eMedicine Specialties > Neurology > Neuromuscular Diseases

Nutritional Neuropathy: Treatment & Medication

Author: R Andrew Sewell, MD, Clinical Instructor in Psychiatry and Mental Illness Research, Education, and Clinical Center (MIRECC) Fellow, Veterans Affairs Connecticut Health Care System, Yale University School of Medicine
Coauthor(s): Lawrence D Recht, MD, Professor of Neurology and Neurosurgery, Department of Neurology and Clinical Neurosciences, Stanford University Medical School
Contributor Information and Disclosures

Updated: Sep 7, 2009

Treatment

Medical Care

If the neuropathy is due to thiamine deficiency in an alcohol-dependent patient, consider instituting an alcohol-withdrawal protocol and providing seizure prophylaxis if indicated.

Surgical Care

  • Prevent trophic changes to the skin and ulceration of the feet with orthotics.
  • Consider surgical prophylaxis of osseous deformities.

Consultations

Refer the patient to an orthopedic surgeon for evaluation of osseous deformities.

Diet

Establishing an exact nutritional deficiency is often difficult. Many etiologies are often present simultaneously, especially in patients with malnutrition. Nutritional supplements are relatively innocuous. Therefore, for many nutritional neuropathies, the treatment is empirical and establishes the diagnosis. The further the disease has progressed, the lower the likelihood of reversing the symptoms.

  • Alcohol: Discontinue alcohol; give folate 1 mg intramuscularly (IM) once daily (qd) for 3 days and thiamine (vitamin B 1 ) 50 mg IM qd and/or 50 mg orally (PO) 3 times daily (tid) for 3 days followed by a maintenance dose of 5-10 mg PO qd.
  • Thiamine (vitamin B 1 ) deficiency: Administer parenteral B-complex vitamins, then oral thiamine, 50 mg IM qd for 3 days or 50 mg PO tid for 3 days; the maintenance dose is 5-10 mg PO qd. A maintenance dose of 0.5 mg/100 kcal is required.
  • Niacin (vitamin B 3 ) deficiency: The peripheral neuropathy of pellagra does not respond to niacin supplements alone; both niacin and pyridoxine must be added to the diet. Niacin causes a vasocutaneous flush; therefore, administer nicotinamide 100 mg IM or intravenously (IV), followed by 200 mg PO tid. The RDA is 11.3-13.3 niacin equivalents, so named because tryptophan is a niacin precursor such that 60 mg tryptophan is equivalent to 1 mg niacin. This RDA is increased in pregnant women and in those with diets high in leucine (eg, millet).
  • Pyridoxine (vitamin B 6 ) deficiency: Treat with excessive amounts of pyridoxine. Be careful of competitive inhibition with thiamine.
  • Cyanocobalamin (vitamin B 12 ) deficiency: Give cyanocobalamin (vitamin B 12 ) supplementation and treat the underlying disease responsible for the deficiency state. Administer IM injections 1 mg/day for 1 week followed by 1 mg/week for 1 month. If malabsorption is the etiology, prescribe 1 mg/mo for life. Oral supplementation of 1 mg/d is acceptable if the integrity of the GI tract is preserved; this yields an absorption of 10 mcg/d.
  • Folate deficiency: Give 1 mg PO qd. Do not give folate until cyanocobalamin (vitamin B 12 ) deficiency has been positively excluded. Folate corrects the hematologic abnormalities but worsen the neurologic dysfunction.
  • Alpha-tocopherol (vitamin E) deficiency: Treatment varies depending on the cause, as follows:
    • Cystic fibrosis - 5-10 IU/kg qd
    • Cholestatic disease - 15-25 IU/kg qd
    • Abetalipoproteinemia - 100-200 IU/kg qd in divided doses with vitamin A 15,000-20,000 IU qd
    • Short bowel syndrome - 200-3600 IU qd
    • Vitamin E transporter deficiency - 800-3500 IU qd
  • Gluten sensitivity: The ideal management is unclear, but a gluten-free diet appears prudent.
  • Malnutrition: Thiamine replenishment alone is usually not sufficient to cause resolution of the symptoms; increase the protein in the diet slowly to 1.5-2 g/kg body weight qd.

Activity

Physical therapy is recommended to prevent joint contractures. Therapy consists of daily exercises though full range of motion, the use of splints to prevent foot drop, and the use of orthotics to minimize ulceration at denervated pressure points.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Vitamins

To treat a nutritional neuropathy, replacing the deficient nutrients is necessary. This may involve administration of folate, thiamine (vitamin B 1 ), nicotinamide, pyridoxine (vitamin B 6 ), cyanocobalamin (vitamin B 12 ), alpha-tocopherol (vitamin E), vitamin A, or protein.


Thiamine (Thiamilate)

For thiamine deficiency syndromes.

Adult

50 mg IM qd for 3 d or 50 mg PO tid for 3 d, then maintenance dose of 5-10 mg PO qd

Pediatric

Not established

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions (intradermal test-dose recommended if sensitivity suspected); deaths have resulted from IV use; administer before or with dextrose-containing fluids in suspected thiamine deficiency


Niacinamide (Vitamin B 3 )

Source of niacin used in tissue respiration, lipid metabolism, and glycogenolysis.

Adult

100 mg IV/IM then 200 mg PO tid

Pediatric

Not established

May potentiate effects of ganglion-blocking and vasoactive drugs, resulting in postural hypotension; may be inactivated by bile-acid sequestrants (colestipol, cholestyramine)—wait 4-6 h before ingestion

Documented hypersensitivity; active liver disease or unexplained, significant increases in AST and ALT levels; large doses of niacin, especially sustained release, associated with severe hepatotoxicity; definite and recent history of peptic ulcer disease can reactivate ulcers

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 those with gallbladder disease, diabetes, or predisposition to gout; monitor blood glucose level; may elevate uric acid levels; pregnancy category C at doses above RDA


Cyanocobalamin (Crystamine)

Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B 12 in humans. Vitamin B 12 synthesized by microbes but not humans or plants. Vitamin B 12 deficiency may result from intrinsic factor deficiency (pernicious anemia), partial or total gastrectomy, or diseases of distal ileum.

Adult

1 mg qd IM for 1 wk then 1 mg/wk for 1 mo
Maintenance dose: 1 mg qmo for life

Pediatric

Not established

Documented hypersensitivity; hereditary optic nerve atrophy

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Severe hypokalemia may result in vitamin B 12 -megaloblastic anemia (may be fatal) due to increased cellular potassium requirements when anemia corrects


Folate (Folvite)

Important cofactor for enzymes used to produce RBCs.

Adult

1 mg PO qd

Pediatric

Not established

May decrease phenytoin to subtherapeutic levels, increasing seizure frequency

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Benzyl alcohol present in some products as preservative; associated with fatal gasping syndrome in premature infants; resistance may occur with alcoholism and deficiencies of other vitamins; do not administer until cyanocobalamin (vitamin B-12) deficiency ruled out


Alpha-tocopherol (Vita-Plus E Softgels, Vitec, Aquasol E)

Protects polyunsaturated fatty acids in membranes from attack by free radicals and protects RBCs against hemolysis.

Adult

Cystic fibrosis: 5-10 IU/kg PO qd
Cholestatic disease: 15-25 IU/kg PO qd
Abetalipoproteinemia: 100-200 IU/kg in divided doses with 15,000-25,000 IU PO qd of vitamin A
Short bowel syndrome: 200-3600 IU PO qd
Isolated familial vitamin E deficiency: 800-3500 IU PO qd

Pediatric

Not established

Mineral oil decreases absorption of vitamin E; vitamin E delays absorption of iron and increases effects of anticoagulants

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Large doses of vitamin E is pregnancy category C; vitamin E may induce vitamin K deficiency; necrotizing enterocolitis may occur with large doses


Multiple vitamins (MVI-12, Cernevit-12)

Dietary supplement.

Adult

MVI-12: 10 mL/24h IV
Cernevit: 5 mL/24h IV

Pediatric

MVI-12
<12 years: 5 mL/24h IV
>12 years: Administer as in adults
Cernevit
<12 years: 2.5 mL/24h IV
>12 years: Administer as in adults

Hydralazine and isoniazid may decrease effect of pyridoxine; pyridoxine may decrease effect of levodopa

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Pregnancy category C if doses above RDA recommendations; caution in severe renal or liver failure; children may require additional vitamin A

More on Nutritional Neuropathy

Overview: Nutritional Neuropathy
Differential Diagnoses & Workup: Nutritional Neuropathy
Treatment & Medication: Nutritional Neuropathy
Follow-up: Nutritional Neuropathy
Multimedia: Nutritional Neuropathy
References

References

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  2. Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG, Norell JE, Dyck PJ. A controlled study of peripheral neuropathy after bariatric surgery. Neurology. Oct 26 2004;63(8):1462-70. [Medline].

  3. Kesler A, Pianka P. Toxic optic neuropathy. Curr Neurol Neurosci Rep. Sep 2003;3(5):410-4. [Medline].

  4. Tanyel MC, Mancano LD. Neurologic findings in vitamin E deficiency. Am Fam Physician. Jan 1997;55(1):197-201. [Medline].

  5. Chang CG, Adams-Huet B, Provost DA. Acute post-gastric reduction surgery (APGARS) neuropathy. Obes Surg. Feb 2004;14(2):182-9. [Medline].

  6. Diamond I, Messing RO. Neurologic effects of alcoholism. West J Med. Sep 1994;161(3):279-87. [Medline].

  7. Erbsloh F, Abel M. Deficiency neuropathies. In: Bruyn GW, Vinken PJ, eds. Handbook of Clinical Neurology. Vol 7: Diseases of Nerves, Part I. New York: Wiley Interscience Division; 1970:558-638.

  8. Forbes CD, Jackson WF. A Colour Atlas and Text of Clinical Medicine. 1993. Aylesbury: Hazell Books Ltd; 428.

  9. Hattori N, Koike H, Sobue G. [Metabolic and nutritional neuropathy]. Rinsho Shinkeigaku. Nov 2008;48(11):1026-7. [Medline].

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

  11. Kumar N, EcEvoy KM, Ahlskog JE. Myelopathy due to copper deficiency following gastrointestinal surgery. Arch Neurol. 2003;60:1782-1785.

  12. Le Quesne PM. Persisting nutritional neuropathy in former war prisoners. Br Med J (Clin Res Ed). Mar 19 1983;286(6369):917-8. [Medline].

  13. Li K, McKay G. Images in clinical medicine. Ischemic retinopathy caused by severe megaloblastic anemia. N Engl J Med. Mar 23 2000;342(12):860. [Medline].

  14. Pallis CA. Neurological manifestations of nutritional disorders. Practitioner. Apr 1974;212(1270 Spec No):509-17. [Medline].

  15. Theodoropoulos DS. Optic neuropathy in vitamin B12 deficiency [letter; comment]. Lancet. Jul 11 1998;352(9122):146-7. [Medline].

  16. Weber GA, Sloan P, Davies D. Nutritionally-induced peripheral neuropathies. Clin Podiatr Med Surg. Jan 1990;7(1):107-28. [Medline].

Further Reading

Keywords

malabsorption neuropathy, alcohol neuropathy, Strachan syndrome, Jamaican neuritis, camp foot, dry beriberi, wet beriberi, deficiency amblyopia, nutritional optic amblyopia, tobacco-alcohol amblyopia, pellagra, subacute combined degeneration, vitamin deficiency, nutritional deficiency, peripheral neuropathies

Contributor Information and Disclosures

Author

R Andrew Sewell, MD, Clinical Instructor in Psychiatry and Mental Illness Research, Education, and Clinical Center (MIRECC) Fellow, Veterans Affairs Connecticut Health Care System, Yale University School of Medicine
R Andrew Sewell, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, American Pain Society, and American Psychiatric Association
Disclosure: Nothing to disclose.

Coauthor(s)

Lawrence D Recht, MD, Professor of Neurology and Neurosurgery, Department of Neurology and Clinical Neurosciences, Stanford University Medical School
Lawrence D Recht, MD is a member of the following medical societies: American Academy of Neurology, American Association for Cancer Research, American Neurological Association, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Milind J Kothari, DO, Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Hershey Medical Center
Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Glenn Lopate, MD, Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Chief of Neurology, St Louis ConnectCare, Consulting Staff, Barnes Jewish Hospital
Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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