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Nutritional Neuropathy Follow-up

  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
 
Updated: Dec 28, 2015
 

Further Outpatient Care

After the diagnosis is made and treatment is initiated, the primary care physician can follow up with the patient.

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Deterrence/Prevention

See the list below:

  • Pyridoxine (vitamin B6) deficiency
    • Patients receiving isoniazid should receive pyridoxine 30 mg/d as prophylaxis.
    • Those receiving penicillamine should receive pyridoxine 100 mg/d.
    • Doses of more than 0.2 g/d have been associated with chronic sensory neuropathy.
    • The recommended daily allowance for men is 2 mg/d.
  • Alpha-tocopherol (vitamin E)
    • In patients with cystic fibrosis, short-bowel syndrome, or deficiency of vitamin E transporter, monitor the serum a-tocopherol level.
    • In those with cholestatic disease, monitor the ratio of serum a-tocopherol level to total serum lipid level.
    • For those with abetalipoproteinemia, use the adipose tissue percentage or results of erythrocyte hydrogen peroxide assay. (Serum a-tocopherol measurements are inaccurate in this disorder.)
  • Bariatric surgery
    • The chance of developing peripheral neuropathy is less in those who have surgery performed at the Mayo Clinic, do not have a jejunoileal bypass, take vitamin and calcium supplements, and attend nutritional clinics postoperatively.
    • Increased risk is associated with greater and faster weight loss; lower postsurgery BMI; lower serum albumin and transferrin; prolonged postoperative nausea, vomiting, diarrhea, and dumping; postoperative complications requiring rehospitalization; inadequate vitamin and calcium supplementation; and poor compliance. Accentuated and rapid weight loss appears to be the crucial risk factor.
    • Unrelated factors appear to be age, weight and BMI, diabetes, HgA1C, cholesterol, triglycerides, and length of hospitalization.
    • In the absence of a deficit, monitoring every 6 months for the first 2 years then annually after that is appropriate, giving oral B 12 supplementation when it is in the low-normal range.
    • In the presence of a deficit, give 0.5 mg/d oral B 12 supplementation, switching to 1.0 g/mo IM if the deficits are not corrected in 3 months or if anemia is also present.
    • Copper deficiency can present decades following surgery, so should be considered as a potential cause for neuropathy in anyone with even a remote history of bariatric surgery.
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Prognosis

See the list below:

  • An acute decrease in vitamin levels causes acute symptoms of vitamin deficiency but few morphologic changes. However, as the deficiency becomes chronic over months to years, such changes eventually take place.
    • In severe chronic deficiency states, response to pharmacologic treatment may be partial or nonexistent, as axonal degeneration can be halted but sometimes not reversed.
    • Improvement is always slow and, although peripheral nerves regenerate at a rate of 1 mm/d, full recovery cannot occur if the neuronal cell body or proximal neuron is damaged or if central pathways have been damaged.
  • Thiamine (vitamin B 1 ) deficiency: Recovery is slow, often leaving residual muscular weakness and atrophy. In areas of endemic deficiency, the mortality rate from cardiac causes if untreated is 25-70%.
  • Cyanocobalamin (vitamin B 12 ) deficiency: Rapid improvement occurs almost immediately after treatment is begun. Gradual improvement occurs over the next 4-6 months.
  • Alcohol neuropathy: Slow incomplete recovery occurs in weeks to months.
  • Vitamin E neuropathy: Recovery is incomplete.
  • Pyridoxine (vitamin B 6 ) excess: Most patients improve with discontinuation; few cases resolve entirely.
  • Malnutrition neuropathy: About 5% of patients have permanent and symptomatic neurologic damage because of extensive degeneration in the distal ends of posterior column fibers. Another 5% have deficiencies, as noted on physical examination.
  • Bariatric surgery: Only about 15% can expect complete resolution of their symptoms, although most respond to treatment.
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Patient Education

See the list below:

  • Dietary information on nutrition should be provided.
  • Patients who use nutritional supplements should be warned that, although pyridoxine is water soluble and excreted in the urine, they still should not take too much.
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Contributor Information and Disclosures
Author

Jasvinder Chawla, MD, MBA Chief of Neurology, Hines Veterans Affairs Hospital; Professor of Neurology, Loyola University Medical Center

Jasvinder Chawla, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Consulting Staff, Department of Neurology, 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, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Additional Contributors

Milind J Kothari, DO Professor, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Neurological Association, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Acknowledgements

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.

R Andrew Sewell, MD Associate Research Scientist in Psychiatry and Mental Illness Research, Education,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.

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Pernicious anemia. Characteristic lemon-yellow–tinged pallor with raw-beef tongue lacking filiform papillae. Used with permission from Forbes and Jackson.
Ischemic retinopathy caused by severe megaloblastic anemia.
 
 
 
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