Current deficits in diagnosis of pediatric b12 deficiency

For more than a century, the medical literature has clearly defined the effects of B12 deficiency on the brain and nervous system. These effects include cerebral atrophy, demyelination, degeneration of cortical neurons, and decreased production of neurotransmitters. B12 deficiency causes an array of neuropsychiatric manifestations including depression, apathy, paranoia, hallucinations, psychosis, self-injury, paresthesias, balance and gait problems, tremor, neuropathy, visual problems, taste, smell, and hearing problems, dizziness, and vertigo.

Unfortunately, the common diagnostic practice is to identify B12 deficiency only in the presence of anemia and macrocytosis. However, these symptoms often are not detectable even in people with advanced B12 deficiency. This is particularly true now that foods are heavily fortified with folic acid, which masks the hematologic effects of B12 deficiency. Moreover, many women have iron deficiency, which can mask a B12 deficiency, as can thalassemia and sickle cell anemia. (Note: Some of the children reported in the medical journals did have macrocytosis, which is a known sign of B12 deficiency, yet their physicians initially failed to diagnose it. By neglecting to perform further tests or provide treatment, these physicians allowed the deficiency to worsen until severe neurologic signs and symptoms were present as well as brain atrophy documented on CT or MRI scans.)

The prevalence of B12 deficiency is not known for children under the age of four years. There are also no standard of care guidelines for

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