Qualitative assessment of dementia.

Abstract

To the Editor: We would like to make the following observations regarding Coen et al's recent JAGS article describing the Dementia of the Alzheimer's Type Inventory (DAT).1 First, it is important to recognize that the DAT is making a qualitative distinction between the clinical presentation of Alzheimer's disease (AD) and that of non-AD/subcortical dementia. This distinguishes the DAT and similar qualitative instruments, ie, Hachinski's Ischemia Index and our own Qualitative Evaluation of Dementia (QED), from traditional quantitative rating scales such as the Mini-Mental State Examination (MMSE). Qualitative assessment provides a degree of specificity in the differential of dementia that has been previously available only after complex and expensive radiological or laboratory evaluation.2, 3 Second, although the DAT ostensibly seeks to discriminate diseases (ie, AD and vascular dementia), it may actually be discriminating syndromes (ie, cortical and noncortical dementia).4 This distinction is crucial to understanding the utility of instruments such as the DAT and the QED. Multiple anatomically or pathologically defined diseases can share the phenomenological features of a single clinical syndrome. We find that Frontal Type dementia (FTD) for example, can present identically to NINCDS Probable AD in the phenomenological space defined when the QED is mapped against a quantitative measure of dementia such as the Executive Interview (EXIT) (although adding the MMSE may discriminate them at any given EXIT score).5, 6 The DAT and the QED have trouble discriminating AD from FTD because both disorders share a common executive dyscontrol syndrome.4 It is the overwhelming prevalence of AD in geriatric samples, and the lack of important treatment differences between AD and FTD, that makes a qualitative approach to AD's assessment possible. Similarly, major depression, Parkinson's disease, non-cortical vascular dementia, and schizophrenia with deficit symptoms may all share a single passive dementia syndrome characterized by apathy and executive dyscontrol.4, 7 Nonetheless, syndromal differences can be very useful. The cortical dementias AD and FTD share clinical features that can be used to discriminate them from subcortical dementias at the bedside. Social disinhibition and environmental dependency are prominent in both AD and FTD and should lead to different types of problem behavior, caregiver burdens, or behavioral interventions relative to passive, environmentally indifferent subcortical cases.4 Syndromal features may, therefore, prove useful, both in the differential of dementia and in the development of syndrome specific treatment plans. Although different diseases can overlap in their syndromal features, a single disease may change it's syndromal presentation at different points in its natural history or if a concurrent illness is added. Qualitative changes may, therefore, lead to the discovery of superimposed co-morbid conditions or suggest evolving patterns of pathology at various stages in natural history. All cases of mixed AD + depression we have examined present within the 90% confidence limits for subcortical dementia without depression when mapped into an EXIT × QED space,8 even with objective cortical impairment on their mental state exams. This phenomenon is also suggested by Coen et al's finding that AD + MID or other noncortical impairment can change the presentation of AD to that of a “sub-cortical” dementia on the DAT. Only when AD remains uncomplicated by other conditions does it present within the EXIT × QED 90% confidence ellipse for “cortical dementia,” or as “AD” on the DAT. This brings us to our final point. If qualitative instruments such as the DAT or the QED can accurately discriminate uncomplicated AD patients from both noncortical dementia and AD + sub-cortical pathology at the bedside, is any further dementia workup required? After all, consider that (1) the tests being used in standard dementia workups target conditions presenting as noncortical dementias. These can now be discriminated from uncomplicated AD at the bedside using the DAT or the QED. (2) Usually, it is the non-cortical diseases, not AD or the FTDs, that are potentially reversible. (3) Mixed disorders with potentially reversible “excess disability” do not seem to be at risk of being mistakenly labeled “uncomplicated AD” by either the QED or the DAT.9 This means that AD patients with potentially reversible functional impairment can be discriminated qualitatively from uncomplicated AD after a very limited evaluation. Since AD is the most common cause of dementia in old age, a full dementia workup of all patients will subject many uncomplicated AD cases to tests for diseases that can be discriminated qualitatively from AD at the bedside. Until rational and effective pharmacotherapy becomes available for AD, it may not be necessary, or even desirable, in clinical practice for an assessment to identify Alzheimer's disease, per-se, independently of its syndromal features.