EDITORIAL REVIEW Vitamin B 12 Deficiency and Dementia
The association of mental disturbance with vitamin B 1 2 deficiency has been recognized since Thomas Addison (1 849) first described pernicious anaemia and noted that 'the mind occasionally wanders'. Dementia was reported in later studies (Holmes, 1956;Droller and Dossett, 1959), but in these instances, the cognitive impairment did not respond to B12 replacement and it was frequently unclear whether the vitamin deficiency was just coexistent with the dementia or of aetiological significance. Subsequently, vitamin B 12 deficiency was included in many medical textbooks as a reversible cause of dementia (Harvey et al., 1984; Braunwald et al., 1987) despite the lack of definitive evidence of a causal relationship.
In recent years, screening with serum B12 assay in dementia has been widely recommended as a standard procedure (Wivel, 1988). However, surprisingly little systematic research has been carried out to examine the specific cognitive effects of B12 deficiency and there are few clinical guidelines about how to proceed if a low serum B12 is detected. This leads to the paradoxical situation in clinical practice where clinicians routinely screen demented patients with serum B12 assay but often ignore the finding of a low B12 level (Thompson and Freedman, 1989). Furthermore, some authors have challenged the existence of a reversible dementia due to B12 deficiency altogether (Byrne, 1987;Hector and Burton, 1988).
A few previous reviews examined the relationship between B 12 deficiency and various psychiatric symptoms or dementia. Zucker et af. (1981) reviewed the literature regarding cases of psychiatric disturbance linked to B12 deficiency. Criteria for including cases were as follows: (1) no other causes of organic mental illness; (2) a non-relapsing course;
(3) poor response to treatment other than B 12 replacement; (4) positive response to B12 replacement; and (5) two of the following: B12 level less than 250 pg/ml, macrocytosis or hyper-