Nutritional Neuropathy Follow-up

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

• 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.

• 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.