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Neuroradiology |
1 From the Departments of Neuroradiology, University of Technology, Fetscherstrasse 74, D-01307 Dresden, Germany (R.v.K., H.B.); Università La Sapienza, Rome, Italy (S.B., L.B.); and University of Toulouse, France (C.M.); the Department of Neurology, University of Heidelberg, Germany (W.H.); and Boehringer-Ingelheim, Germany (D.M.). Received April 24, 2000; revision requested June 12; revision received July 17; accepted August 11. Address correspondence to R.v.K. (e-mail: kummer-r@rcs.urz.tu-dresden.de).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Serial CT scans obtained within 6 hours of stroke onset, at 22–96 hours (median, 1 day), and at 2–36 days (median, 7 days) after symptom onset in 786 patients with ischemic stroke were prospectively studied, and follow-up CT scans were used as the reference. Clinical variables were assessed prospectively and independently of CT evaluation.
RESULTS: The specificity and positive predictive value of ischemic edema at baseline CT for brain infarcts were 85% (95% CI: 77%, 91%) and 96% (95% CI: 94%, 98%), respectively. Sensitivity and negative predictive values were 64% (95% CI: 60%, 67%) and 27% (95% CI: 23%, 32%), respectively. Patients without early CT findings were less severely affected (P < .001), developed smaller infarcts (P < .001), had fewer intracranial bleeding events (P < .001), and had a better clinical outcome at 90 days (P < .001) compared with patients with hypoattenuating brain tissue at early CT.
CONCLUSION: After ischemic stroke, x-ray hypoattenuation at CT is highly specific for irreversible ischemic brain damage if detection occurs within the first 6 hours. Patients without hypoattenuating brain tissue have a more favorable clinical course.
Index terms: Brain, CT, 10.12111 • Brain, infarction, 10.781 • Brain, ischemia, 10.781
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Information on whether the ischemic brain has a chance to survive or is already dead is important to assess the effect of treatment. Because of time constraints, a reliable method of cerebral blood flow measurement that could clearly facilitate the prediction, from cerebral blood flow values, of which brain regions will die and which will survive is not routinely applicable. Even with histologic staining, identification of irreversible damage is difficult in experimental animals within the first hours after arterial occlusion (5). It was shown (6–8), however, that brain tissue affected by severe ischemia with a perfusion level of less than 15 mL/100 g per minute takes up water. This process becomes irreversible within a short time (9).
We studied the hypothesis that an increase in brain tissue water content, indicated by a decrease in x-ray attenuation, might herald irreversible ischemic tissue damage. We used the prospective computed tomography (CT) protocol of the European Cooperative Acute Stroke Study II (ECASS II) (10), a large multicenter trial on thrombolysis, to study the capability of CT in the early prediction of irreversible ischemic brain damage. We further studied whether the extent of ischemic brain edema at initial CT is associated with the clinical course.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Patients
Patients (325 women, 461 men; median age, 68 years; age range, 18–84 years) were enrolled in Europe, Australia, and New Zealand from October 1996 to January 1998 after informed consent was obtained and if they were 18–80 years of age and had a moderate to severe hemispheric stroke within the last 6 hours. Intracranial hemorrhage, a hypoattenuating area exceeding one-third of the middle cerebral artery (MCA) territory at CT, severe stupor, coma, and recovery before treatment initiation were among the exclusion criteria (10). Four hundred nine patients were assigned to receive recombinant tissue plasminogen activator (0.9 mg per kilogram of body weight, with an upper limit of 90 mg, and 391 were assigned to receive placebo.
CT Evaluation
All local investigators of ECASS II (532 physicians; 372 (70%) neurologists, 69 (13%) radiologists, 64 (12%) neuroradiologists, and 27 (5%) internists or others) participated in training courses to improve the quality of both the CT scanning procedure and CT scan evaluation (11). Baseline and follow-up CT scans were obtained without contrast enhancement and with the same scanner if possible. Windows and center levels were set to optimally distinguish gray and white matter.
Following the prospective ECASS protocol, all CT scans were evaluated twice, first by the local investigators and then independently by three members of the CT reading panel, who were blinded to treatment allocation, follow-up CT findings, and the reading results of the local investigators. The chairman of the CT reading panel gathered the categorized findings from the panel members, checked them for disagreements, disclosed disagreements to the other panel members, and discussed each discrepant CT finding to achieve a consensus. The final judgments were sent to the data management center, which then was allowed to send the follow-up scans to the members of the CT reading panel.
The members of the CT reading panel were informed which hemisphere was affected and reviewed the CT scans for hypoattenuating arterial territories responsible for the symptoms of acute stroke. We defined hypoattenuation as a visible decrease in x-ray attenuation of brain tissue compared with the attenuation in other portions of the same anatomic structure or its contralateral counterpart. We categorized the extent of hypoattenuation of the MCA territory as no hypoattenuation, 33% or less (small), or greater than 33% (large). On follow-up scans, we measured the volume of acute ischemic lesions by multiplying the maximum diameter of the hypoattenuating area, the maximum diameter of the area perpendicular to it in the same section, the number of sections affected, the section distance, and a conversion factor of 0.5 by using the formula for irregular volumes.
In patients with hemorrhagic transformation, the entire lesion was measured. We classified hemorrhagic events as hemorrhagic infarction or parenchymal hematoma according to the definitions used in the ECASS II.
Clinical Assessments
Local investigators used the National Institutes of Health Stroke Scale (NIHSS) to assess the neurologic deficits of the patients at baseline; at 24 hours after symptom onset; and at 7, 30, and 90 days (SD, 14). The NIHSS is a 42-point scale that is used to quantify neurologic deficits in 11 categories. For example, a mild facial paresis is assigned a score of 1, and a complete hemiplegia with aphasia, gaze deviation, hemianopia, dysarthria, and sensory loss is assigned a score of 25.
The investigators used the Barthel index and the modified Rankin score at 90 days ± 14 (SD) as clinical endpoints. The Barthel index is a reliable and valid measure of the ability of the patient to perform activities of daily living. A score of 100 indicates complete independence. The modified Rankin scale is a simplified overall assessment of function in which a score of 0 indicates absence of symptoms and a score of 6, death. If values were missing, data from the last observation were used. For the modified Rankin score and the Barthel index, a worst-case imputation was made for missing values at day 90. The primary endpoint of ECASS II was the proportion of patients who had a favorable outcome (score < 2) on the modified Rankin scale.
Data Analysis
We used an intention-to-treat analysis for the radiographic endpoints. Ischemic lesions at follow-up CT as described by the CT reading panel served as the reference for irreversible tissue damage irrespective of whether they were detected 22–96 hours (first follow-up CT) or 2–36 days (second follow-up CT) after symptom onset. In four patients with missing CT scans from day 1, we used the information provided at CT on day 7. The findings of the first follow-up CT examination were used in 38 patients with missing second follow-up CT findings.
Baseline CT findings were considered true-positive if follow-up CT scans confirmed the ischemic lesion in the same location, and they were considered true-negative if baseline and follow-up CT scans did not reveal an ischemic infarct. If follow-up CT scans did not show the typical development (increased hypoattenuation, sharper demarcation) of an ischemic lesion seen on the baseline scan or if they were normal in the location indicated at baseline CT, we classified the finding at baseline as false-positive. We then reviewed the false-positive findings for an explanation, such as obliquity of the scan or partial volume artifacts. Normal baseline scans with ischemic lesions at follow-up were called false-negative.
On the basis of these definitions, we calculated sensitivity, specificity, positive and negative predictive values, and accuracy with their 95% CIs. The positive predictive value is the proportion of findings on the baseline scans that are confirmed on follow-up scans. The negative predictive value describes the proportion of negative findings on baseline scans that are still negative on the follow-up scans.
Statistical Analysis
Numeric variables are presented as means with SDs or 95% CIs. All proportions are presented with 95% CIs. To calculate the 95% CI, we used the formula suggested by Berry (12). Differences between the distributions were tested with the Mann-Whitney U test and the Kruskal-Wallis test. Differences between proportions were tested with the 
2 test and the McNemar test. We accepted .05 as a level of significance.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Findings at Baseline CT
The local investigators of ECASS II identified 294 (37%; 95% CI: 34%, 41%) patients with ischemic hypoattenuation at baseline CT; among them were 271 (34%) patients with true-positive findings and 23 (3%) patients with false-positive findings compared with the findings at follow-up CT. Their findings were true-negative in 84 patients. Follow-up CT showed infarcts in 408 (52%) patients that were not seen at baseline (Table 1).
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Remarkably, the mean infarct volume increased between days 1 and 7 from 48 mL ± 77 to 61 mL ± 93 (Mann-Whitney U test, P < .001). Despite the increase in mean infarct volume, the median NIHSS score improved from 8 to 6 (Mann-Whitney U test, P < .001) between days 1 and 7. The infarct volume at the second follow-up CT correlated directly with the NIHSS at day 7 (r2 = 0.47, P < .001), at day 90 (r2 = 0.32, P < .001), and indirectly with the Barthel index at day 90 (r2 = -0.29, P < .001).
Patients with infarcts at follow-up CT (n = 679) had a poorer clinical outcome at 90 days than patients without a detectable infarct (n = 107). The mean Barthel index was 68 ± 37 in patients with infarct and 89 ± 26 in patients without infarct at follow-up CT (Mann-Whitney U test, P < .001). Only 227 (33%) of 679 patients with infarct at follow-up CT had a modified Rankin score of 0 or 1 compared with 75 (70%) of 107 patients without infarct (odds ratio, 0.21; 95% CI: 0.14, 0.33).
Treatment did not affect the number of infarcts detected at follow-up CT. The mean infarct volume increased similarly during CT follow-up in both treatment groups.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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In addition to the local investigators of ECASS II, three experienced neuroradiologists individually evaluated the CT scans and had the opportunity to consult each other. The finding of hypoattenuating brain tissue at baseline CT had a high positive predictive value for an ischemic infarct at follow-up CT, irrespective of whether the local investigators or the CT reading panel assessed the CT scans. The local investigators were less sensitive and less specific (difference not significant) in detecting hypoattenuating brain tissue than were the neuroradiologists. The difference can be explained by the different settings in which the CT scans were read: The local investigators had to evaluate the CT findings as quickly as possible to allow early randomization and treatment. In contrast, the three neuroradiologists could evaluate the scans without any time constraints and could finally consult each other, but they had less clinical information. This setting was chosen to determine the capability of CT under optimal conditions. Training and experience may also have contributed to the neuroradiologists’ higher sensitivity and specificity.
In agreement with others (13), we did not observe a single patient with resolution of tissue hypoattenuation within the first 24 hours after stroke onset in both treatment groups. Infarcts seen at the first follow-up CT at 24 hours were confirmed by the second follow-up CT at 7 days, with only four (0.5%) exceptions that are best explained by a fogging effect, a transient increase of hypoattenuation within ischemic brain lesions at CT in the 2nd and 3rd week (14,15). Only pitfalls such as partial volume artifacts, motion artifacts, scan obliquity, or ischemic subcortical demyelination impaired the specificity of the baseline CT findings.
These observations are in line with those of others (13,16–18) and suggest that hypoattenuating brain tissue covering an arterial territory that appeared on a CT scan after a stroke is a distinct pathophysiologic finding that represents irreversible damage. During the initial 3 hours of ischemia, an increase in water and sodium contents is almost exclusively confined to gray matter (6,19). Brain cortex water content increases immediately after arterial occlusion (7,8) if perfusion decreases below 12 mL/100 g per minute, the critical flow level for structural integrity (3). If brain tissue water content increases by 1%, x-ray attenuation decreases by 2–3 HU (20). In animal experiments, x-ray attenuation declined by 7.5 HU ± 1.6 within 4 hours of MCA occlusion (21). Brain tissue hypoattenuation after arterial occlusion may, therefore, be interpreted as ischemic edema, and it may be used as an indicator for severe focal ischemia with subsequent necrosis. Ischemic edema appearing in gray matter first causes a diminished contrast to adjacent white matter and, thus, a loss of anatomic margins. Such gray matter hypoattenuation explains negative phenomena such as obscuration of lentiform nucleus and loss of the insular ribbon (17,22).
The subtlety of early ischemic gray matter edema at CT may be one reason to explain why ischemic infarcts are often missed at CT during the first 6 hours after symptom onset, as the ECASS II local investigators did, and the interobserver agreement is only moderate (23,24). It does not explain, however, why experienced reviewers do not detect any ischemic edema at CT in about one-third of infarcts that appear later at CT. In this study, the proportion of patients with x-ray hypoattenuation within the first 6 hours of stroke was in the range (56%–92%) of that of other studies (13,17,18, 22,25–27), which is higher than that assumed in recent reviews (28–30).
A normal CT finding in a patient with acute stroke can be explained by focal ischemia above the critical flow level of structural integrity, by an early stage of ischemic edema causing hypoattenuation below contrast resolution, by ischemia mainly confined to white matter, or by small volumes of ischemic brain tissue or lesions near the skull base where beam hardening artifacts impair recognition. We presume that the development of ischemic edema is delayed beyond the first 6 hours in a considerable proportion of patients. This delay occurred in 246 (73%) of 337 patients with normal initial CT findings in ECASS II. A standard for irreversible ischemic brain damage is not available for the first few hours after stroke onset. Areas of disturbed proton diffusion at diffusion–weighted magnetic resonance imaging may be unspecific for permanent damage (31,32). Therefore, problems may arise in the assessment of the sensitivity and accuracy of early CT for irreversible tissue damage. Low values may be due to a delay in the development of such tissue changes and not caused by the incapability of CT.
Like others (18), we found that hypoattenuating brain tissue at CT within the first 6 hours of stroke is associated with a larger infarct volume, more severe symptoms, a less favorable clinical course, and a high risk for secondary cerebral hemorrhage and death compared with normal findings at CT. The association between the extent of hypoattenuation at baseline CT and the frequency of cerebral deaths was similar to that in ECASS I (33). This observation supports the assumption that patients with less severe strokes and a good prognosis develop no, delayed, or only small ischemic brain lesions (18,34). The association between CT findings and clinical performance explains the lower proportion of positive CT findings in less severely affected patients examined in the 6th hour after stroke onset. As in ECASS I, the feature of ischemic infarctions at CT was not stable even after 24 hours after stroke in our study (35).
New infarcts appeared on the CT scans in 16 patients, and the mean volume of lesions increased between days 1 and 7, although the patients clinically improved, on average. These findings reflect that the symptoms of stroke are not directly linked to the underlying ischemic tissue damage. The eloquence of brain regions is different, and enlargement of ischemic edema may occur even with clinical recovery. We have no information on whether other lesions may appear even after 7 days after stroke onset and whether these lesions further increase in volume beyond our observation period. We found, however, a significant correlation between the presence of lesions and their volume at the follow-up CT, with clinical outcome at 90 days. This correlation suggests that ischemic lesions, as assessed at day 7 after stroke onset, are clinically relevant and that the possibility of their early detection is worth investigating.
In summary, we found that CT is highly specific in the detection of irreversible ischemic brain tissue damage within the first hours of stroke onset. Ischemic edema is present within the first 6 hours of symptom onset in about two-thirds of patients. A normal early CT scan in a patient with stroke indicates a less severe disease. Ischemic tissue damage is delayed in these patients.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Author contributions: Guarantor of integrity of entire study, R.v.K.; study concepts and design, all authors; definition of intellectual content, all authors; literature research, R.v.K., H.B.; clinical studies, R.v.K., D.M., W.H.; data acquisition, R.v.K., S.B., L.B., C.M., D.M.; data analysis/interpretation, all authors; statistical analysis, R.v.K.; manuscript preparation, all authors; manuscript editing, D.M., W.H., R.v.K.; manuscript revision/review and final version approval, all authors.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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), in patients with small hypoattenuating tissue volumes of 33% or less of the MCA territory (n = 412, 
), and in patients with greater than 33% MCA territory hypoattenuation (n = 37, 
) at baseline (NIHSS 0), at day 1 (NIHSS 1), at day 7 (NIHSS 7), at day 30 (NIHSS 30), and at day 90 (NIHSS 90) after stroke onset. The NIHSS is used to score the neurologic deficit with a 42-point scale; 0 means no deficit, and 42, a severe deficit. Patients with normal CT findings within 6 hours of stroke onset had a better score at baseline and a better clinical course than patients with positive CT findings. Patients with small hypoattenuation at early CT improved clinically, as did the patients with normal CT findings. Patients with hypoattenuation exceeding 33% of the MCA territory did not improve during the first 3 months after stroke.