(Stroke. 1999;30:773-779.)
© 1999 American Heart Association, Inc.
Original Contributions |
Confusional State in Stroke
Relation to Preexisting Dementia, Patient Characteristics, and Outcome
From the Stroke Unit (H.H., I.D., O.G., C.L., D.L.) and Memory Unit (H.H., F.L., F.P.), Department of Neurology, University of Lille (France), for the Research Group on Cognition in Degenerative and Vascular Disorders. Reprint requests to Didier Leys, MD, Stroke Unit, Department of Neurology, Hôpital Roger Salengro, F-59037 Lille, France.
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Abstract |
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Background and Purpose—Acute confusional state (ACS) is frequent in hospitalized stroke patients. We previously showed that 16% of patients admitted for a stroke have preexisting dementia. The extent to which preexisting cognitive decline is associated with a risk of ACS at the acute stage of stroke remains to be systematically examined. The aim of this study was to evaluate the prevalence of ACS in acute stroke patients, to study the influence of preexisting cognitive decline and other patient characteristics, and to evaluate the influence of ACS on outcome.
Methods—We diagnosed ACS using DSM-IV criteria and the Delirium Rating Scale with a cutoff of 10 in 202 consecutive stroke patients aged 40 years or older (median age, 75 years; range, 42 to 101 years). Cognitive functioning before stroke was assessed with the Informant Questionnaire on Cognitive Decline in the Elderly.
Results—Forty-nine stroke patients (24.3%; 95% CI, 18.3% to 30.2%) had an ACS during hospitalization. Using logistic regression analysis, we found preexisting cognitive decline (P=0.006) and metabolic or infectious disorders (P=0.008) to be independent predictors of ACS. Functional, but not vital, prognosis was worse in patients with ACS at discharge and 6 months after stroke.
Conclusions—ACS occurs in one fourth of stroke patients older than 40 years. Its occurrence requires inquiry for a preexisting cognitive decline, which usually remains unrecognized in the absence of a systematic evaluation.
Key Words: confusion • delirium • dementia • stroke, acute
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Acute confusional state (ACS) is frequent in hospitalized elderly patients.1 ACS is associated with increased functional decline during hospitalization, risk of hospital-acquired complications, increased duration of hospital stay, need for long-term care, and high short-term mortality rate.2 Several predisposing factors for ACS in hospitalized patients have been identified irrespective of the cause of admission: age,3 4 male sex,4 drugs,3 5 somatic or metabolic disorders,3 6 7 dementia,3 4 7 8 and focal brain lesions of any origin,3 5 6 7 especially stroke.3 In stroke patients, ACS has been reported in single case reports,9 small groups of patients,10 11 and retrospective studies.12 The only prospective study conducted in 145 stroke patients13 found ACS in 48% of patients. In this study, ACS was more likely to occur in elderly patients, men, patients with severe neurological deficits, hemorrhagic strokes, and left-sided hemispheric lesions.13 We previously showed that preexisting dementia is present in one sixth of patients admitted for stroke14 but remains unrecognized in most cases in the absence of a systematic evaluation.14 It is, however, important to diagnose early preexisting dementia in stroke patients because in these patients, the duration of in-hospital stay should be as short as possible, the rehabilitation should be adapted to the patient's abilities, and the treatment introduced for the secondary prevention of stroke may be modified. To our knowledge, the extent to which ACS is associated with preexisting cognitive decline in stroke patients has never been systematically evaluated. The aim of this study was to evaluate the influence of preexisting cognitive decline on the occurrence of ACS in stroke patients and the relationship to patient characteristics and outcome.
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Subjects and Methods |
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Patients
The study population was recruited over a 28-week period (November 2, 1995, to May 12, 1996). Patients were included in a cohort of 202 patients involved in a prospective systematic study of preexisting and new-onset dementia in stroke patients; the objectives and first results of this study have been already published.14 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 in origin (ischemic or hemorrhagic) with exclusion of subarachnoid hemorrhage. Criteria for stroke were clinical symptoms or signs of focal disturbance of cerebral function lasting >24 hours or leading to death, with no apparent cause other than of vascular origin; criteria for transient ischemic attacks (TIAs) were episodes of focal cerebral dysfunction, presumably ischemic in origin, lasting <24 hours and followed by return to normality. We excluded (1) patients with TIA, (2) patients with stroke due to cerebral venous thrombosis, (3) patients younger than 40 years, (4) patients who were not fluent French speakers, (5) patients without a reliable informant, (6) patients with history of severe head trauma or neurosurgery at any time before stroke, (7) patients referred from another hospital to avoid selection bias, and (8) patients who did not live in the urban community of Lille. Previous stroke or TIA were not exclusion criteria. Patients with hemorrhagic infarcts were classified as having cerebral ischemia.
Methods
Patients were examined at admission by 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, B-mode echo
tomography of the cervical arteries, and bidimensional
transthoracic echocardiography were
performed within 24 hours. A delayed CT scan was performed within 8 to
10 days, except in patients who died before that time or had an MRI
scan. Other examinations were performed in selected patients: cerebral
MRI scan, 24-hour continuous 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 or 
8 years of schooling); presence of arterial
hypertension (defined as systolic blood pressure 160
mm Hg or diastolic blood pressure 90 mm Hg either
before stroke onset or lasting >1 month after stroke onset or current
treatment with antihypertensive drugs); diabetes mellitus (defined as
fasting 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/wk; cigarette
smoking (>10 cigarettes a day or cessation <5 years earlier); and
presumed cause of stroke, according to Trial of Org 10172 in Acute
Stoke Treatment (TOAST) criteria.15 The severity of
the clinical deficits was scored according to the Orgogozo rating
scale.16 The level of consciousness was evaluated in each
patient at admission by mean of the ad hoc item of the Orgogozo
scale.16 Data were recorded as soon as possible after
onset and always within 24 hours.
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),17 according to a protocol previously
described.14 The aim of this questionnaire is to detect a
fall from a high previous to a lower present intellectual
level.17 The score obtained does not reflect the severity
of the cognitive impairment but the severity of intellectual decline
occurring over the last 10 years. This questionnaire, applied to a
close relative, has a good reliability between and within
raters.18 19 The correlation between the score obtained on
the Mini-Mental State Examination (MMSE)20 and IQCODE
scores is good.18 19 The main advantage of the IQCODE at
the acute stage of stroke is that it does not require any participation
of the patient at a stage of the disease when neuropsychological
functions may be influenced by stroke itself. An IQCODE score of 78 was
obtained when patients had no cognitive decline before stroke. We
classified patients with IQCODE scores 104 as having preexisting
dementia. The assessment of independent daily living activities was
performed with the informant-completed measure of activities of daily
living and behavior in elderly patients with cognitive
impairment.21
CT scans were performed without contrast on an Elscint 2004 Elite Plus machine, with 5-mm contiguous slices. We determined on CT scans 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-Vehier et al.22 Leukoaraiosis was assessed on the hemisphere opposite a unilateral focal vascular lesion, if any, and on the right hemisphere in the remainder and was scored by means of the 0- to 3-point rating scale of Blennow et al.23 Cerebral atrophy was scored according to the method of Leys et al.24 The location of stroke was determined as a function of the side (right, left) and of the territory involved (anterior superficial hemispheric territory, posterior superficial hemispheric territory, deep hemispheric territory, cerebellum–brain stem) according to the procedure of Tatemichi et al,25 with the addition of small centrum ovale infarcts (<15 mm) that were included in the deep infarct group. Determination of the stroke location was performed on the neuroimaging data that was judged the most appropriate, ie, a delayed CT (87 patients) or MRI (82 patients) scan. In 33 patients it was not possible to perform a delayed CT or MRI scan because of patient death or refusal; if the stroke lesion was not seen on the first CT scan, the location of the stroke was considered undetermined.
Occurrence of ACS during hospitalization in the acute stroke unit
(median duration of stay, 12 days) was defined according to the
criteria of the Diagnostic and Statistical Manual of
Mental Disorders, Fourth Edition (DSM-IV).26
Symptoms of ACS were quantified with the use of the Delirium Rating
Scale of Trzepacz et al,27 which quantifies
multiple parameters affected by delirium such as temporal
onset of symptoms, perceptual disturbances, hallucinations,
delusions, psychomotor behavioral disturbances, cognitive
status deficits, sleep-wake cycle disturbances, lability of
mood, and variability of symptoms. This scale fulfills 4 essential
criteria for usefulness in diagnosis of delirium28 :
specific validation for use in delirium; capability of distinguishing
delirium from dementia; assessment of multiple features of delirium;
and feasibility in delirious patients.27 Patients needed
to have a score 10 to be diagnosed as having ACS, to avoid demented
patients or patients with aphasia being erroneously diagnosed as
confused.
We recorded potential factors of confusion during hospitalization, as follows: (1) epileptic seizures occurring during hospitalization; (2) metabolic or infectious disorders, defined as natremia <130 or >150 mmol/L, glycemia <2.8 or >16.6 mmol/L, urea nitrogen >35.7 mmol/L, calcemia <2.0 or >2.75 mmol/L, severe hypoxemia (SaO2 <90%), hyperthermia (>38.5°C), or clear evidence of urinary, pulmonary, or systemic infections; and (3) drugs known to induce ACS (psychotropic agents such as benzodiazepines, barbiturates, carbamazepine, antidepressants, neuroleptics, antiparkinsonian drugs, analgesics, corticoids, cimetidine, antihistamines, and all drugs with anticholinergic effects).
At discharge, we studied the intrahospital mortality rate and assessed the functional outcome with the Barthel Index29 and the Rankin Scale.30 Six months after stroke onset, we determined the mortality rate by telephoning the patient, the family, and/or the general practitioner. In survivors who underwent the 6-month visit, the functional outcome was evaluated with the Barthel Index,29 Rankin Scale,30 and Weintraub questionnaire,21 and we performed a short evaluation of the patient's cognitive function by means of the MMSE.20 In patients who did not undergo the 6-month visit, the functional outcome was evaluated by telephone with the patient, the family, and/or the general practitioner by means of the Rankin Scale.30
Statistical Analyses
Data were analyzed with the SPSS/Macintosh package. The
first step of the statistical analysis consisted of a
description of the prevalence of ACS, with a 95% CI.
The second step consisted of a bivariate analysis comparing
variables between patients with and patients without ACS. We used
the 
2 test, with Yates correction, or
Fisher's exact test when appropriate, and the odds ratio (OR) method
with 95% CI to compare qualitative factors between groups. We used the
Mann-Whitney U test to compare quantitative variables.
Variables compared between groups were demographic characteristics,
risk factors for stroke, risk factors for dementia, preexisting
cognitive decline, potential causes of ACS, severity of the
neurological deficit at admission, type of stroke (infarct or
hemorrhage), stroke topography and subtype, CT scan findings,
and outcome (duration of hospitalization in acute stroke unit,
in-hospital and 6-month death, and functional outcome) (Tables 1
and 2).
We also evaluated the influence of ACS on the MMSE score after
exclusion of patients with preexisting dementia by means of bivariate
analysis.
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The third step of the statistical analysis consisted of a
logistic regression analysis31 with ACS
(classified as 1 when present and 0 when absent) as dependent
variable (Table 3). The independent
variables included in this analysis were selected from the
bivariate analysis, with a 0.25 level as a screening criterion
for selection of candidate variables.31 Assumptions
underlying the use of such a regression model were tested according to
recommended procedures.32
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We then determined (1) the predictive factors of ACS in patients with an IQCODE score of 78 and (2) the predictive factors of ACS in patients with an IQCODE score >78 by means of bivariate analysis and logistic regression analysis,31 with ACS (classified as 1 when present and 0 when absent) as dependent variable.
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Results |
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During the 28-week recruitment period, 258 patients with stroke, who were aged 40 years or older, native French speakers, and without history of severe head trauma or neurosurgery were admitted in the acute stroke unit. Fifty-six (27.7%) were excluded because of the lack of informant or impossibility of meeting the informant within 48 hours of stroke onset. The informants were spouse in 78 cases (39%), child in 104 cases (51%), brother or sister in 11 cases (5.5%), and a close friend in 9 cases (4.5%).
The study population consisted of 105 women and 97 men with a median age of 75 years (range, 42 to 101 years); 25 patients (12.4%) had a deep intracerebral hemorrhage and 177 (87.6%) an ischemic stroke; 147 patients (72.8%) had a first-ever stroke, and 55 (27.2%) had had a previous stroke or TIA. Of 202 patients, 68 had an IQCODE score of 78, and 134 had an IQCODE score >78. At admission, 152 patients (75.2%) had no reduction in consciousness (score on the ad hoc item of the Orgogozo scale of 15), and 50 (24.8%) had mild to severe reduction in consciousness (37 had a score of 10; 8 had a score of 5; 5 had a score of 0).
Of the 202 patients, 49 (24.3%; 95% CI, 18.3% to 30.2%) had an ACS
during hospitalization in the acute stroke unit. In the subgroup of
patients with ischemic stroke, 43 (24.3%; 95% CI, 18.0% to
30.6%) had an ACS, while 6 (24.0%; 95% CI, 7.3% to 40.7%) had an
ACS in the subgroup of patients with deep intracerebral
hemorrhage. Among 68 patients without any cognitive decline
before stroke (IQCODE score 
78), only 9 (13.2%; 95% CI, 4.5% to
18.6%) developed an ACS. Among 101 patients with cognitive decline
before stroke but without dementia (IQCODE scores >78 and <104), 25
(24.7%; 95% CI, 16.3% to 33.2%) developed an ACS; among 33 patients
with preexisting dementia (IQCODE score 104), 15 (45.5%; 95% CI,
28.5% to 62.4%) developed an ACS during hospitalization
(P=0.002). Among the 152 patients without
disturbances of consciousness at admission, 29 (19.1%)
developed an ACS during hospitalization; among the 50 remaining
patients, 20 (40.0%) developed an ACS (P=0.003).
The results of the bivariate analysis performed on the whole
population are detailed in Tables 1
and 2. Patients with
ACS were older, less likely to be smokers, less likely to have
posterior fossa lesions, and more likely to have metabolic
or infectious disorders. They had higher IQCODE scores and loss of
autonomy in daily living activities before stroke, more severe clinical
deficits at admission with lower scores on the Orgogozo rating scale,
and higher leukoaraiosis and cerebral atrophy scores on the initial CT
scan (Table 1).
The logistic regression analysis performed on the whole
population with presence of ACS as dependent variable found IQCODE
scores (P=0.006) and presence of metabolic or
infectious disorders (P=0.008) as independent variables
(Table 3).
Of the 202 patients, none was lost to follow-up. Twenty-seven died during hospitalization, and 33 died within 6 months. Thirty-two patients did not undergo the 6-month visit for at least 1 of the following reasons: too poor physical condition, insurance refusal, patient or family refusal, or move to another area or country. In 9 of these 32 patients, we could not get enough information by telephone contact to obtain a reliable Rankin score. ACS had occurred in 3 of these 9 patients (33.33%) and in 29 of the 133 survivors (21.80%) from whom we obtained information concerning outcome (P=0.421). One hundred ten patients underwent the 6-month visit and underwent the MMSE. ACS had occurred in 10 of the 32 survivors (30.30%) who did not undergo the 6-month visit and in 22 of the 110 patients (20%) who did (P=0.180).
The intrahospital and 6-month mortality rates did not differ between
patients with and without ACS, although functional scores were worse in
patients with ACS (Table 2). Patients with ACS had lower MMSE
scores 6 months after stroke (P=0.002), even after exclusion
of patients with preexisting dementia (P=0.042).
Nine of the 68 patients without any cognitive decline before stroke (IQCODE score=78) had an ACS during hospitalization. Using bivariate analysis, we found confused patients with an IQCODE score of 78 to be more likely to have arterial hypertension (P=0.007), to have metabolic or infectious disorders (P=0.028), and to have more severe neurological deficits at admission (P=0.016) than patients who were not confused. The logistic regression analysis performed on the 68 patients with IQCODE score of 78 with presence of ACS as dependent variable found history of arterial hypertension (P<0.001; ß=3.691; SE=1.395), history of excessive alcohol consumption (P=0.003; ß=2.839; SE=1.113), and presence of metabolic or infectious disorders (P=0.022; ß=1.997; SE=0.964) as independent variables (overall prediction of the model=89.71%).
Forty of the 134 patients with IQCODE score >78 had an ACS during hospitalization. Using bivariate analysis, we found confused patients with IQCODE score >78 to be more likely to have higher IQCODE scores (P=0.027), a right superficial lesion (P=0.009), and metabolic or infectious disorders (P=0.041). The logistic regression analysis performed on the 134 patients with IQCODE score >78 with presence of ACS as dependent variable found IQCODE score (P=0.023; ß=0.031; SE=0.014) and presence of a right superficial lesion (P=0.011; ß=1.148; SE=0.450) as independent variables (overall prediction of the model=70.90%).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Our study has shown that ACS occurred in one fourth of stroke patients older than 40 years and was independently associated with preexisting cognitive decline and metabolic or infectious concomitant disorders. Patients with ACS had a worse functional outcome at discharge and 6 months after stroke.
The prevalence of ACS in our study population (24.3%; 95% CI, 18.3% to 30.2%) is lower than that observed in 2 previous studies: 48%13 and 33.3%.12 However, one study12 was retrospective and considered disorientation and ACS as a single entity. Erkinjuntti et al33 showed that in elderly hospitalized patients, 40% of patients with dementia were considered confused, and 25% of patients with ACS were considered demented, in the absence of a structured evaluation of the cognitive status. The diagnosis of ACS in stroke patients may be difficult because loss of consciousness and neurological dysfunction may be symptoms of stroke. The use of both the Delirium Rating Scale27 and DSM-IV criteria26 could have increased our diagnosis accuracy. The prevalence of ACS in the study of Gustafson et al13 was surprisingly high (48%), even in patients with TIA (29%). There is no clear explanation for this discrepancy, but since preexisting cognitive decline is a major contributor to ACS and was not systematically assessed in the study of Gustafson et al,13 we cannot exclude a higher proportion of patients with preexisting cognitive decline in this study.13 The inclusion/exclusion criteria in our study may have led to a selection of patients who had a reliable informant and who could be easily followed up; we cannot exclude that this study population has a lower risk of ACS.
Preexisting cognitive decline was the most important factor for ACS in our study. This is not surprising since dementia is an important factor for ACS in elderly hospitalized patients.8 33 However, most patients were not considered demented, and the cognitive decline was not obvious to the relatives.14 This finding suggests that even if ACS may be related to stroke, the presence of ACS requires investigation for preexisting cognitive decline, which is often not recognized in the absence of a formal evaluation. It is important to diagnose dementia as early as possible because (1) new treatments are emerging for Alzheimer's disease that are effective in mild to moderate forms of the disease34 35 36 ; (2) an early diagnosis of dementia could allow a better medical and social management of demented patients and caregivers, which could lead to an improvement in the quality of life for patients and family and to a delayed institutionalization of the patients37 38 ; and (3) the choice of the treatments used in the prevention of stroke recurrence may be influenced by the presence of cognitive decline.
However, the presence of cognitive decline before stroke is not the only factor leading to the development of ACS in stroke patients. Excessive alcohol consumption before stroke and metabolic or infectious disorders may play an important role in the development of ACS in patients without preexisting cognitive decline. Moreover, the presence of cognitive decline before stroke does not lead to ACS in all stroke patients: only 30% of patients with cognitive decline existing before stroke develop ACS during hospitalization. The location of stroke may therefore play a role. Many locations have been reported to be associated with ACS: right middle cerebral artery territory,10 39 left posterior cerebral artery territory,40 hippocampal area, lingual and fusiform gyrus,41 and thalamus.42 In the whole population, according to bivariate analysis, ACS tended to be more frequent in right superficial lesions and was less frequent in posterior fossa lesions. Moreover, right superficial lesion was more frequent in patients with preexisting cognitive decline who developed ACS during hospitalization than in patients who did not. This is in agreement with the literature: ACS has been reported to be more frequent in right than in left hemispheric lesions.12 43 The presence of dysphasia may mask the behavioral and cognitive changes, leading to an underestimation of the prevalence of ACS in patients with lesion of the left hemisphere. However, the use of the Delirium Rating Scale of Trzepacz et al,27 which quantifies multiple parameters affected by delirium, minimized this potential bias in our study. The nondominant hemisphere has a critical role in spatial and bodily perception and orientation44 45 and plays a major role in perceiving emotion45 46 : disturbance of both spatial and emotional orientation might increase the likelihood of misinterpretation of the environment, leading to a higher risk of ACS in patients with right hemisphere lesion. ACS was more frequent in patients who had consciousness disturbances at admission. The level of consciousness at the moment of ACS was modified in all patients, because fluctuating consciousness disturbances are required for a diagnosis of ACS, according to DSM-IV criteria. According to bivariate analysis, ACS appeared to be more frequent in patients with severe neurological deficit at admission. Since reduction in consciousness is associated with a higher severity of stroke, it is difficult to determine whether the occurrence of an ACS was related to the reduction in consciousness or to the severity of the stroke. However, according to multivariate analysis, the severity of the neurological deficits at admission did not appear to be an independent predictor of ACS.
Our study showed that the mortality rates at discharge and after 6 months were not influenced by ACS. The reason may be that mortality at the acute stage is probably influenced more by the severity of stroke than by the cognitive status. However, the functional outcome was worse at discharge and after 6 months, and patients with ACS were less likely to live at home 6 months after the stroke. These patients may be more likely to have cognitive decline, which has been shown to be associated with a worse long-term outcome in stroke patients.47
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Acknowledgments |
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This study was supported by the CH&U de Lille (grant 9306), association pour la recherche et l'enseignement en pathologie neurovasculaire (APREPAN), association d'étude et de recherche sur la maladie d'Alzheimer (ADERMA), ADRINORD, a travel grant from the IPSEN Foundation to Dr Hénon, and the grant MENRT from the French Ministry of Education, Research, and Technology for the Research Group on Cognition in Degenerative and Vascular Disorders (grant EA 2691). We thank J. Campos for technical assistance and S. Polley and C. Mouly for neuropsychological assistance.
Received November 10, 1998; revision received January 4, 1999; accepted January 4, 1999.
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