An adequate supply of vitamin B12 is crucial for the normal function of the nervous system and production of red blood cells. B12 deficiency injures the brain, spinal cord and peripheral nerves. The term "B12 neuropathy" refers to both spinal cord and peripheral nerve disease, since they frequently occur together and are difficult to distinguish. It affects 40 percent of people with B12 deficiency and is often the first indication of inadequate vitamin stores.
How It Happens
B12 neuropathy is caused by damage to the spinal cord and bundles of long peripheral nerves extending throughout the body. These include sensory nerves for pain and touch, motor nerves controlling muscles, and autonomic nerves regulating blood pressure, bowel and bladder function. A lack of B12 damages myelin, the protective coating surrounding nerve fibers. Without this insulation, nerves do not function properly and gradually deteriorate. The damage usually begins in the fingers and toes and spreads up the arms and legs.
Symptoms
The symptoms of B12 neuropathy reflect the specific types of nerves involved. In the early stages, sensory nerves are primarily affected. Numbness and tingling tend to affect the feet and legs more than the hands and arms. Shaky movements, unsteadiness and difficulty walking are also common. Leg weakness, poor coordination and bowel and bladder problems develop in advanced cases.
Neurological Examination
A neurological examination tests sensation, muscle strength, reflexes, coordination and walking. B12 neuropathy impairs the ability to feel pain, touch and vibration in the hands and feet. Decreased sensitivity to vibration when a tuning fork is placed on the foot or ankle is the most common abnormality detected. Reflexes are diminished or absent at the ankles and knees. Weakness in the legs is often associated with a loss of muscle mass. B12 neuropathy causes an unusual manner of walking with feet widely spread on the floor and a tendency to teeter from side to side.
Clinical Severity
When untreated, B12 neuropathy typically progresses over weeks to months. Initial sensory symptoms worsen and new problems such as unsteadiness and difficulty walking may develop. The severity of the neuropathy depends on the duration of symptoms prior to diagnosis. A study in "Medicine" in 1991 found that neurologic symptoms present for less than six months were typically mild. In contrast, abnormalities persisting for more than one year were more severe and often disabling. Neurological symptoms can occur without anemia or other blood cell abnormalities. In fact, people without anemia tend to have more extensive nervous system disease. The severity of the neuropathy is unrelated to the B12 level.
Diagnosis
The diagnosis is based on the characteristic neurological abnormalities and several diagnostic tests. Nerve conduction studies measure how fast nerves carry electrical signals. An abnormal test result indicates a neuropathy, but does not prove B12 deficiency as the cause. The B12 level in the blood is usually low, but occasionally normal. Methylmalonic acid and homocysteine are substances which build up in the blood when B12 is deficient. High levels confirm the diagnosis when other findings of B12 neuropathy are present. A trial of B12 replacement is used when the diagnosis is uncertain.
Treatment
B12 therapy halts progression of the neuropathy. Early diagnosis and treatment can prevent irreversible nerve damage. B12 stores are replaced with either intramuscular injections or pills. B12 injections act rapidly and are more reliably absorbed than pills. Oral B12 is an option after correction of B12 deficiency and neurologic recovery. Large daily doses are required because of variable and unpredictable absorption. A 1998 study in "Blood" showed that a daily 2,000 mcg B12 pill was as effective as a monthly 1,000 mcg B12 injection for maintaining optimal B12 reserves. However, oral B12 treatment of peripheral neuropathy has not been adequately studied.
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
- "Lancet Neurology"; Vitamin B12, Folic Acid, and the Nervous System; E. Reynolds; Volume 5 pg 949-960; 2006
- "Blood"; Effective Treatment of Cobalamin Deficiency with Oral Cobalamin; A. Kuzminski, E. Del Giacco, R. Allen, S. Stabler and J. Lindenbaum; Volume 92 pg 1191-1198; 1998
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