THE FREQUENTLY LOW COBALAMIN LEVELS IN DEMENTIA USUALLY SIGNIFY TREATABLE METABOLIC, NEUROLOGIC AND ELECTROPHYSIOLOGIC ABNORMALITIES

Cobalamin levels are frequently low in patients with dementia, but it is unclear if they represent definable deficiency and what the mechani sms are. Therefore, patients being evaluated for dementia who had low cobalamin levels but no obvious evidence of deficiency were studied he matologically, neurologically and with metabolic tests and were re-eva luated after cobalamin treatment. Abnormalities suggestive of or diagn ostic for deficiency were documented in most of the 16 demented and no ndemented patients. Metabolic results: 50% of patients tested had abno rmal deoxyuridine suppression and 44% had increased serum methylmaloni c acid and/or homocysteine levels; these test results correlated with each other. Neurologic results: 73% of patients had clinical abnormali ties, primarily mild neuropathies, not attributable to other causes, 7 5% had electroencephalographic abnormalities, 77% had abnormal visual evoked potentials and 33% had abnormal somatosensory potentials. Metab olic and neurologic dysfunction were present together or absent togeth er in all but 2 cases. Cobalamin therapy improved 50-100% of the vario us types of abnormalities, although it did not improve cognitive funct ion in the 13 demented patients. Food-cobalamin malabsorption was foun d in 60% of the patients. Despite the absence of megaloblastic anemia and rarity of traditional malabsorption of free cobalamin, low cobalam in levels in demented patients frequently represent mild cobalamin def iciency and are often associated with food-cobalamin malabsorption. Pe rhaps most importantly, this is accompanied not only by metabolic chan ges but by evidence of mild neurologic dysfunction. Their frequent rev ersibility by cobalamin confirms that these defects indeed arise from cobalamin deficiency. Although the long-standing dementia does not imp rove, treating such patients with cobalamin has other concrete benefit s.