Vitamin B12 is an essential nutrient required for the normal function of the nervous system and production of red blood cells. A deficiency of B12 causes serious complications such as anemia and nerve damage. Neurologic abnormalities develop in approximately 40 percent of people with B12 deficiency. B12 neuropathy may involve the brain, spinal cord and the peripheral nerves extending throughout the body. Even a mild deficiency may cause disabling neurologic symptoms.
Initial Treatment
Early treatment is crucial to prevent permanent nerve damage. Intramuscular B12 injections rapidly correct B12 deficiency, and are absorbed more reliably than pills. The recommended dose of 1,000 mcg is large, since lower doses could delay the response with the risk of irreversible neurologic damage. B12 injections are initially given daily for one week, and then weekly for four weeks. The particular schedule is not important as long as it includes eight to twelve injections during the first two to three months.
Long-Term Treatment
After correction of B12 deficiency, a monthly 1,000 mcg injection is usually adequate to maintain optimal B12 stores. There is no evidence that higher or more frequent doses are more effective for B12 neuropathy. B12 injections are required for at least three to six months to reverse neurologic abnormalities. They must be continued for life if the underlying cause of the deficiency is not correctable.
Response
Most neurologic symptoms improve with B12 injections. Abnormal sensations such as numbness and tingling usually improve first, often during the first two weeks of treatment. Unsteadiness, difficulty walking, and muscle weakness resolve more slowly over several months. In rare cases, symptoms transiently worsen initially, but then invariably improve with continued treatment. Neurologic abnormalities usually improve within three months, with a maximal response by six months. However, recovery is occasionally slow and may continue after a year or more of treatment.
Outcome
B12 injections prevent progression and reverse nerve damage, although the rate and degree of improvement varies. In a study in Medicine in 1991, half of patients had a complete recovery from their neuropathy, and half had a significant partial response. Moderate to severe neurologic abnormalities are permanent in 5 to 10 percent of cases. Neurologic symptoms that persist after six to 12 months of B12 therapy are often irreversible.
Predictors of Response
The duration and severity of symptoms prior to treatment are the most important factors determining the response to B12 injections. People with less severe symptoms for a shorter length of time have the best chance of a complete recovery. In contrast, a delay in treatment frequently results in irreversible nerve damage. In the 1991 Medicine study, neurologic abnormalities were often permanent when symptoms were present more than six months before B12 treatment. None of the patients with a severe neuropathy made a full recovery.
Younger people with less advanced neuropathy detected by magnetic resonance imaging or MRI also have a better response to B12 injections. A 2006 study in the Journal of General Internal Medicine found that patients under age 50 with less extensive MRI evidence of spinal cord involvement had the highest rate of complete recovery. The absence of anemia at the time of diagnosis is associated with more severe nerve damage before and after B12 treatment.
B12 Trial
People with unexplained neurologic symptoms should be tested for B12 deficiency since early diagnosis may prevent permanent nerve damage. However, B12 neuropathy may occur with a normal B12 level. A study in Blood in 2005 found normal B12 levels in 90 percent of patients with serious neurologic abnormalities that improved after B12 injections. Thus, all people with possible B12 neuropathy should receive a trial of B12 injections for at least three months. A response to B12 confirms that B12 deficiency is the cause.
References
- "Bailliere's Clinical Haematology"; Neurological Complications of Acquired Cobalamin Deficiency: Clinical Aspects; D. Savage and J. Lindenbaum; Volume 8 pg 657-678; 1995
- "Medicine"; Neurologic Aspects of Cobalamin Deficiency; E. Healton, D. Savage, J. Brust, T. Garrett and J. Lindenbaum; Volume 70 pg 229-245; 1991
- "Journal of General Internal Medicine"; Potential Outcome Factors in Subacute Combined Degeneration; O. Vasconcelos, E. Ooehm, J McCarter, W. Campbell and Z. Quezado; Volume 21 pg 1063-1068; 2006
- "Blood"; Cobalamin-Responsive Disorders in the Ambulatory Care Setting: Unreliability of Cobalamin, Methylmalonic Acid and Homocysteine Testing; L. Solomon; Volume 105 pg 978-985; 2005
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