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(Stroke. 1996;27:904-905.)
© 1996 American Heart Association, Inc.

Articles

Do Silent Brain Infarctions Predict the Development of Dementia After First Ischemic Stroke?

N. M. Bornstein, MD; A. Y. Gur, MD, PhD; T. A. Treves, MD; I. Reider-Groswasser, MD; B. D. Aronovich, MD, PhD; S. S. Klimovitzky, MD; D. Varssano, MD A. D. Korczyn, MD, MSc

From the Department of Neurology, Tel Aviv Medical Center, and the Sackler Faculty of Medicine, Tel Aviv University (Israel).

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Silent brain infarctions (SBI) are common findings in advanced age, but their relationship to dementia is still uncertain. The present study was designed to evaluate whether SBI predict the development of dementia after first clinical ischemic stroke.

Methods We blindly studied admission CT scans of 175 consecutive nondemented patients presenting with ischemic stroke that clinically was their first stroke episode. SBI were defined as CT evidence of infarcts not compatible with the acute event. The patients were subsequently followed for their mental state for 5 years. Survival analysis, wherein onset of dementia was the end point, was performed on the total sample population and conducted separately on those with and without SBI at admission.

Results Dementia developed in 56 patients (32%), including 22 of the 63 (35%) with SBI and 34 of the 112 (30%) without SBI. Thus, dementia was not related to SBI.

Conclusions Our data indicate that SBI do not predict the development of dementia after stroke.

Key Words: cerebral infarction • computed tomography • dementia

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
With advancements in neuroimaging, silent brain infarctions (SBI) were recognized as a common finding in the elderly, including patients with first-ever symptomatic stroke.^{1 2 3} Data are available concerning prevalence, risk factors, and CT characteristics of SBI in patients with ischemic stroke, but the clinical significance of SBI is still controversial.^{4 5 6 7 8 9} It would not be surprising if such silent infarctions could predict the subsequent development of dementia. The possibility that SBI may indicate predisposition to dementia is important because cognitive impairment after ischemic stroke is frequent, but factors leading to its occurrence are poorly understood. Furthermore, several recent studies showed that dementia after stroke does not necessarily appear to have "typical" vascular features, such as acute onset.^{10 11 12} In the present study we assessed the predictive value of SBI in relation to the development of cognitive decline in patients after what clinically appeared to be their first-ever ischemic stroke.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Between May 1988 and December 1990, 441 patients with acute cerebrovascular disease were admitted to our department. Of these, 64 (14.5%) had transient ischemic attacks and 30 (6.8%) had cerebral hemorrhage. Among the 347 patients with ischemic stroke, 23 (6.6%) died during hospitalization, 72 (20.7%) had severe aphasia or coexisting cerebral or serious medical disorders, 26 (7.5%) reported previous cerebral insults, and 27 (7.8%) were reported to have had cognitive impairment before the stroke. The present study included the remaining 199 patients with clinical first-ever ischemic stroke, 175 of whom underwent brain CT examinations within 48 hours of admission and who were followed up later.

The patients' mean±SD age was 72.3±6.8 years. All were examined and evaluated according to a standard protocol, including medical and neurological examinations as well as a Short Mental Test including 26 questions regarding orientation, registration, attention, calculation, general knowledge, recent memory, language through naming, repetition, comprehension of verbal commands, writing and reading, constructional abilities, and abstraction.¹³ The patients were followed up with biannual evaluations of their mental status for 5 years. The diagnosis of dementia was based on criteria according to the Diagnostic and Statistical Manual of Mental Disorders, edition 3, revised.¹⁴ CT examinations were performed shortly after admission with the use of an Elscint 2400 Elite scanner. Contrast material was not used routinely. The type, size, and vascular territory of the strokes were recorded. SBI was diagnosed if the CT examination revealed an infarct in a site not compatible with the clinical symptoms. For the present analysis, all scans were retrieved and read by the same neuroradiologist (I.R.-G.), who had no knowledge of the clinical data.

Statistical Analysis
The Cox regression analysis was used to control for any differences between the groups in age, sex, and major vascular risk factors. The prevalence of SBI among the patients who did or did not develop dementia was compared by a nonparametric test (²). Patients who died or were lost to follow-up without developing dementia during the 5-year period were censored at the time of their last examination.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Dementia developed in 56 patients (32%), including 22 of the 63 (35%) with SBI and 34 of the 112 (30%) without SBI (Table 1). There were no differences in age or sex in the demented and nondemented patients (Table 2). No statistically significant differences were found in the two groups pertaining to major vascular risk factors (arterial hypertension, atrial fibrillation, diabetes mellitus, hyperlipidemia, ischemic heart disease) (P=.3, Cox regression analysis).

View this table: [in this window] [in a new window]   Table 1. Silent Brain Infarctions and Subsequent Development of Dementia After First-Ever Ischemic Stroke

View this table: [in this window] [in a new window]   Table 2. Mean Age and Sex of Patients With and Without Dementia After First-Ever Ischemic Stroke

As for the noncensored data of patients with SBI, 22 of 55 (40%) subsequently developed dementia as opposed to 34 of 102 (33%) without SBI. Obviously, SBI did not affect subsequent cognitive decline in these patients (odds ratio, 1.3; confidence interval, 0.6 to 3.0; P=.5). Seventy-eight percent of the SBI were lacunar and 22% were cortical, with no differences in later development of dementia (P=.4).

The number of SBI also did not predict the development of dementia. Thus, in 34 patients with a single SBI, 14 (41%) developed dementia compared with 21 patients who presented with two of more SBI, of whom 8 (38%) developed dementia. Of the 102 patients with no SBI, 34 (33%) developed dementia (confidence interval, 0.7 to 4.1; ²=2.3; P=.3).

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Previous studies have demonstrated the equivocal value of SBI in predicting the development of dementia after stroke.^{5 7 9} However, all recent reports are based on different groups of patients with a low incidence of dementia. Brott et al⁵ investigated patients with asymptomatic severe carotid artery stenosis (Asymptomatic Carotid Atherosclerosis Study), while Feinberg et al⁷ studied patients with nonvalvular atrial fibrillation (Stroke Prevention in Atrial Fibrillation Study). Fukuda et al¹⁵ demonstrated a correlation between mental deterioration and severity of lesions in white matter. Their study was based on patients with symptomatic multiple lacunar infarcts rather than SBI. However, almost all authors indicated the necessity of establishing a relationship between SBI and dementia by evaluating an adequate number of patients with and without dementia and, in parallel, an adequate number of patients with and without SBI.^{5 6 7 9 16}

This is the first prospective study aimed at determining whether there is a relationship between SBI and any future development of dementia after clinical stroke.

Our study included a sufficient number of patients in each previously delineated group and demonstrated a lack of correlation between SBI and the development of dementia after first-ever symptomatic ischemic stroke (odds ratio, 1.3; P=.5). This confirms the speculation by Brust¹⁷ that multiple small subcortical infarcts are unlikely to cause dementia. Wolfe et al¹⁸ noted that the effects of multiple infarcts are synergistic and not simply additive.

In a previous study we investigated the likelihood of subclinical cognitive dysfunction due to primary degenerative dementia in those patients who subsequently developed cognitive decline after stroke.¹⁹ The present results support this view and perhaps may be useful to define the causes of cognitive impairment after stroke. Jorgensen et al²⁰ and Culebras et al¹⁶ concluded that SBI do not influence the prognosis of stroke or neurological outcome, and the present study additionally shows that SBI are not significant in the development of poststroke dementia.

	Footnotes

 
Reprint requests to Dr N.M. Bornstein, Department of Neurology, Tel Aviv Sourasky Medical Center, 6 Weizmann St, Tel Aviv 64239, Israel.

Received October 10, 1995; revision received December 18, 1995; accepted January 18, 1996.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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