subacute combined degeneration, B12 deficiency, malabsorption, nitrous oxide

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Updated October 12, 2014.

Written or reviewed by a board-certified physician. See About.com's Medical Review Board.

The term "myelopathy" refers to a disorder of the spinal cord. A myeloneuropathy is a disease process that effects both the spinal cord and peripheral nerves. Symptoms can include an unsteady gait, numbness, weakness, or bowel and bladder problems. The numbness in a myeloneuropathy is usually in a "stocking and glove" distribution beginning in the feet.

The causes of myelopathy are diverse, and include autoimmune disorders, tumors, toxins, vitamin deficiencies and more.

Appropriate treatment of the disorder will depend on the underlying diagnosis.

Vitamin B12 deficiency is the most classic form of myeloneuropathy due to a nutritional deficiency. The vitamin is usually found in animal proteins, but is common enough in supplemented cereals and some yeast products that it is very rare to become deficient based off dietary restriction alone. Vitamin B12 is absorbed in a complex manner that relies on a substance called intrinsic factor being secreted from the stomach and reacting with the vitamin to allow proper absorption in the small intestine.

Longstanding vegetarians who do not take care to supplement may develop B12 deficiency, but more commonly the problem results from poor absorption. Some people have an autoimmune disorder" in whichantibodies attack the cells that secrete intrinsic factor. As a result, B12 cannot be absorbed. Gastric bypass surgeries or inflammatory disorders like celiac disease can also lead to vitamin malabsorption. Medications like metformin and histamine H2 receptor antagonists may also lower B12 levels.

The myelopathy caused by low vitamin B12 has been called subacute combined degeneration: "subacute" because symptoms develop slowly, "combined" because multiple neurological symptoms are impacted, and "degeneration" because cells can die as a result. The major part of the spinal cord that is damaged is the posterior columns, which carries information about light touch, vibration, and position sense (proprioception) to the brain. As a result, people feel numbness and may feel tingling as well. The autonomic nervous system can also impaired, since these fibers also run in the spinal cord. A mild peripheral neuropathy also contributes to these symptoms. In addition, the optic nerve may be compromised, leading to diminished vision, and the olfactory bulb degenerates, resulting in a decreased sense of smell. Finally, people can develop a dementia, which is why this vitamin is routinely checked before diagnosing someone with a disease like Alzheimer's.

Diagnosis of B12 Deficiency

In addition to neurological changes, B12 deficiency a case a decrease in red blood cells, known as an anemia, and the disorder may be detected when checking a complete blood count that shows both low hematocrit and increased corpuscular volume (blood cell size). In addition, some people with a low normal B12 may still have problems if other laboratory measures such as methylmalonic acid and homocysteine are increased.

Vitamin B12 deficiency can be confirmed by a simple blood measurement of the vitamin level. Further studies used in the diagnosis of B12 deficiency include spinal cord magnetic resonance imaging (MRI), somatosensory evoked potentials or visual-evoked potentials. The MRI will show a bright signal in the posterior part of the spinal column. Evoked potentials show slowing in the visual and sensory pathways. Autonomic testing can confirm orthostatic hypotension due to a dysautonomia.

Beyond simply confirming the presence of B12 deficiency, it may be important to find the reason for that deficiency. While most of the time it is a simple dysautonomia, more severe problems like celiac disease or even a gastric tumor should not be missed.

B12 deficiency can be treated by either oral or intramuscular injections of the vitamin. Because so many cases of B12 deficiency are because the vitamin is not being well absorbed after being taken normally by mouth, initially intramuscular injections are preferred. If possible, the cause of the B12 deficiency should be addressed, though this is frequently never fully determined.

Nitrous Oxide Myeloneuropathy

Nitrous oxide is a commonly used anesthetic, and is often sometimes abused in the form of whipped cream cannisters or small containers called "whippets." Nitrous oxide can provide a "high," but also can lead to damage of the spinal cord in a manner very much like B12 deficiency.

There is a common but erroneous belief that nitrous oxide lowers B12 levels. This is not quite correct. Nitrous oxide interferes with the B12 molecule and changes it to an inactive form not useful to the nervous system. If B12 is already low, even a single dose of nitrous oxide, such as that used by a dentist's office, can precipitate neurological impairment as the remaining B12 is inactivated.

The treatment of nitrous oxide toxicity is similar to B12 deficiency. High levels of the vitamin are given to overcome the inactivating effects of the nitrous oxide. Of course, cessation of the drug is critical.

Recovery from B12 Deficiency

Recovery from B12 deficiency takes time. Typically it requires lifelong supplementation with vitamin B12. Improvement may continue for up to 6 to 12 months of supplementation, though some people will suffer from lasting deficits. Working with a physical or occupational therapist ay help people accommodate to any residual problems.

Sources:

Brent P. Goodman, Diagnostic Approach to Myeloneuropathy; Continuum: Spinal Cord, Root, and Plexus Disorders Volume 17, Number 4, August 2011

AH Ropper, MA Samuels. Adams and Victor's Principles of Neurology, 9th ed: The McGraw-Hill Companies, Inc., 2009.
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