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Age and Ageing 2005 34(6):544-545; doi:10.1093/ageing/afi203
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© The Author 2005. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Reversible dementia—the implications of a fall in prevalence

When I took my oral exams in geriatric medicine in the mid 1980s, according to the literature which we then parroted, the percentage of dementias considered to be reversible was at least 20% [1]. However, only a few years later and in the same month, two separate reviews were published pointing out that the prevalence was in fact much lower, that is, just over 11% [2, 3]. By the mid-1990s, [4] and again just over 8 years later in 2003 in an update to the 1988 meta-analysis [5], the prevalence of reversibility was reported to have decreased to less than even 1%.

What can explain such a rapid fall and what are the clinical implications? Firstly, it is possible that some of the conditions which make up most of the underlying causes of reversibility such as the use of drugs which can cause reversible cognitive decline (benzodiazepines, alcohol, etc.), metabolic causes (such as B12 deficiency or hypothyroidism) or cognitive decline secondary to depression, have fallen for reasons not entirely clear to us. Secular trends often confound our understanding of disease processes. On the other hand, the prevalence may have stayed the same but these conditions are now being diagnosed earlier and treated more effectively. Finally, there may have been changes in reporting.

To begin with the possibility of a change in the natural history of the reversible dementias, there is little evidence that the prevalence of the underlying diseases has fallen. It is, however, possible that the elderly are indeed better cared for today. For example, Weytingh et al. [4] adduce some indirect evidence that improvements in primary care may have contributed to fewer patients with reversible dementia being referred to the relevant diagnostic frameworks. In support of this proposition, if one compares the data from the 2003 study [5] which updates the 1988 meta-analysis [3], in the more recent study there is evidence of less selection bias in that far fewer studies now emanate from inpatient units. Many more patients were examined either in outpatient settings or in the community where Alzheimer’s disease [AD] (the most common cause of dementia and to date still irreversible) is much more likely to be found [6]. As well, patients who made it into the more recent meta-analysis were both older and more likely to be female than those reported earlier, more clearly reflecting the dementia seen in the community, almost all of which will turn out to be AD [6].

There is also some evidence that better general education for primary care physicians in the principles of geriatric pharmacology has had a positive effect. For example, while medication as a cause of dementia (not necessarily reversed) was reported in 1.5% of all cases of dementia in 1988, by 2003 this particular aetiology had dropped almost to zero.

Perhaps a more careful use of standardised assessment instruments, consensus diagnosis and sufficient follow-up as a positive spin-off from the increasing number of drug trials for dementia has increased our diagnostic accuracy, both of dementia and of reversibility. Again, support for this hypothesis can be found in an examination of the proportion of cases initially suspected as dementia judged to indeed be suffering from some other condition. In the 1988 meta-analysis this percentage was only 3.7% whereas in the later review [5] it had risen to almost a fifth (18.6%). In the latter case, due to better diagnosis many conditions such as delirium or aphasia would have been excluded from studies, thus lowering the prevalence of reported reversibility.

Additional evidence for better assessment over the last few years can also be found in the work of Walstra et al. [7] who examined 169 patients for reversibility in a dementia clinic. Initially, they found that on clinical impression alone, it did appear that five patients had actually shown cognitive improvement after a potentially reversible aetiology had been treated. However, upon close follow-up (a practice which was not always observed in earlier studies), careful assessment could not confirm any true reversal.

If indeed, dementia reversibility occurs so infrequently, what are the clinical implications? Firstly, for good reasons other than the possibility of uncovering reversibility, old people with cognitive decline require an accurate diagnosis. Perhaps they are not demented. Even if they are, patients and their families will want a clear prognosis. Most patients with dementia will be elderly and as such, often suffer from various co-morbidities. It has become a truism that many of the frail elderly with symptoms of functional decline benefit from comprehensive geriatric assessment [8]. One need not adduce the possibility of dementia reversibility to justify properly examining old people.

However, if the clinician is convinced that reversibility is an extremely rare event, then the search for it should be more focused. If, on the other hand, one believes the prevalence to really be higher, there would be more of a justification for broadening the diagnostic chase, with all of the clinical and resource implications.

This issue has been much debated for example, relating to the question of a universal versus focused recommendation for neuro-imaging. Much ink has been spilt on this question, some of it with passion [9]. To me the choice boils down to what I call the ‘Canadian approach’ [10], more focused and clinical, versus the ‘American approach’ [11], which argues for a more universal and aggressive testing strategy.

This issue is not a trivial one. An intrusive diagnostic approach, especially if the odds for finding anything are slim, can often do more harm than good, in particular in the frail elderly [12]. With respect to dementia reversibility, it does appear to be a rare event. While older people with cognitive decline need and deserve a careful assessment, the search for reversibility should not be what primarily leads the clinician. Sometimes in geriatric care, it is best to make haste slowly.

A. Mark Clarfield

Department of Geriatrics, Soroka Hospital, PO Box 151, Beer-sheva 84101, Israel Fax (+972) 8 628 6599

Email: marklclar{at}bgu.ac.il

References

  1. Neshkes RE, Jarvik LF. The central nervous system—dementia and delirium in old age. In Brocklehurst JC ed. Textbook of Geriatric Medicine and Gerontology. Churchill Livingstone, Edinburgh, 1985, pp. 309–327.
  2. Barry P, Moskowitz MA. The diagnosis of reversible dementia in the elderly: a critical review. Arch Intern Med 1988; 148: 1914–18.[Abstract/Free Full Text]
  3. Clarfield AM. The reversible dementias: do they reverse? Ann Intern Med. 1988; 109: 476–86.[Abstract/Free Full Text]
  4. Weytingh MD, van Crevel H. Reversible dementia: more than 10% or less than 1%? A quantitative review. J Neurol 1995; 242: 466–71.[CrossRef][Web of Science][Medline]
  5. Clarfield AM. The decreasing prevalence of reversible dementias: an updated meta-analysis. Arch Int Med 2003; 163: 2219–29.[Abstract/Free Full Text]
  6. Evans DA, Funkenstein H, Albert MS et al. Development of Alzheimer disease in a community population of older persons: higher than previously reported. JAMA 1989; 262: 2551–56.[Abstract/Free Full Text]
  7. Walstra GJM, Teunisse S, van Gool WA, van Crevel H. Reversible dementia in elderly patients referred to a memory clinic. J Neurol 1997; 244: 17–22.[CrossRef][Web of Science][Medline]
  8. Stuck AE, Siu AL, Wieland GD, Adams J, Rubinstein LZ. Comprehensive geriatric assessment: a meta-analysis of controlled trials. The Lancet 1993; 342: 1032–36.[CrossRef][Web of Science][Medline]
  9. Wild D. Study: incidence of reversible dementias very low. CNS News 2004; 6: 35.
  10. Patterson CJS, Gauthier S, Bergman H et al. The recognition, assessment and management of dementing disorders: conclusions from the Canadian Consensus Conference on Dementia. CMAJ 1999; 160 (suppl 12): S1–S15.
  11. Knopman DS, DeKosky ST, Cummings JL et al. Practice parameter: diagnosis of dementia. Neurology 2001; 56: 1143–53.[Abstract/Free Full Text]
  12. Mold JW, Stein AF. The cascade effect in the clinical care of patients. N Eng J Med 1986; 314: 512–14.[Web of Science][Medline]

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