Only one-third of patients with low vitamin B_{a dozen} levels receive adequate therapy. 50 Parenteral substitution remains the surest form of vitamin B₁₂ replacement. The recommended dosage is 1,000 ?g cobalamin im daily for 1 week, weekly for 1 month, then monthly. 10,33 Occasionally deaths have been reported in early phases of replacement due to the fall of potassium in patients with megaloblastosis. For patients with this condition, monitoring of potassium levels and a lower starting dose of vitamin B₁₂ is recommended (5 ?g/day in the first days). 10 Folate administration in patients with vitamin B₁₂ deficiency can partially correct megaloblastosis but may aggravate encephalopathy; therefore both values should be monitored together. 10 Frequently iron deficiency occurs together with vitamin B₁₂ deficiency and requires replacement. 51

Prognosis

Whereas hematological abnormalities normalize within 2 months of vitamin B₁₂ substitution, 11 the reversal of neurological symptoms depends on their severity and duration. 3,4 Mental symptoms have also been described to be partially or completely reversible after cobalamin substitution. 4,14,52,53 Chatterjee et al. 54 even reported the partial reversal of associated white matter lesions. Interestingly, in a recent case report cognitive improvement under cobalamin substitution was paralleled by a significant improvement of the P300 latency. 55 P300 has previously been suggested as a valuable parameter in the assessment of dementia 56,57 and has been used in the follow-up of treatment studies. 58

The improvement of mental impairment seems to be possible only in early stages, however; after longer duration there may be structural changes without the possibility of neuronal repair. Martin et al. 59 found improvement of cognitive dysfunction in 11 of 18 patients with low serum cobalamin only if symptoms persisted for less than 1 year. Similar observations were reported by other authors. 53,60 Chronic dementia seems to respond poorly but should, nevertheless, be treated if there is metabolic evidence for vitamin B₁₂ deficiency. 61

Talk

In the two case reports we presented, cobalamin deficiency is a likely contributor to the neuropsychiatric malfunctioning. In Patient 1, a borderline low vitamin B₁₂ serum level, pathological Schilling test, and histologically proven atrophic gastritis imply cobalamin deficiency. Patient 2 had long been known to suffer from pernicious anemia but had refused regular vitamin B₁₂ therapy. Cobalamin deficiency was confirmed by a low vitamin B₁₂ serum titer, macrocytosis, and a pathological Schilling test. Substitution of vitamin B₁₂ together with additional treatment resulted in improved cognitive function, which was documented by psychological retesting (Patient 1) or was indicated clinically by restored orientation (Patient 2).

Although in our patients, as well as in previously reported cases, the effects of vitamin B₁₂ substitution cannot be positively distinguished from the effects of co- medication, supporting therapeutic measures, and retest improvement, there is substantial evidence supporting the crucial involvement of vitamin B₁₂ in several pathophysiological conditions affecting the CNS, reaching from myelination to transmitter function. ₁₂ deficiency, which today can be unambiguously identified, is a common condition in the elderly population. Considering the devastating impact of dementia on the quality of life of the individual and also the vast costs this often incurable condition causes, the proper diagnosis and inexpensive treatment of cobalamin deficiency should not be missed, especially in the early phases of cognitive decline.

Modern diagnostic tools like the measurement of HY and MMA, as well as longitudinal testing of cognitive function and neurophysiological parameters, will help to further define the role of vitamin B₁₂ deficiency as a cofactor in the development of dementia and to elucidate why not all cobalamin-deficient patients develop mental symptoms.

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Several important functions have been attributed to vitamin B₁₂ as a coenzyme. 10,29,30 Both cobalamin and folate are needed for the methylation of homocysteine to methionine and in the synthesis of S- adenosylmethionine, a major methyl donor in the CNS. S-adenosylmethionine participates in various methylation steps involving proteins, phospholipids, DNA, and neurotransmitter metabolism. A defect in methylation processes is thought to play a central role in the biochemical basis of the neuropsychiatry of these vitamin deficiencies. 30