We thank Dr Martin for his thoughtful comments. We agree with him that the dilemma for the clinician may be, in part, the accurate categorization of exactly which psychiatric symptoms he or she faces in a given patient. We contend, however, that usage of DSM-III criteria1 should make the distinction between a delirious patient and a demented patient clear. Certainly, a demented patient may also be delirious, but it would then be the delirium that begs address, in the hope of returning to what represents normalcy for that patient. In clinical practice the difficulty in separation of these two entities seems to stem more from their definitions not being clearly understood than from disagreement on the manner of presentation of the patient. Regarding the references cited in support of correlating white matter neuropathologic changes with mental status aberrations, we offer the following comments: Given the well-known neuropathological changes in subacute combined degeneration of the spinal cord, and the plethora of psychiatric symptoms associated with hypovitaminosis B-12,2 we are astonished that the literature is not replete with detailed descriptions of cerebral white matter changes specific for this clinical entity. It is not. Woltman's3 wonderfully descriptive case series of seven necropsies is great fun to read, but obviously describes no single diagnostic entity. Adams4 describes two cases of moribund anemic patients who died within approximately a week of their hospital admission, whose anemia seemed to be responding to liver therapy. Diagnostic specificity aside (either case might have been a patient with folate deficiency) Adams concludes that “the order of involvement of the central nervous system is posterior columns, then lateral and anterior columns and finally cerebral white matter.” It could be argued that in our more modern era, vitamin B-12 deficiency rarely progresses to this extreme. Holmes5 describes fourteen patients with disorders of mood, confusion and memory deficits, slowing of mental processes, depression, delusions, and hallucinations. Two died, and only one had any cerebral white matter changes. We are forced to conclude that three cases does not constitute “abundant” (enough) neuropathological data from which to draw any conclusion—except that we need more data. Finally, we reiterate our original assertion: those who contend that vitamin B-12 deficiency causes dementia face the inertia of an impressive amount of clinical work that fails to support that association.