodenoscopy~ is used to rule out physical obstruction as a cause of
gastrointestinal (GI) symptoms.
Isotope studies may indicate gastropare& (decreased gastric motility).
VCUG (voiding; cvstourethronram) may show decreased bladder emptying caused by damage to
the nerves controlling the bladder.
Other tests may be performed to determine the presence and extent of other neurological losses.
Treatment goals (assuming the immediate alcohol problem has been addressed) include controlling
symptoms, maximizing ability to function independently, and preventing injury. The following
paragraphs describe what may happen in treatment.
Physical therapy and/or the use of orthopedic appliances such as splints may be necessary to
muscle function and to maintain useful positioning of the limbs.
Medication may be used if necessary to treat pain or uncomfortable sensations. Response to
medications varies. The least amount of medication needed to reduce symptoms is advised, to reduce
dependence and other side effects of the chronic use of medications.
Common medications used may include over-the-counter analgesics such as aspirin (see salicylates-
&), ibuprofen, or acetaminophen - oral to reduce pain. Stabbing pains may respond to tricyclic
antidepressents or anticonvulsant medications such as phenytoin or carbamazepine.
A nutritious diet should be encouraged. Nutritional supplements may be recommended.
Positioning, or the use of a bed frame that keeps the covers off the legs, may reduce pain for some
Treatment of autonomic dysfunction (such as blood pressure problems, difficulty with urination, and
slow gastrointestinal movement) may be necessary. Treatment may be chronic, long-term, and
response to treatment is varies. Many treatment! may be tried before finding one that is successfull in
reducing symptoms. Use of elastic stockings, sleeping with the head elevated, or medications such as

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fludrocortisone may reduce postural blood pressure changes (orthostatic hypotension), Manual
expression of wine, intermittent catheterization, or medications such as bethanzchol may be necessary
to treat bladder dysfunction.
Impotence, diarrhea, constipation, or other symptoms are treated as appropriate. These symptoms
respond poorly to treatment.
Protection from injury to an extremity with reduced sensation is important. This may include
the temperature of bath water to prevent bums, change in footwear, frequent inspection of shoes to
reduce injury caused by pressure or objecls in the shoes, or other measures. Extremities should be
guarded to prevent injuries from pressure.
Use of alcohol should be stopped to reduce progression of the damage. Treatment of alcoholism may
include psychiatric interventions, social support such as AA (Alcoholics Anonymous), medications,
behavior mod
Expectations (prognosis):
Damage to nerves from alcoholic neuropathy is usually permanent and may be progressive if' use of
alcohol is not stopped. Symptoms vary from mild discomfort to severe disability. The disorder is
usually not life threatening, but may severely compromise the quality of life.
Complications :
discomfort or chronic
injury to extremities
Calling your health care provider:
Call for an appointment with your health care provider if symptoms indicate alcoholic neuropathy
be present.

    The Neuropathy Association Inc. ® does not endorse any treatments, medications, articles, abstracts or products that
    may be discussed herein. You should consult a neurologist with any questions you have about your condition.

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