(Stroke. 2004;35:1268.)
© 2004 American Heart Association, Inc.
Original Contributions |
Editorial Comment—Dementia After Stroke
Consultant Neurologist, Department of Neurology, Royal Free Hospital, London, UK
Stroke and dementia were implicitly associated by the advent of the concept of multi-infarct dementia, but it was Tatemichi et al1 who put this in temporal context and brought it to popular attention by observing a 26.3% dementia incidence 3 months after hospitalization for stroke. Several subsequent studies largely confirmed Tatemichi’s work but gave incidence estimates for poststroke dementia from 6% to 32%,2,3 with most studies producing estimates toward the upper end of this range. As Ivan et al4 point out, these works are potentially inaccurate for several reasons, including cross-sectional study design, the use of hospital-based cohorts with the risk of selection bias, lack of controls, and no (or imperfect) exclusion of previous dementia, to which should be added the effect of the diagnostic criteria used.
What is remarkable about the data from Ivan et al is that it took 
10 years for 19.3% of the cases of dementia to develop, a level that in most other studies would have been achieved within 3 months. Approximately 40% of apparently incident cases in most studies are caused by preexisting dementia, most of which is Alzheimer disease (AD).5–7 Nine such cases were excluded for that reason here and, if these are added to the numerator and denominator, would amount to 18% of cases, largely explaining the difference. The remainder may be accounted for other reasons among the 28 cases that were not followed-up with cognitive examination at 6 months.
Thus, Ivan et al have produced a much lower estimate for the incidence of poststroke dementia than previous studies. However, the single most common manifestation of vascular dementia (VaD) is now known to be a subcortical dementia based on small-vessel disease rather than the older concept of multiple larger cortical infarcts. The mini-mental state examination (MMSE) is useful as a screening tool for AD but is insensitive to subcortical dementia;8 in addition, the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) definition of dementia is based on AD. Both of these factors will result in an underestimate of the incidence of VaD, a feature common to all poststroke dementia studies to date.
The incident cases have been classified into VaD, AD, and mixed dementia using the Alzheimer’s Disease Diagnostic and Treatment Centers (ADDTC)9 criteria to identify VaD. None of the criteria for VaD are validated and they produce wildly varying results, even when applied to the same population.10,11 The ADDTC, used here, is one of the more sensitive but might still underestimate cases by 15%. There are no criteria at all for mixed dementia and the authors have not stated how this diagnosis was made. Thus the dementia etiologies reported by Ivan et al must be regarded as approximate. Because screening for dementia (the MMSE) and its confirmation (DSM IV) were both based on AD and the tool for identification of VaD identified vascular events, this methodology is likely to classify mixed dementia as VaD.12 This is also probable for statistical reasons, because the Medical Research Council Cognitive Function and Ageing Study (MRC-CFAS) study13 showed that 78% of the elderly have cerebrovascular disease at autopsy. The absolute figure further supports this notion because 7% of the stroke cases demented with an AD component as compared with 8.7% of the controls. Coexistent stroke does not protect against AD, rather, quite the converse; it profoundly accelerates its progression and advances its presentation.14 There should, therefore (and paradoxically), have been more mixed and AD cases recognized as an absolute proportion of the whole stroke group.
The MRC-CFAS study13 also raised doubts about the validity of the criteria for the histological diagnosis of AD. Furthermore, there are no histopathological criteria at all for diagnosing VaD; pathologists often make very subjective decisions.15 That the diagnoses of 16 cases were confirmed at autopsy is therefore not as strong a statement as it initially appears.
This work has the great strength of detailed premorbid knowledge of the study population and the consequent ability to exclude preexisting dementia and the presence of a stroke-free control group, so that the true effects of stroke can be more clearly assessed. It does not fully resolve the question of the magnitude of the incidence of poststroke dementia because the definitions used here will underestimate the incidence of VaD and mixed dementia. Nonetheless, the error will be an underestimate, and the study shows that dementia occurs after stroke in 19.3% of stroke cases as compared with 11% in a stroke-free matched group. This amounts to a minimum of 58 000 additional cases of dementia in the United States each year. Unlike AD, these are preventable by the modification of stroke risk factors. The numbers involved also indicate the importance of assessing cognition as part of the evaluation of stroke outcome, especially in research and also in routine clinical practice.
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[Abstract/Free Full Text]
Related Article:
- Dementia After Stroke: The Framingham Study
- Cristina S. Ivan, Sudha Seshadri, Alexa Beiser, Rhoda Au, Carlos S. Kase, Margaret Kelly-Hayes, and Philip A. Wolf
Stroke 2004 35: 1264-1268.[Abstract] [Full Text] [PDF]
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