Nutritional Neuropathy Follow-up

Updated: Sep 25, 2017
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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Further Outpatient Care

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



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.



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. In 2017, researchers suggested that acute or subacute axonal neuropathy in patients due to a variety of reasons including alcohol abuse, bariatric surgery or dietary deficiency is one syndrome, caused by micronutrient deficiencies. Therefore, it should be treated accordingly. [22]


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.