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(Stroke. 1997;28:2429-2436.)
© 1997 American Heart Association, Inc.

Articles

Preexisting Dementia in Stroke Patients

Baseline Frequency, Associated Factors, and Outcome

H. Hénon, MD; F. Pasquier, MD, PhD; Durieu, MD; O. Godefroy, MD, PhD; C. Lucas, MD; F. Lebert, MD; D. Leys, MD ;

From the Department of Neurology, Stroke Unit (H.H., I.D., O.G., C.L., D.L.) and Memory Clinic (H.H., F.P., F.L.), University of Lille (France).

Correspondence and reprint requests to Florence Pasquier, MD, PhD, Department of Neurology, Memory Unit, Hôpital Roger Salengro, F-59037 Lille, France. E-mail pasquier{at}chru-lille.fr

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose The link between stroke and degenerative dementia, especially Alzheimer's disease, is closer than expected by chance. Dementia after stroke may be due to the cumulative effect of vascular and degenerative changes. The prevalence of dementia just before stroke onset remains unsettled. The aim of this study was to determine the frequency of preexisting dementia in stroke patients, associated factors, and consequences on outcome.

Methods We evaluated the cognitive functioning prior to stroke in 202 consecutive patients with ischemic or hemorrhagic stroke by means of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). We classified in the dementia group patients with IQCODE scores of 104 or more. Six months after stroke onset, survivors underwent a battery of neuropsychological tests.

Results Thirty-three patients were demented before stroke (16.3%; 95% confidence interval, 11.2 to 21.4). There was no diagnosis of dementia in 32 of these 33 patients. We determined by logistic regression analysis that female sex, family dementia, leukoaraiosis, and cerebral atrophy are independently associated with prestroke dementia. All survivors who had IQCODE scores of 104 or more at the acute stage met criteria for dementia 6 months later.

Conclusions Our study showed that one sixth of stroke patients have preexisting dementia. Therefore, some patients with so-called "poststroke dementia" probably had unrecognized preexisting dementia.

Key Words: Alzheimer's disease • dementia • intracerebral hemorrhage • stroke, acute • stroke, ischemic

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Dementia syndromes diagnosed after stroke are usually considered to be vascular in origin. However, the link between stroke and degenerative dementia, especially Alzheimer's disease (AD), is probably closer than expected by chance: (1) some cases of dementia occurring after stroke have a progressive onset and course, which suggests a degenerative process^{1 2 3} ; (2) stroke, risk factors for stroke, and AD share common genetic factors, such as the 4 allele of the apolipoprotein E gene^{4 5 6 7} ; (3) stroke-free elderly subjects with dementia have an increased risk for stroke⁸ ; and (4) Alzheimer's disease and vascular lesions of the brain are frequently associated at autopsy.^{9 10 11} Therefore, dementia occurring after stroke may be the consequence of the effects of stroke and degenerative changes^{1 12 13 14} : when a stroke occurs at a preclinical stage of AD, the period of preclinical AD may be shortened by the stroke lesion.^{14 15}

The prevalence of dementia is increased after an ischemic stroke,^{1 16 17 18 19} with a relative risk of 5.5 at 4 years, even when patients who were demented immediately after stroke are excluded.¹⁸ On the basis of the neurologist's judgment, approximately 16% of stroke patients in the Stroke Data Bank Cohort¹ had dementia within 10 days after stroke onset. Poststroke dementia is usually considered to be related to stroke. However, dementia may also be related to associated nonvascular pathology. Using modified DSM-III criteria, Tatemichi et al found that 26.3% of stroke patients were classified as "demented" 3 months after stroke.¹⁷ Among these demented patients, 34.6% were considered to have Alzheimer's disease with stroke, because functional and memory impairments preceded the index stroke.¹⁷ This finding suggests that at least 8% of stroke patients had cognitive disturbances before stroke.¹⁷ In another stroke cohort study,²⁰ nearly 40% of patients had cognitive decline before stroke. However the frequency of preexisting dementia was not systematically studied at the acute stage of stroke in these studies.^{17 20} Therefore, some dementia syndromes recognized after a stroke may be due, at least in part, to unrecognized preexisting dementia.^{1 14} If some dementia syndromes occurring after stroke are due to the summation of vascular and degenerative lesions, a systematic evaluation of preexisting cognitive functions should find cognitive decline before stroke onset in a significant proportion of stroke patients. The aim of this study was to determine the frequency of preexisting dementia in stroke patients by means of a standardized questionnaire; ancillary objectives were to determine factors associated with preexisting dementia and relation to outcome.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Patients
The recruitment of the study population was conducted over a 28-week period (November 2, 1995, to May 12, 1996). All consecutive patients admitted to the acute stroke unit of the Lille University Hospital were eligible. This unit admits adults whose pathology is likely to be vascular (ischemic or hemorrhagic) in origin. Criteria for stroke are clinical signs of focal disturbance of cerebral function lasting more than 24 hours or leading to death, with no apparent cause other than being of vascular origin; criteria for transient ischemic attack (TIA) were episodes of focal cerebral dysfunction, presumably ischemic in origin, lasting less than 24 hours and followed by return to normality. Patients with hemorrhagic infarcts were classified in the ischemic group. We excluded from the study those patients (1) with TIA, (2) with stroke caused by cerebral venous thrombosis, (3) younger than 40 years of age, (4) who were not fluent French speakers, (5) who were not Caucasian, (6) without a reliable informant, (7) with history of severe head trauma or neurosurgery, (8) referred from another hospital to avoid selection bias, and (9) who did not live in the urban community of Lille (1.2 million inhabitants), because the follow-up was usually performed in other centers. Previous stroke or TIA was not an exclusion criterion.

Methods
Patients were examined at admission by a neurologist-in-training and a board-certified neurologist and underwent standard blood and urine tests (blood and urinary ionograms, blood count cell, coagulation tests with Quick time, and erythrocyte sedimentation rate); 12-lead ECG; and noncontrast CT scan. Doppler ultrasonography and B-mode echotomography of the cervical arteries, bidimensional transthoracic echocardiography, and tests for syphilis and hyperfibrinogenemia were performed within 24 hours. A delayed CT scan was performed within 8 to 10 days. The following examinations were performed in selected patients: cerebral MRI scan; 24-hour ECG; transesophageal echocardiography; cerebral angiography; and tests for hypercoagulability.

Medical history was determined from all available records (general practitioner's letter or telephone call) and sources (patient, family, or general practitioner). We prospectively collected the following data: age; sex; education level (<8 years of education, 8 years of education); first- or second-degree relative with history of migraine, stroke, depression, or dementia; presence of arterial hypertension (defined as systolic blood pressure >160 mm Hg or diastolic blood pressure >90 mm Hg or current treatment with antihypertensive drugs either before stroke onset or lasting more than 1 month after stroke onset); diabetes mellitus (defined as serum glucose level >1.20 g/L or current use of antidiabetic drugs); hyperlipidemia (defined as fasting serum level of triglycerides >1.5 g/L or fasting cholesterol serum level >2.3 g/L; history of peripheral artery disease with intermittent claudication; previous TIA or stroke; mean alcohol consumption >300 g/week; cigarette smoking (>10 cigarettes per day or cessation <5 years earlier); high- and medium-risk cardiopathies, according to TOAST criteria²¹ ; and significant stenosis of the internal carotid arteries, defined as a narrowing of 50% or more of the lumen documented by Doppler ultrasonography, B-mode echotomography, MR angiography, or conventional angiography. The severity of the clinical deficits was scored according to the Orgogozo rating scale,²² which was constructed to include items reflecting global severity and has been shown to have a high interrater reliability for individual items and for the additive score.²³ The rating scale, widely distributed and easily applicable, is used in many centers. Data were recorded as soon as possible after stroke onset and always within 24 hours. Stroke subtypes were defined at discharge, according to TOAST criteria.²¹

CT scans were performed, without contrast, on an Elscint 2004 Elite Plus machine by means of 5-mm contiguous slices. We determined on CT scan the number and location of old infarcts, defined as infarcts seen at admission on CT scans and not related to the index stroke. We defined silent infarcts as old infarcts found on CT scan in patients without a history of stroke, according to the criteria of Mounier-Vehieret al.²⁴ Leukoaraiosis was defined according to the criteria of Inzitari et al²⁵ and scored by means of the 0-to-3-point rating scale of Blennow et al.²⁶ Leukoaraiosis was assessed on the hemisphere opposite to a unilateral focal vascular lesion, if any, and on the right hemisphere in the remainder. Cerebral atrophy was scored according to the method of Leys et al,²⁷ with cerebral atrophy scores of 0 (no atrophy), 1 (mild atrophy), 2 (moderate atrophy), and 3 (severe atrophy).

The assessment of preexisting dementia was conducted within 48 hours of stroke onset by means of a French translation of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE).²⁸ This questionnaire, administered to a close relative, consists of 26 questions concerning the changes experienced by the patient over the last 10 years in aspects of daily behavior requiring memory and other intellectual abilities. Each item carries a score of 1 to 5 (1, has become much better; 2, has become a bit better; 3, has not changed; 4, has become a bit worse; and 5, has become much worse). The global score, the addition of the scores of all items, ranges from 26 to 130 points. The informant should have known the patient for at least 10 years and meet him or her at least once a week. The questionnaire has a good reproducibility between and within raters.^{29 30 31} There is a good correlation between the score and the Mini-Mental State Examination (MMSE)³² and IQCODE scores.^{30 31 33 34} This questionnaire is a valuable tool in community studies³⁵ to screen dementia, irrespective of its severity and cause. It is not influenced by patients' previous intelligence, education level, or socioeconomic class^{29 30 31 35 36} because its aim is to detect a fall from a higher previous to a lower present intellectual level.²⁸ This screening tool has been validated not only in AD patients³⁷ but also in population samples of elderly subjects.^{29 34 35} In most studies,^{31 34 35 37 38} criteria for dementia were the DSM-III-R criteria³⁹ and in one case²⁹ the ICD-9 criteria⁴⁰ . The score obtained with the IQCODE does not reflect the severity of cognitive impairment but instead the severity of decline occurring along the last 10 years. To our knowledge, this questionnaire has never been tested in the evaluation of the severity of cognitive impairment. However, it has been found to be more effective than the MMSE³² in the detection of mild dementia diagnosed according DSM-III-R criteria.³⁵ The value of the IQCODE at the acute stage of stroke is that it does not require the participation of the patient at a stage of the disease when neuropsychological functions may be influenced by stroke. We classified as having preexisting dementia those patients with IQ code scores of 104, because this cutoff point accurately classifies 92.7% of demented patients as actually demented and 88.1% of the general population sample as normal, leading to a diagnosis accuracy of 90.4%.³⁰ The assessment of independent ADL was performed with the informant-completed measure of ADL and behavior in elderly patients with cognitive impairment,³⁶ which quantifies the loss of independence in daily living activities and allows follow-up, irrespective of the presence of motor or perceptual handicaps.³⁶

At discharge, we studied the intrahospital mortality rate and the functional outcome by means of the Barthel Index⁴¹ and the Rankin Scale.⁴² Occurrence of an acute confusional state during hospitalization was evaluated according to the Delirium Rating Scale (DRS),⁴³ which quantifies multiple parameters affected by delirium, such as temporal onset of symptoms, perceptual disturbances, hallucinations and delusions, psychomotor behavior, cognitive status, presence of physical disorder, sleep-wake cycle disturbance, liability of mood, and variability of symptoms.

Six months after stroke onset, survivors underwent a battery of neuropsychological tests. We performed a global evaluation of cognitive functions by means of the Mattis dementia rating scale (MDRS),⁴⁴ which evaluates a broad array of cognitive functions because it includes subtests of attention, initiation, perseveration, construction, conceptualization, and verbal and nonverbal memory. Cognitive functions assessed included the following: attention and frontal lobe functions (mental control portion of the Wechsler Memory Scale⁴⁵ , target detection tasks,⁴⁶ trail-making test B,⁴⁷ Stroop,⁴⁸ subtests of the MDRS⁴⁴ ); short-term verbal memory (digit span,⁴⁵ immediate recall of the Free and cued selective reminding test^{49 50} ); long-term verbal memory (Free and cued selective reminding test,^{49 50} subtests of the MDRS⁴⁴ ); visual memory (BEM 144,⁵¹ Corsi block-tapping test,^{46 52} subtests of the MDRS⁴⁴ ); orientation (orientation items of the MMSE³² ); executive functions (subtests of the MDRS,⁴⁴ Wisconsin Card Sorting Test,⁵³ verbal fluency); language ability, including naming (confrontation naming of 36 figures) and the shortened version of the Token test⁵⁴ ; gestual praxis (subtests of the MDRS⁴⁴ symbolic gesture, pantomiming of object use without objects); gnosia (identification of famous faces and naming of pictures of objects); constructional and visuospatial functions (subtests of the MDRS,⁴⁴ construction of the MMSE³² ); concept formation (subtests of the MDRS,⁴⁴ the Wisconsin Card Sorting Test⁵³ ); and reasoning (calculation, arithmetic problem solving, evaluation of judgment by the criticism of verbal absurdities). The MMSE³² was also administered as a measure of the severity of cognitive impairment but was not used for the purpose of dementia diagnosis. Presence of functional impairment was evaluated by means of Weintraub's questionnaire.³⁶ A structured interview for psychiatric symptoms and disorders was administered that consisted of the CAMDEX⁵⁵ and MADRS⁵⁶ scales. We chose an interval of 6 months after stroke for neuropsychological testing to have optimal regression of the acute consequences of stroke and to increase the number of patients able to undergo the neuropsychological testing, because a stable physical course is often obtained at month 6. All available information gathered from the neurological, neuropsychological, and functional assessments administered at the 6-month visit was reviewed at a diagnostic case conference attended by the examining neurologist and two neuropsychologists experienced in the diagnosis of dementia. Dementia was determined according to DSM-IV criteria,⁵⁷ which require patients to have memory impairment (short- and long-term memory impairment in at least one of the following domains: executive functions, language, praxis, and gnosis. For a diagnosis of dementia in testable aphasic patients, impairment in nonverbal memory was required. Moreover, consistent with DSM-IV criteria,⁵⁷ functional impairment due to cognitive decline, apart from any physical disability due to stroke, was an additional diagnostic requirement, with use of information from Weintraub's questionnaire³⁶ and other sources when available. Criteria for AD were those of the NINCDS-ADRDA work group,⁵⁸ and criteria for vascular dementia were those of the NINDS-AIREN group.⁵⁹ We classified patients who had an IQCODE score of 104 at the acute stage into one of the following groups: AD, vascular dementia, other dementia, alive without dementia, and dead. In survivors, MRI scans were performed whenever possible.

Statistical Analyses
The first step of statistical analysis consisted of a description of the prevalence of preexisting dementia, with 95% CIs. The second step consisted of a bivariate analysis comparing variables between patients with IQCODE scores 104 and those with IQCODE scores <104. We used the ² test, with Yates' correction or Fisher's exact test when appropriate, and the odds ratio (OR) method with 95% CIs to compare qualitative factors between groups, and we used Mann and Whitney's U test to compare quantitative variables. Variables compared between groups were demographic characteristics; risk factors for stroke; risk factors for dementia, infarct or hemorrhage; severity of the neurological deficit at admission; and stroke subtype. The third step of statistical analysis consisted of a logistic regression analysis⁶⁰ with IQCODE score (quoted 1 when 104 and 0 when <104) as a dependent variable. Because we used a high cutoff of the IQCODE score to determine the diagnosis of dementia, there could be some demented patients in the subgroup of patients with an IQCODE score of <104. To avoid the effect of a cutoff, we performed a multiple linear regression analysis with the IQCODE as a dependent variable. The last step of statistical analysis consisted of three logistic regression analyses evaluating the following: (1) factors predicting in-hospital death; (2) factors predicting dependence at discharge in survivors- (for this purpose, we considered two groups of patients, those independent at discharge [defined as those with a Rankin score of <3] and those who were dependent [Rankin score of 3]); and (3) factors predicting death at month 6. The independent variables included in the analysis were selected from the bivariate analysis, with a 0.25 level as a screening criterion for selection of candidate variables.⁶⁰ Data were analyzed with the SPSS/Macintosh package.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
During the 28-week recruitment period, 258 patients with stroke, aged 40 years, French speakers, without history of severe head trauma or neurosurgery, were admitted into the acute stroke unit. Fifty-six (27.7%) were excluded because of the lack of an informant or the impossibility of meeting the informant within 48 hours of stroke onset.

The study population consisted of 202 patients (105 women and 97 men), with a median age of 75 years (range; 42 to 101 years). Twenty-five patients had a deep intracerebral hemorrhage and 177 an ischemic stroke. One hundred forty-seven patients had a first-ever stroke, and 55 had suffered a previous stroke or TIA.

The informants were spouse in 78 cases (39%), a child in 104 (51%), another first-degree relative in 11 (5.5%), and a close friend in 9 (4.5%).

Of the 202 patients, 33 (16.3%; 95% CI, 11.2 to 21.4) had an IQCODE score of 104. Only 1 was known to have presented with AD; his IQCODE score was 124. The breakdown of patients with IQCODE scores of 104 in various age categories was as follows: 3 of 68 patients between 40 and 69 years of age (4.4%; 95% CI, 0.0 to 9.3), 6 of 62 patients between 70 and 79 years (9.7%; 95% CI, 2.3 to 17.0), and 24 of 72 patients aged 80 years (33.3%; 95% CI, 22.4 to 44.2), In the subgroup of 147 patients with a first-ever stroke, 23 (15.6%; 95% CI, 9.8 to 21.5) had a IQCODE score of 104. In the subgroup of patients with ischemic stroke, 27 (15.25%) had an IQCODE score of 104, whereas in the subgroup of patients with deep intracerebral hemorrhage, 6 (24%) had an IQCODE score of 104 (P=.41). There was no statistically significant difference between IQCODE scores of patients with hemorrhage and those with infarct using Mann and Whitney's U test (P=0.37). The results of the bivariate analysis are provided in Table 1.

View this table: [in this window] [in a new window]   Table 1. Baseline Characteristics of Patients According to IQCODE Scores

The logistic regression analysis with IQCODE score (quoted 1 if 104 and 0 if <104) as dependent variable found the following independent variables (overall prediction of the model: 89.6%): leukoaraiosis score (P=.0002), female sex (P=.0002), family history of dementia (P=.0016), cerebral atrophy score (P=.0102). The multiple linear regression analysis found the same independent variables (Table 2). The equation obtained was IQCODE score=78.39+(4.1 x cerebral atrophy score)+(9.44xfamily history of dementia)+ (4.38xleu-koaraiosis score)-(4.55xsex).

View this table: [in this window] [in a new window]   Table 2. Results From the Multiple Linear Regression Analysis

Using bivariate analysis, the intrahospital mortality, functional outcome at discharge and 6-month mortality were worse in patients with IQCODE scores of 104 (Table 3). However, the IQCODE score was not a significant predictor of short-term outcome when a multivariate statistical analysis was performed. The logistic regression analysis with in-hospital death (quoted 1 if dead and 0 if alive) as dependent variable found the following independent variables (overall prediction of the model: 88.1%): cerebral atrophy score (P=.0008), Orgogozo's score at admission (P<.0001), hospitalization for deep hemorrhage (P=.0010). The logistic regression analysis with dependence at discharge in survivors (quoted 1 if Rankin score 3 and 0 if Rankin score < 3) as the dependent variable found the following independent variables (overall prediction of the model: 80%): leukoaraiosis score (P<.0001), Orgogozo score at admission (P<.0001), history of coronary heart disease (P<.0001), history of atrial fibrillation (P=.0006), < 8 years of education (P=.0489). The logistic regression analysis with death within 6 months (quoted 1 if dead and 0 if alive) as dependent variable found the following independent variables (overall prediction of the model: 87.13%): age (P=.0183), cerebral atrophy score (P=.0112), Orgogozo's score at admission (P<.0001), history of atrial fibrillation (P=.0473), hospitalization for deep hemorrhage (P=.0169).

View this table: [in this window] [in a new window]   Table 3. Short-Term and 6-Month Outcome According to IQCODE Scores

Of the 202 patients, 60 died. Forty patients could not be followed-up for the presence of at least one the following reasons: too poor physical condition, insurance refusal, patient or family refusal, have moved to another area or country. One hundred and ten patients underwent the 6 month visit: 8 patients did not undergo the neuropsychological examination: 4 because they were too severely aphasic and 4 because they refused the tests. Using DSM-IV criteria, we found 33 patients out of 102 who underwent the neuropsychological evaluation (32.4%) to be demented at the 6 month visit. Of 33 patients with an IQCODE score of 104 or more, 18 died within 6 months. None of them underwent autopsy. Of the 15 survivors, 11 underwent the neuropsychological evaluation 6 months after stroke onset and fulfilled criteria for dementia. Only 2 underwent MRI; 2 had a pace-maker and 7 had too severe cognitive disturbances with agitation or opposition. The median score obtained at the MMSE³² was 22 (range,: 12 to 26). Depressive symptoms were present in 7 of 11 patients, but none of them fulfilled the DSM-IV criteria for major depression. Only one patient was currently treated with antidepressive drug: however she was free of depressive symptom at month 6. Three patients with severe intercurrent disorders could not undergo the neuropsychological evaluation at month 6, and 1 patient refused; for these 4 patients we obtained information by telephone that confirmed memory disturbance and functional impairment. Of 11 patients who met criteria for dementia 6 months after stroke onset, 8 fulfilled criteria for possible AD; these patients had a neuropsychological profiles suggestive of AD and, according to the relatives at the 6-month visit, a progressive course of their cognitive deficits before stroke and no obvious worsening after stroke. In this group of 8 patients, 1 had no leukoaraiosis. The leukoaraiosis score was 1 in 2 patients, 1.5 in 1 patient, 2 in 1 patient, 2.5 in 1 patient, and 3 in 2 patients. In 3 patients silent infarcts were demonstrated on CT scan performed at admission: lacune of the white matter of the right hemisphere in 1 patient, lacune of the white matter of the right hemisphere and of the right putamen in 1 patient, and infarct of the posterior fossa in 1 patient. The location of the index stroke was right superficial middle cerebral artery territory in 2 patients, left superficial middle cerebral artery territory in 2 patients, lacune of the white matter of the left hemisphere in 2 patients, left posterior fossa in 1 patient, and left thalamic hemorrhage in 1 patient. For the 2 patients who underwent MRI, the diagnosis remained possible AD because the vascular abnormalities were not considered relevant for the diagnosis of vascular dementia. Two patients with previous strokes, with each stroke leading to a worsening of the cognitive functions, met criteria for probable vascular dementia. In one patient, the cause of dementia remained unsettled because the severity of the neuropsychological deficits did not permit a reliable neuropsychological evaluation and because we did not obtain enough information about the course of the disease.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Preexisting dementia was found in one sixth of stroke patients and was not usually recognized before stroke. It was associated with cerebral atrophy, leukoaraiosis, familial history of dementia, and female sex, and it does not appear to influence the short-term outcome.

Prestroke dementia was diagnosed according to the IQCODE:, to evaluate the patient's cognitive functions before stroke onset, this questionnaire was completed, with the help of a patient's close relative, as soon as possible after the admission of the patient to the acute stroke unit. The information of these relatives has proved useful for the diagnosis of dementia when recorded in the unstructured manner of the clinical history^{61 62} as well as the in structured interviews used for epidemiological studies,^{63 64} even after the patient's death.⁶⁴

As we wanted to avoid an overestimation of this prevalence, we used a cutoff of 104 for the IQCODE, as used by Jorm and Jacomb in their first study,³⁰ even if the best cutoff to discriminate between demented and nondemented patients with the French version of the IQCODE seems to be of 94.³⁷ Therefore, according to previous studies, we probably correctly classified 90% of patients, and the risk of misclassification of patients who had an IQCODE score of 104 is about 7%.³⁰ Our study has probably underestimated the number of patients with dementia prior to stroke. The only patient known to be demented prior to stroke had an IQCODE score of 124. However, this method is as sensitive as the MMSE³² to screen for mild dementia.³⁵ The patient in our study who had an MMSE³² score of 26 at month 6 was a patient with a high educational level and a high socioprofessional occupation; an MMSE³² score of 26 reflects cognitive decline. Moreover, we have shown that patients with IQCODE scores of 104 had significantly more severe impairment in everyday functioning, supporting the diagnosis of dementia in patients with high IQCODE score. Finally, among patients who had an IQCODE score of 104 at stroke onset, all the survivors actually met criteria for dementia 6 months later.

The baseline frequency of preexisting dementia was about 16%. However, in this age category, this frequency may reflect the prevalence of dementia in the community. Although it was not the purpose of this study to determine whether dementia is more frequent in patients who will have a stroke than in the community, the prevalence of preexisting dementia was slightly higher than that reported in European community–based studies,⁶⁵ especially in those over 80 years of age (Table 4). Figures obtained in our study can hardly be compared with those obtained in community-based studies because of different methodologies. However, this is an argument for an overrepresentation of dementia in stroke patients that requires confirmation in a case-control study. This finding supports the hypothesis that a same patient could have an increased risk of stroke and degenerative disease. However, because CT scans were used rather than MRI and because systematic neuropathologic studies were not performed in patients who died, cerebrovascular disease as a basis for premorbid dementia may have been underestimated in our study.

View this table: [in this window] [in a new window]   Table 4. Age-Specific Prevalence (%) of Preexisting Dementia in Stroke Patients and of Dementia (Whatever the Etiology) in Community-Based Studies

We pooled patients with ischemic and hemorrhagic stroke, although the mechanisms underlying those stroke subtypes may differ. For instance, amyloid angiopathy, which is typically found in patients with degenerative dementia, may result in cerebral hemorrhage. However, although there was a tendency for a higher prevalence of preexisting dementia in the subgroup of patients with cerebral hemorrhage, the difference between groups was not statistically significant.

In the bivariate analysis, the prevalence of dementia was significantly related to age. The largest increase in frequency of dementia occurred between the groups 70 to 74 years and 75 to 79 years, as in a previous study¹ that focused on very early (within 10 days) dementia occurring after stroke. However, although the association between brain atrophy and dementia may be confounded in part by normal aging effects,⁶⁶ cortical atrophy seems to be a strong determinant of prevalence of prestroke dementia, because it has been found to be a strong determinant of poststroke dementia, even after adjustment for age.¹

Factors independently associated with preexisting dementia are those usually associated with degenerative dementia rather than those associated with vascular dementia: cerebral atrophy, leukoaraiosis, family history of dementia,and female sex. Previous stroke or TIA, silent infarcts, and the presence of old infarcts on CT scan were not associated with preexisting dementia in this study; moreover, of 10 patients who met criteria for dementia 6 months after stroke onset, 8 would have fulfilled criteria for probable AD because of a progressive course before and after stroke, which suggests a degenerative process, with no worsening or only transient worsening of cognitive status after stroke. However, they had a history of stroke and were therefore considered to have possible AD; only 2 patients met criteria for probable vascular dementia. These results lead to the hypothesis that most cases of preexisting dementia are of degenerative rather than of vascular origin. Recognition of degenerative pathology in a patient with poststroke dementia is important because of the emergence of effective treatments for AD.⁶⁷ Neuropathologic studies are now necessary to determine the proportion of cases of dementia occurring after a stroke that are degenerative in origin.

Dementia occurring after stroke is associated with an increased risk of loss of autonomy and death, even after adjustment on other potential confounders.⁶⁸ Preexisting dementia does not influence the very-short-term prognosis. We did not take into account the impact of factors occurring after stroke, such as poststroke dementia, because our objective was to determine whether preexisting dementia influence outcome. However, we do not know yet the influence of cognitive disturbances before stroke on functional and cognitive outcome at 6 months and later. Functional outcome at discharge and 6-month mortality may well be affected also by the presence of stroke-related dementia. This will be evaluated in further study. A follow-up of these patients is now necessary to know whether the 16% rate of preexisting dementia in stroke patients should be taken into account in the management of stroke patients: The high rate of stroke patients with unrecognized preexisting dementia might interfere with the results of drug trials at the acute stage of an ischemic stroke. To avoid differences between groups due to an unbalanced number of patients with preexisting dementia, an evaluation of cognitive functions before inclusion might allow a stratification for this variable; use of the IQCODE requires less than 15 minutes. Finally, the most important question that should be addressed now is to determine whether recognition of preexisting dementia in stroke patients, and differentiating degenerative from vascular origin, should lead to a different approach at the acute stage of stroke.

	Selected Abbreviations and Acronyms

 

AD = Alzheimer's disease DSM-III-R = Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revision 3 DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, 4th Edition ICD-9 = International Classification of Diseases, 9th Revision IQCODE = Informant Questionnaire on Cognitive Decline in the Elderly MDRS = Mattis Dementia Rating Scale MMSE = Mini-Mental State Examination

	Acknowledgments

 
This study was supported by direction de la recherche et des études doctorales (DRED) grant ER 153, CH&U de Lille grant 9306, association pour la recherche et l'enseignement en pathologie neurovasculaire (APREPAN), and association d'étude et de recherche sur la maladie d'Alzheimer (ADERMA). We thank Drs H. Petit, A. Destée, J.P. Pruvo, C. Daems, and P. Rogelet for their contributions; Mrs J. Campos for her technical assistance; and Mrs S. Polley and Mrs C. Mouly for neuropsychological assistance.

Received April 28, 1997; revision received August 13, 1997; accepted August 28, 1997.

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