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Incidence of Vascular Dementia in Rochester, Minn, 1985-1989
David S. Knopman, MD;
Walter A. Rocca, MD, MPH;
Ruth H. Cha, MS;
Steven D. Edland, PhD;
Emre Kokmen, MD
Arch Neurol. 2002;59:1605-1610.
ABSTRACT
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Objective To examine the contribution of cerebrovascular disease to dementia.
Methods We used the records-linkage system of the Rochester Epidemiology Project
to ascertain incident cases of dementia in Rochester, Minn, for 1985 through
1989. We defined dementia using the criteria of the Diagnostic
and Statistical Manual of Mental Disorders, Fourth Edition. To define
dementia types, we reviewed neuroimaging reports, which were available for
two thirds of dementia cases, in addition to medical histories and neurologic
examination results. Vascular dementia (VaD) was defined by 1 of the following
criteria: dementia onset or worsening within 3 months of a clinical stroke
or bilateral gray matter infarctlike lesions shown by imaging that fulfilled
specified location criteria (critical imaging lesions).
Results We found 482 incident cases of dementia. Overall, 10% of patients had
onset or worsening of their dementia within 3 months of a stroke. Eleven percent
of the incident dementia cases had bilateral gray matter lesions on imaging
that were considered critical. Eighteen percent of patients had one or the
other of these features (VaD by our criteria), but only 4% of patients had
both. The incidence rate of VaD increased steeply with advancing age and was
similar in men and women. Our incidence rates were similar to those from a
recent European meta-analysis.
Conclusion The presence of either a stroke temporally related to dementia onset
or worsening or of critical imaging lesions was common among dementia patients,
whereas the occurrence of both features together was rare.
INTRODUCTION
THE CONTRIBUTION of cerebrovascular disease (CVD) to dementia has been
difficult to define, and epidemiologic studies show considerable variability
in the proportion of dementia attributed to CVD. These studies used clinical
diagnostic criteria for vascular dementia (VaD)1-7
that lack sensitivity and specificity8 and
measure different aspects of CVD.9-10
The divergence in estimates of prevalence11-18
and incidence19-24
of VaD suggests that the concept of VaD itself needs further investigation.
We investigated the incidence of VaD in Rochester, Minn, from 1985 through
1989. Although diagnoses of dementia in retrospective series may undercount
mild cases, the diagnosis of stroke through record review is accurate.25 Therefore, the records-linkage system of the Rochester
Epidemiology Project allows a population-based view of the relationship between
stroke and dementia. In contrast to most other studies of the incidence of
dementia, we report rates for specific features of CVD, including imaging
studies, in addition to rates based on several particular diagnostic criteria
for VaD. Incidence rates for Alzheimer disease (AD) have been reported separately.26
METHODS
CASE ASCERTAINMENT
We ascertained cases of dementia through the records-linkage system
of the Rochester Epidemiology Project as described previously.27-28
Medical care for the population of Rochester and Olmsted County, Minnesota,
is provided largely by the Mayo Clinic at the primary, secondary, and tertiary
levels. Additional health care providers in the community participate in the
Rochester Epidemiology Project, which provides the infrastructure for indexing
essentially all the medical information of the local population. Each provider
in the community uses a dossier system whereby all medical information for
each individual is accumulated in a single file. Medical diagnoses, surgical
interventions, and other key information from the dossier are routinely abstracted.
The abstracted information is coded using the International
Classification of Diseases adapted code for hospitals (H-ICDA) and
entered into computerized indices.29 Therefore,
each individual in the system can be searched for a given condition through
extensive indices of clinical or histologic diagnoses and surgical procedures.
We searched these indices for 112 specific H-ICDA codes that might indicate
dementia. Any patient with at least 1 of the study codes was considered as
a potential case. Cases of dementia in the general population may remain undetected
for a number of years30-31 but
may be eventually diagnosed as having dementia at some point during their
natural history. To increase the likelihood of capturing these individuals,
the indices were searched for the study interval and for 6 additional years
following the last year of the study interval. Cases of dementia identified
in the 6 subsequent years were then reviewed for evidence of dementia onset
in 1985 through 1989. All medical records of each potential case were screened
by a specifically trained nurse abstractor and a diagnosis obtained, as previously
described.27-28 The primary study
neurologist (E.K.) confirmed the presence of dementia, classified the dementia
by type, and determined the year of onset. To standardize and operationalize
the diagnoses, each cardinal feature required for a diagnosis of dementia
(see "Diagnostic Criteria" subsection that follows) was considered and scored
separately. All medical records, including physician and nurse notes, were
reviewed and all available data pertinent to the criteria were abstracted.
To be included in the study, patients with dementia were required to
reside in Rochester in the year of onset of dementia and for at least 1 preceding
year. Dementia cases who moved to Rochester for the management of a preexisting
dementing illness were excluded. All study procedures were reviewed and approved
by the Mayo Institutional Review Board. Persons obtaining medical care at
the Mayo Clinic and other medical services affiliated with the Rochester Epidemiology
Project are given the opportunity to deny access to their medical records
for research purposes.32 Ten individuals were
excluded from our study for this reason, and their dementia status remained
unknown.
DIAGNOSTIC CRITERIA
The principal sources of diagnostic information were the medical history,
neurologic examinations, and neuroimaging studies as recorded historically
in the patient dossier of the records-linkage system. Diagnostic criteria
for dementia were those of the Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition (DSM-IV).1 The criteria for dementia in DSM-IV include the following features: memory impairment
as a prominent early feature; at least 1 of the following: aphasia, apraxia,
agnosia, or disturbance of executive function; and loss of function sufficient
to interfere with social or occupational activities. The criteria were scored
separately, and the diagnosis of dementia was made only if all of the requirements
for the diagnosis were fulfilled. However, we were unable to estimate the
severity of dementia through our retrospective chart review.
Clinical stroke was defined as a medical record documentation of a focal
neurologic deficit of acute onset that persisted for more than 24 hours and
occurred at any time before the onset of dementia. All types of stroke were
included. For a stroke to be considered temporally related to dementia, it
had to precede the onset of the dementia by no more than 3 months or to cause
an abrupt worsening of cognitive function in patients with prior cognitive
deficits. We also reviewed the neurologic examinations at the time of the
diagnosis of dementia to document the presence of the following focal neurologic
signs: hemiparesis, lower facial palsy, extensor toe signs, sensory deficits,
hemianopia, dysarthria, or other signs traditionally observed in CVD.
It was not possible to review the actual computed tomography (CT) or
magnetic resonance (MR) scans of our patients; however, the primary study
neurologist (E.K.) reviewed the radiologists' written reports of these studies.
Most imaging studies were CT; only 8% of cases with imaging (28 of 354) had
at least 1 MR scan. We classified infarctlike lesions as likely to undermine
cognition (which we will refer to as critical lesions) when they fulfilled
1 of the following 2 criteria: (1) bilateral frontal, temporal, or parietal
lobe cortical infarctions or (2) bilateral thalamic or basal ganglia infarctions.
We further required that the imaging occurred in the time window from 1 year
before through 3 years after the onset of dementia to avoid considering imaging
lesions that clearly postdated the onset of dementia. We also noted the presence
of bilateral diffuse subcortical or periventricular white matter lesions;
however, because of the uncertain relationship of white matter lesions to
infarction, we excluded purely white matter lesions from our definition of
critical lesions.
For the diagnosis of VaD, we required 1 of the following 2 criteria:
(1) clear evidence for the onset or worsening of dementia within 3 months
of a clinical stroke or (2) bilateral gray matter infarctlike lesions shown
by imaging and judged to be critical. In addition, we independently applied
3 sets of published diagnostic criteria for VaD to our incident series: the DSM-IV criteria,1 the National
Institute of Neurological Disorders and Stroke and the Association Internationale
pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria,2 and the International Classification
of Diseases, 10th Revision (ICD-10) criteria.7
DATA ANALYSIS
We described the distribution of clinical strokes, imaging lesions,
focal signs, and their combination in all incident cases of dementia. In addition,
we calculated age- and sex-specific incidence rates using different diagnostic
criteria. The number of person-years at risk was estimated from census data
with an adjustment for prevalent cases of dementia. Demographic data for the
city of Rochester by sex and single year of age were available for the census
years 1980 and 1990. Counts for the intercensal years were estimated by linear
interpolation. These numbers were corrected by removing patients already affected
by dementia and therefore not at risk, as described elsewhere.27
Average annual incidence rates were reported by sex and 5-year age classes
between 50 and 99 years. The objectives of this study were descriptive. Because
the study covered the target population completely, no sampling was involved,
and we did not use statistical tests to interpret our findings.27
RESULTS
There were 482 incident cases of dementia who were residents of Rochester
in the 5 years from 1985 through 1989; 479 of them were between the ages of
50 and 99 years and 3 were older than 99 years. Figure 1 shows the principal subsets of cases. Of these 482 cases,
59 had other medical or neurologic diseases, such as brain tumor, head injury,
and a number of miscellaneous conditions that either antedated the dementia
or occurred simultaneously with the dementia, and were thought to cause their
dementia. Two (3%) of these 59 patients also had critical imaging findings,
suggesting that CVD may have contributed to their dementia. Eight (14%) of
these 59 patients also had a stroke; however, none had a stroke with a clear
temporal relationship to the dementia.
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Figure 1. Distribution of incident cases
of dementia according to history of stroke, infarctlike lesions on imaging,
and the presence of other medical or neurologic diseases that caused the dementia,
Rochester, Minn, 1985 through 1989.
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Fifty (12%) of the 423 patients with no other cause of dementia had
a history of a clear temporal relationship (within 3 months) between a stroke
and onset or worsening of their dementia (Figure 1), of whom only 16 also had a critical imaging lesion. Of
the 50 patients who exhibited the temporal relationship between a clinical
stroke and their dementia, onset of dementia occurred with the stroke in 26
and exacerbation of existing dementia occurred in the remainder.
Imaging studies were available in 354 (73%) of the entire group of 482
patients. There were 51 cases with critical imaging lesions (Figure 1). The location of critical infarctlike lesions on imaging
was bilateral frontal, parietal, or temporal cortex in 51%, bilateral basal
ganglia or thalamus in 33%, and both cortical and subcortical in 16%. Patients
with cortical lesions outnumbered patients with subcortical locations.
Of the 423 patients with no other cause of dementia, 70 (17%) had at
least 1 infarctlike lesion on imaging regardless of its critical status. Of
these 70 patients, 31 also had a clinical stroke, whereas 39 did not (Figure 1). An additional 94 cases (22%) had
white matter lesions, of which 45 (11%) met NINDS-AIREN imaging criteria.2 Six of these 45 patients also had a stroke with temporal
relationship and were included in our definition of VaD.
Among the 482 patients, 132 (27%) had at least 1 focal neurologic sign.
Among the 423 patients with no other cause of dementia, 109 (26%) had 1 or
more focal signs on examination, 73 (17%) had 2 or more, and 47 (11%) had
3 signs or more. Twenty-three (39%) of the 59 patients with dementia due to
other medical or neurologic diseases also had focal neurologic signs.
The overlap of clinical strokes and critical imaging lesions was small;
only 16 (32%) of the 50 patients with dementia temporally related to a stroke
also had critical imaging lesions. On the other hand, of the 51 cases with
critical imaging lesions and no other cause of dementia, 35 (69%) lacked a
history of clinical stroke temporally related to the onset or worsening of
dementia, and 27 (53%) had no history of clinical stroke ever.
Focal neurologic signs and clinical strokes were related. Of the 50
patients with dementia temporally related to stroke, 42 (84%) had at least
1 focal sign at the time of onset of dementia. In contrast, of the 109 patients
with at least 1 focal finding at the time of onset of dementia, 79% had a
history of stroke but only 39% had strokes within the 3-month time frame.
There was a variable association between focal signs and critical lesions
on imaging. Among the 51 patients with critical imaging lesions and no other
cause of dementia, only 27 (53%) had at least 1 focal neurologic sign. However,
if the enumeration was limited to cases who had both critical imaging lesions
and at least 1 clinical stroke regardless of its temporal relationship to
dementia, 22 (92%) of the 24 had at least 1 focal sign.
Table 1 provides the operational
criteria used to define VaD in our study and by others and gives the proportion
of all cases of dementia assigned to VaD using different criteria. By our
criteria (a history of stroke within 3 months of the onset or worsening of
dementia or critical imaging lesions on imaging), VaD was present in 18% of
incident cases of dementia in Rochester in 1985 through 1989. Age- and sex-specific
incidence rates using our definition are shown in Table 2 and Figure 2.
For comparison, Table 2 and Figure 2 also show the incidence rates obtained
when only patients who underwent a clinical stroke temporarily related to
dementia were included in the analysis. The incidence of VaD continued to
increase with age. However, VaD represented 21% of all dementia cases with
onset before the age of 80 years but only 16% of dementia cases with onset
at 80 years and older.
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Table 1. Number of Incident Cases of Vascular Dementia According to
Different Criteria, Rochester, Minn, 1985-1989*
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Table 2. Age- and Sex-Specific Incidence Rates (per 100 000 Person-years)
of Vascular Dementia in Rochester, Minn, 1985-1989*
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Figure 2. Incidence of vascular dementia
in men and women separately, using 2 sets of criteria. Without imaging: dementia
temporally related to clinical stroke alone. With imaging: dementia temporally
related to clinical stroke or critical imaging lesions.
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COMMENT
We studied the incidence rates of specific features of CVD that may
play a role in causing dementia in a well-defined population. Eighteen percent
of our incident dementia cases had onset or worsening of dementia within 3
months of a clinical stroke or had bilateral gray
matter infarctlike critical lesions shown by imaging (critical lesions). We
suggest that the presence of either feature is sufficient to assume that CVD
is contributing to the origin and course of the dementia. Requiring the presence
of both features for a diagnosis of VaD (which is the core of the NINDS-AIREN
criteria) may lead to an underrecognition of relevant CVD in patients with
dementia. We observed both features in only 4% of our incident cases. Neuropathologic
correlation studies in our series of incident cases of dementia have shown
moderate sensitivity and specificity of our criteria and poor sensitivity
of the NINDS-AIREN criteria for "pure" VaD (D.S.K., Joseph E. Parisi, MD,
W.A.R., Bradley F. Boeve, MD, R.H.C., Hulya Apaydin, MD, Alessandro Salviati,
MD, S.D.E., unpublished data, 2002).
Application of different diagnostic criteria in our incidence study
of dementia resulted in significantly different estimates of VaD frequency,
a result observed by others.10, 33
The estimated incidence rates of VaD were much higher using our criteria than
using the NINDS-AIREN criteria,2 but lower
than using the DSM-IV1
or ICD-107 criteria.
Perhaps because of the averaging of results from studies using various criteria
and diverse interpretations of the same criteria by different groups, the
estimated incidence of VaD from the pooled European studies of 17.6% was similar
to our estimate of 18%.19 Age-specific incidence
rates were also similar in Rochester and the pooled European studies19 (Figure 3).
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Figure 3. Comparison of incidence rates
of vascular dementia in Rochester, Minn (dementia temporally related to clinical
stroke or critical imaging lesions), and Europe (pooled estimate).19
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We did not attempt to distinguish between "pure" VaD and combined VaD
and AD. Given the low sensitivity of the diagnostic criteria for VaD,8 we chose to report only the rates for cases that we
thought had relevant CVD. To avoid confusion by adding new terms, we have
used the term VaD, but a better designation for epidemiologic studies should
acknowledge the inability to distinguish between pure VaD and VaD combined
with AD.
The strengths of our study were its basis in a well-defined population;
the use of the records-linkage system, which covers virtually all residents
of Rochester; the accurate detection of clinical strokes through the system;
and the availability of routine imaging reports on 73% of dementia cases.
It has been shown that the records-linkage system is sensitive in detecting
cases of stroke in the population.25
The drawbacks of a retrospective analysis such as ours are important
and include the difficulties in the assignment of diagnoses based on record
review alone. The lack of consistently available data on all patients can
make assignment of a diagnosis of dementia difficult. The fact that neurologists
did not examine all patients might have led to an undercounting of focal neurologic
signs. In our methods, we were conservative in diagnosing dementia, and we
may have failed to identify individuals with milder illnesses. We were also
unable to characterize the severity of the dementia at onset. Individuals
with mild dementia can only be detected using direct neuropsychological testing.27 However, in our studies of mortality in this cohort,
the median survival of our patients with AD was comparable to that reported
from prospectively recruited patients.34
The use of CT images in our study instead of MR images may have underestimated
the burden of infarcts. Although CT may have failed to detect some chronic
infarctions, those missed were likely too small and well below our threshold
to be critical. Some CT scans may have been performed in the acute stroke
period when a new infarct could have been missed. Another source of underestimation
of cerebral infarctions was the unavailability of imaging for 27% of our cases.
Although it was unlikely that the patients who did not undergo imaging had
the same frequency of critical infarcts as those who underwent imaging, we
have no basis for imputing the burden of infarcts in those without imaging
studies.
Cerebral cortical infarctlike lesions predominated, but subcortical
gray matter infarctlike lesions were also common among critical imaging lesions,
which is consistent with other studies in our series. A prior study35 in Rochester found an association between multiple
infarctions and dementia; however, that study did not investigate infarct
location. In selected series of patients, infarction in the territory of the
middle cerebral artery and the left hemisphere region of the thalamocortical
radiations were more closely associated with dementia after stroke than were
infarctions in other regions.36-38
We are not aware of any other population-based studies that have detailed
the locations of infarctions in patients with dementia. We adopted most of
the NINDS-AIREN perspective on critical infarctions in dementia.2
We did not accept the broader view that any infarctlike
lesion on imaging is critical.4, 18, 24
More quantitative work is needed to define better the locations of infarctions
that are invariably associated with dementia.
We excluded extensive white matter lesions from our definition of critical
lesions. We did not accept them as imaging evidence for stroke.2
In contrast, DSM-IV and ICD-10 criteria include white matter lesions (Table 1). Although white matter lesions are seen with considerable
frequency in patients thought to have VaD,39-40
the preponderance of evidence is that white matter lesions do not usually
represent infarction per se.40-42
In addition, white matter lesions lack specificity for VaD because they are
seen also in AD.43-44 If we accepted
bilateral and extensive subcortical white matter lesions as critical lesions,
39 additional patients would have been classified as VaD by our criteria,
increasing the VaD representation from 18% to 26% of all cases of dementia
(Table 1).
Only about half of the patients with critical imaging lesions had a
clinical history of stroke or focal neurologic signs. Clinically silent critical
imaging lesions were a major contributor to the increasing incidence of VaD
in our oldest population. Other studies have found that silent cerebral infarctions
are common and increase with advancing age.45-47
AUTHOR INFORMATION
Accepted for publication April 29, 2002.
Author contributions: Study concept and design (Drs Knopman, Rocca, Edland, and Kokmen); acquisition of
data (Ms Cha and Dr Kokmen); analysis and interpretation
of data (Drs Knopman, Rocca, and Edland and Ms Cha);
drafting of the manuscript (Drs Knopman, Rocca, Edland,
and Kokmen and Ms Cha); critical revision of the manuscript for important
intellectual content (Drs Knopman, Rocca, and Edland);
statistical expertise (Dr Rocca and Ms Cha); obtained
funding (Dr Kokmen); and administrative, technical,
and material support (Drs Knopman, Rocca, Edland, and Kokmen).
This work was supported in part by grants AG 06786 (Mayo Alzheimer's
Disease Patient Registry) and AG 16574 (Mayo Alzheimer's Disease Research
Center) from the National Institute on Aging, Bethesda, Md, and was made possible
by the Rochester Epidemiology Project grant AR 30582.
Corresponding author and reprints: David S. Knopman, MD, Department
of Neurology, Mayo Clinic, 200 First St SW, Rochester MN 55905 (e-mail: knopman{at}mayo.edu).
From the Departments of Neurology (Drs Knopman, Rocca, and Kokmen)
and Health Sciences Research (Drs Rocca and Edland and Ms Cha), Mayo Clinic
and Mayo Foundation, Rochester, Minn.
The primary neurologist of the
study, Dr Kokmen, died in 2000.
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