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Published online before print April 28, 2005, 10.1148/radiol.2353040571
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(Radiology 2005;235:992-948.)
© RSNA, 2005

Neuroradiology

CT Sign of Brain Swelling without Concomitant Parenchymal Hypoattenuation: Comparison with Diffusion- and Perfusion-weighted MR Imaging1

Dong Gyu Na, MD, Eung Yeop Kim, MD, Jae Wook Ryoo, MD, Kwang Ho Lee, MD, Hong Gee Roh, MD, Sam Soo Kim, MD, In Chan Song, PhD and Kee-Hyun Chang, MD

1 From the Department of Radiology, Seoul National University College of Medicine, Seoul National University Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110–744, Korea (D.G.N., I.C.S., K.H.C.); and Departments of Radiology (E.Y.K., J.W.R., H.G.R., S.S.K.) and Neurology (K.H.L.), Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. Received March 28, 2004; revision requested June 8; revision received July 12; accepted August 18. Address correspondence to D.G.N. (e-mail: dgna@radiol.snu.ac.kr).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To retrospectively evaluate the apparent diffusion coefficient (ADC) on magnetic resonance (MR) images and the perfusion parameters of lesions that show brain swelling without concomitant parenchymal hypoattenuation on computed tomographic (CT) scans.

MATERIALS AND METHODS: Review board approval was obtained, and informed consent was waived. A total of 14 patients (seven men and seven women; mean age, 64 years ± 11) were retrospectively selected from the consecutive 172 patients with acute cerebral ischemia who underwent CT within 6 hours of symptom onset. All patients had brain swelling without parenchymal hypoattenuation, including loss of gray-white matter distinction on CT scans, and they underwent diffusion- and perfusion-weighted MR imaging shortly after CT. CT attenuation, ADC, and perfusion parameters of relative cerebral blood volume (CBV), time to peak (TTP), and relative cerebral blood flow (CBF) were calculated for gray and white matter of the lesion. The measured values were compared with those of the contralateral hemisphere by using the paired t test; comparison of values of perfusion parameters among three subgroups was performed with the Kruskal-Wallis test. Arterial occlusions were determined with MR angiography or conventional angiography.

RESULTS: The mean interval between initial CT and MR imaging was 2.4 hours ± 0.9 (range, 0.4–3.4 hours). The ADC of lesions was similar to that of contralateral normal tissue (mean ADC ratio for gray matter and white matter, 0.99 and 0.97, respectively) (P > .05). Lesions had an increased relative CBV (P < .001), a mild to moderate TTP delay (P < .001), and a variable but not statistically significant reduction of relative CBF. The mean relative CBF of gray matter was less in patients who had complete infarction (0.81 ± 0.16) than that in patients with partial infarction (0.99 ± 0.16) or those with a normal radiologic outcome (1.12 ± 0.22), but this difference was not statistically significant (P > .05). Proximal cerebral artery occlusions were found in all patients. In five (36%) patients, the lesion did not progress to infarction at follow-up.

CONCLUSION: The CT sign of brain swelling without concomitant parenchymal hypoattenuation in patients with acute cerebral ischemia does not represent severe ischemic damage and may suggest ischemic penumbral or oligemic tissue.

© RSNA, 2005


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Brain swelling with sulcal effacement is one of the early ischemic changes noted with computed tomography (CT), and such early ischemic changes have been used as exclusion criteria (the so-called one-third rule) in large clinical trials of both intravenous and intraarterial thrombolytic therapy (1–4). The one-third rule is defined as the presence of early ischemic changes on unenhanced CT scans obtained in one-third or more of the middle cerebral artery territory in the patients with acute ischemic stroke. Early ischemic changes on CT scans include parenchymal hypoattenuation, including loss of gray-white matter distinction, and diffuse or focal brain swelling with effacement of cerebral sulci (1,2,5,6). Although the importance of early ischemic changes remains controversial in patients within 3 hours of symptom onset (6,7), the one-third rule has been used widely and recommended as an exclusion criterion for determining thrombolytic therapy in patients within 6 hours of symptom onset (1–3,8). Early ischemic change of parenchymal hypoattenuation indicates severe ischemic edema of brain tissue and irreversible ischemic injury (9). Patients showing parenchymal hypoattenuation of more than one-third of the middle cerebral artery territory receive no benefit and have higher risk of symptomatic hemorrhage after tissue plasminogen activator treatment, as shown in the European Cooperative Acute Stroke Study I trial (5). However, the prognostic importance of a CT sign of brain swelling without concomitant hypoattenuation is questionable (10), although it is rarely documented. It is not clear whether this CT sign represents severe ischemic change of the brain tissue, which may increase the risk of hemorrhage or a poor outcome after thrombolytic therapy. We hypothesized that brain swelling without concomitant hypoattenuation on CT scans might not represent severe ischemic change. Thus, the purpose of our study was to retrospectively evaluate the apparent diffusion coefficient (ADC) on magnetic resonance (MR) images and the perfusion parameters of lesions showing brain swelling without concomitant parenchymal hypoattenuation on CT scans.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients
Between May 1997 and November 2003, 172 consecutive patients with acute middle cerebral artery infarct and a National Institutes of Health Stroke Scale score of more than 3 underwent CT within 6 hours of symptom onset. Of these patients, we considered for inclusion in our study those who met all of the following inclusion criteria: (a) patients with brain swelling but no concomitant parenchymal hypoattenuation, including loss of gray-white matter distinction on CT scans; (b) patients who underwent MR imaging, including both diffusion-weighted (DW) and perfusion-weighted (PW) MR imaging shortly after CT scanning; and (c) patients who underwent follow-up CT scanning or MR imaging within 10 days of the initial CT examination. We excluded patients who underwent intravenous or intraarterial thrombolytic therapy before MR imaging. The study was approved by the review board of Sungkyunkwan University School of Medicine (Seoul, Korea), and informed consent was waived for our retrospective study.

The Baseline National Institutes of Health Stroke Scale score was obtained for all patients. Two neuroradiologists (D.G.N. and E.Y.K., with 10 and 6 years, respectively, of experience with CT) independently evaluated CT scans to determine the presence of a CT sign of brain swelling without concomitant parenchymal hypoattenuation. Disagreements between interpreters were decided by consensus. The interpreters were blind to the initial MR images, follow-up images, and clinical information, except for information about which hemisphere of the brain was affected. The presence of this CT sign was determined when obvious asymmetric sulcal effacement was observed in more than one section and when there was no concomitant cortical hypoattenuation, including loss of gray-white matter distinction. The 60-HU window width with a 30-HU center level was generally used, and variable window width was also applied in the evaluation of the lesion on unenhanced CT scans.

CT and MR Imaging
All CT scans were obtained with a helical CT scanner (High-Speed Advantage or LightSpeed Ultra; GE Medical Systems, Milwaukee, Wis). The scanning parameters of unenhanced CT were 120 kV and 240 mA, with an image matrix of 512 x 512, a 23- or 24-cm field of view, and a 5-mm section thickness. MR imaging was performed with a 1.5-T unit (Signa or CV/i; GE Medical Systems) with echo-planar imaging sequences, including DW and PW imaging. The typical stroke MR imaging protocol consisted of DW imaging, PW imaging, T2-weighted gradient-echo imaging, gadolinium-enhanced T1-weighted imaging, and three-dimensional time-of-flight MR angiography. Follow-up MR imaging included fast spin-echo T2-weighted and fast fluid-attenuated inversion-recovery (FLAIR) imaging. DW MR images were obtained in 20 sections with b values of 0 and 1000 sec/mm2. Averaged DW MR images were generated online by averaging three orthogonal-axis images. Imaging parameters of DW imaging were as follows: repetition time msec/echo time msec, 6500/96.8; matrix, 128 x 128; field of view, 24 or 28 cm; section thickness, 5 mm; and intersection gap, 2 mm. Perfusion MR imaging was performed with gradient-echo echo-planar sequences (2000/60) during the injection of 0.2 mmol per kilogram of body weight gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) at a rate of 4 mL/sec with an MR-compatible power injector (Spectris; Medrad, Pittsburgh, Pa). The bolus of contrast material was followed by a 15-mL bolus of saline that was administered at the same injection rate. The imaging parameters of T2-weighted and FLAIR images included a matrix of 256 x 192, a field of view of either 23 or 24 cm, a section thickness of 5 mm, and an intersection gap of 2 mm. Two signals were acquired with T2-weighted imaging, and one signal was acquired with FLAIR imaging.

Averaged DW images were processed to generate a trace ADC map based on pixel-by-pixel calculation of signal intensity. Perfusion maps of relative cerebral blood volume (CBV), time to peak (TTP), and relative cerebral blood flow (CBF) were generated off-line at a workstation. After eliminating the recirculation of contrast agent with {gamma}-variate curve fitting, the relative CBV was computed by means of a numeric integration of the curve. The TTP was generated by computing the arrival time of contrast material to maximal concentration. The relative CBF map was obtained with the singular value decomposition deconvolution method (11,12). The shape of the arterial input function was determined from the proximal middle cerebral artery contralateral to the affected hemisphere, and the relative CBF was determined as the height of the deconvoluted tissue curve.

Data Processing and Analysis
All DW and PW images were spatially coregistered to the first volume of CT scans to superimpose the regions of interest (ROIs) delineated on CT scans by use of SPM2 software (Wellcome Department of Cognitive Neuroscience, London, England). All CT scans and MR images were coregistered into the volume data with the same 256 x 256 matrix. After selection of patients with CT evidence of brain swelling without hypoattenuation, two interpreters (D.G.N. and E.Y.K.) selected one CT image in each patient that showed the most obvious brain swelling, by means of consensus. They then independently determined ROIs and manually drew an ROI for the gray matter of the lesion showing gyral swelling without hypoattenuation and another ROI for the subcortical white matter of the lesion. These ROIs were transferred to the corresponding coregistered DW and PW images. The ROI values were averaged from the measurements obtained by the two interpreters. For comparison, mirror ROIs were manually redrawn on CT scans for the gray and white matter of the contralateral hemisphere. An ADC threshold of 1.2 x 10–3 mm2/sec was used to minimize partial volume effect with cerebrospinal fluid. The relative ratios of ADC, signal intensity on DW images, relative CBV, and relative CBF of gray and white matter were calculated by dividing the lesion values by the mirror ROI value of the contralateral hemisphere. TTP delay was defined as the difference between the TTP of a lesion and that of the contralateral hemisphere.

The time to CT and MR imaging after symptom onset, the time between initial CT and MR imaging, and the time to follow-up imaging were assessed. The location of gyral swelling without concomitant hypoattenuation was evaluated on CT scans in each patient, and arterial occlusions were assessed on MR angiograms or conventional angiograms by means of consensus of the two neuroradiologists (D.G.N. and E.Y.K.).

The radiologic outcome of the initial lesion was determined by the same two interpreters in consensus on the follow-up CT scan or FLAIR MR image after completion of evaluation of the initial CT scans and MR images. The radiologic outcome was categorized as normal, partial infarct, or complete infarct according to the presence of cortical infarction, which had gyral swelling on the initial CT scan.

Statistical Analysis
Statistical analysis was performed by using commercially available software (SPSS-PC, version 10.0; SPSS, Chicago, Ill). The normality of each variable was tested by using the Kolmogorov-Smirnov test. Comparisons of the mean values of CT attenuation, ADC, and perfusion parameters between the lesion and contralateral hemisphere were performed with the paired t test. Comparison of mean values of perfusion parameters among three subgroups (normal, partial, and complete infarction) categorized by the radiologic outcome was performed with the Kruskal-Wallis test because normality of the variable was rejected in one subgroup. The values of perfusion parameters of a subgroup with normal or small infarction at follow-up were compared with those of other patients by using an unpaired t test. A P value of less than .05 was considered to indicate a statistically significant difference. The statistical power was assessed for the statistical test of ADC value by using computer software (13). Interobserver agreement concerning the presence of the CT sign of brain swelling was assessed with {kappa} statistics. Interobserver reliability of measured ROI values was assessed by using intraclass correlation coefficients of the ROI sizes determined by the two raters. The coefficients of lesion size on the CT images were 0.730 for gray matter, 0.932 for white matter, and 0.885 for the overall size of the lesion.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
Early ischemic change of brain swelling without concomitant hypoattenuation or loss of gray-white matter distinction was observed in 22 (13%) of the 172 patients. Of these 22 patients, eight were excluded because they did not meet inclusion criteria (n = 6) or had poor PW image quality (n = 2); therefore, 14 patients were included for analysis in this study. Thrombolytic therapy was performed after MR imaging in two of 14 patients (intraarterial thrombolysis in one and intravenous and intraarterial combined therapy in the other). The agreement rate for the presence of a CT sign of brain swelling was 87%, and the k value was 0.50 (moderate) (14). Table 1 shows the demographic data of 14 patients (seven men and seven women; mean age, 64 years ± 11). The mean time to CT and MR imaging ± standard deviation was 2.8 hours ± 1.5 and 5.2 hours ± 1.8, respectively, after symptom onset. The mean interval between initial CT and MR imaging was 2.4 hours ± 0.9, and the mean time to follow-up imaging was 5.7 days ± 1.6. The initial National Institutes of Health Stroke Scale score was 15.0 ± 5.6. The occlusion of proximal cerebral artery (internal carotid artery, 5; M1 segment, 6; middle cerebral artery bifurcation, 2; and M2 segment, 1) was found in all patients who underwent MR angiography (n = 13) or conventional angiography (n = 1). Follow-up CT (n = 5) and MR (n = 9) images showed that lesions with a CT sign of brain swelling without parenchymal hypoattenuation were normal (n = 5) and progressed to partial (n = 6) or complete (n = 3) infarctions (Figs 1–3). In three of six patients with partial infarction at follow-up, there were only small cortical or subcortical infarctions.


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  		TABLE 1. Demographic Data of the 14 Patients

 


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  		Figure 1a. Patient 5. (a) Two ROIs for each area of gray (black outline) and white (white outline) matter were placed manually in both brain hemispheres on unenhanced CT scans. (b) Unenhanced CT scan shows diffuse gyral swelling with asymmetric sulcal effacement in the left frontoparietal lobe (large arrowheads) and focal cortical hypoattenuation (small arrowhead). DW image and ADC map show focal cytotoxic edema in the area of the cortex only and white matter corresponding to a hypointense lesion on the CT scan. Perfusion maps showed a slightly increased TTP delay, increased relative CBV, and no substantial relative CBF reduction in the lesion without hypoattenuation on the CT scan. Follow-up CT (4 days) showed that no cortical infarction was found for the lesion showing gyral swelling without hypoattenuation on the initial CT scan.

 


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  		Figure 1b. Patient 5. (a) Two ROIs for each area of gray (black outline) and white (white outline) matter were placed manually in both brain hemispheres on unenhanced CT scans. (b) Unenhanced CT scan shows diffuse gyral swelling with asymmetric sulcal effacement in the left frontoparietal lobe (large arrowheads) and focal cortical hypoattenuation (small arrowhead). DW image and ADC map show focal cytotoxic edema in the area of the cortex only and white matter corresponding to a hypointense lesion on the CT scan. Perfusion maps showed a slightly increased TTP delay, increased relative CBV, and no substantial relative CBF reduction in the lesion without hypoattenuation on the CT scan. Follow-up CT (4 days) showed that no cortical infarction was found for the lesion showing gyral swelling without hypoattenuation on the initial CT scan.

 


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  		Figure 2. Patient 10. Unenhanced CT scan shows diffuse gyral swelling with asymmetric sulcal effacement in the right inferior frontoparietal lobe (arrowheads). CT scan shows hypoattenuation in the right basal ganglia (arrow). DW image and ADC map shows normal signal intensity in the cortex of the frontoparietal lobe and ADC reduction in the right basal ganglia. Perfusion maps show increased TTP delay in the lateral basal ganglia and inferior frontoparietal gyruses. Perfusion maps show increased relative CBV and no substantial reduction of relative CBF in the right frontoparietal cortex. Perfusion maps also show decreased relative CBV and relative CBF in the right basal ganglia. Follow-up FLAIR MR imaging (7 days) showed progression of infarction in the cortex, which had obviously delayed TTP. This patient underwent combined intravenous and intraarterial combined thrombolytic therapy after MR imaging. Initial conventional angiography (not shown) demonstrated migration of thrombus to proximal M2 segment and recanalization of inferior M2 branches. The occlusion of the proximal superior M2 segment was not recanalized after intraarterial thrombolysis.

 


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  		Figure 3. Patient 12. Unenhanced CT scan shows diffuse gyral swelling with asymmetric sulcal effacement and preserved gray-white matter distinction in the left frontoparietal lobe (arrowheads). DW image and ADC map show normal signal intensity in the cortex and a slight ADC reduction in the subcortical white matter. Perfusion maps show a slightly increased TTP delay and a relative CBF reduction in the lesion. The relative CBV was slightly lower (gray matter, 0.93; white matter, 0.92) in this patient only, and relative CBF in this patient was lowest (gray matter, 0.62; white matter, 0.34) among all patients. Follow-up CT (3 days) showed progression of infarction in the whole parenchyma corresponding to anterior and middle cerebral artery territory (arrowheads).

 
The mean CT attenuation of the gray matter showing gyral swelling was slightly greater than that of the contralateral gray matter, but this difference was statistically significant (31.09 ± 3.55 and 30.61 ± 3.30, respectively) (P = .031) (Table 2). The mean values of ADC and signal intensity on DW images of the lesion were similar to those of the contralateral normal tissue and were not statistically significant (P > .12) (Figs 1, 2). Although not statistically significant, the mean ADC of the white matter (ADC ratio, 0.97 ± 0.10) was slightly less than the control value (Fig 3).


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  		TABLE 2. Mean Values of CT Attenuation, ADC, ADC Ratio, and Signal Intensity Ratio on DW MR Images

 
Lesion relative CBV was significantly greater for gray matter (1.24 ± 0.19; range, 0.93–1.59) (P < .001) and white matter (1.39 ± 0.35; range, 0.92–2.07) (P = .001) (Table 3) than for lesion relative CBV in the contralateral hemisphere. The mean TTP value was slightly or moderately delayed in most patients (P < .001). Lesion relative CBFs were variable, and the difference between lesion relative CBFs and control values was not statistically significant (P > .05). In two patients with no infarction and small partial infarction at follow-up, the relative CBFs of lesions were significantly greater (>1.2) than those of the contralateral hemisphere. The mean relative CBV and TTP delay of the gray matter were similar among patient subgroups with normal radiologic outcome or partial or complete infarction (P > .05). Although the mean relative CBF value of gray matter was less in patients with complete infarction (0.81 ± 0.16) than in those with partial infarction (0.99 ± 0.16) or normal radiologic outcome (1.12 ± 0.22), there was no statistically significant difference (P > .05). The mean relative CBF value of gray matter was significantly greater in the subgroup of patients with normal radiologic outcome or small infarctions at follow-up than in other patients (1.09 ± 0.20 and 0.87 ± 0.14, respectively) (P = .036).


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  		TABLE 3. Mean Values of rCBV, TTP Delay, and rCBF

 
The statistical power of the paired t test for the comparison of mean ADC values between the lesion and the contralateral hemisphere (n = 14) was 0.99 for both gray and white matter. Six patients in each group were required to have a 90% chance of having a difference in means of 92 x 10–6 mm2/sec (2 standard deviations of normal gray matter) for gray matter and 192 x 10–6 mm2/sec (2 standard deviations of normal white matter) for white matter at the 5% level of significance by using the paired t test.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
REFERENCES
 
The results of this study show that the lesion with a CT sign of brain swelling without concomitant hypoattenuation had no cytotoxic edema and no significant decrease of ADC. This lesion had high relative CBV, a mild to moderate TTP delay, and no significant relative CBF reduction. This CT sign was found exclusively in cases of proximal cerebral artery occlusion, and it progressed to partial or complete infarction in 64% of patients.

Brain swelling may be classified into two major groups according to the pathophysiology: It may be classified as either cerebral hyperemia due to increased CBV or cerebral edema due to increased tissue water (15). In cases of traumatic brain injury, the brain swelling may be mainly due to cerebral hyperemia in early hours or days, but brain edema is the major cause of brain swelling several days after head injury (16–18). In acute cerebral ischemia, brain swelling is usually associated with early ischemic edema accompanied by an increase in tissue water. An experimental study (19) showed that brain swelling gradually increases after middle cerebral artery occlusion and is accompanied by ischemic edema and increase of tissue water when the CBF rate falls to less than 10–15 mL · 100 g–1 · min–1. Ischemic brain swelling without edema may be explained by cerebral hyperemia, which can develop due to either compensatory vasodilation after a mild decrease of CBF (20,21) or early postischemic hyperperfusion (22).

Early ischemic change of parenchymal hypoattenuation, including loss of gray-white matter distinction, results from ischemic edema. Attenuation seen on CT scans is linearly proportional to tissue water content (23), and a 1% increase in tissue water content causes a 2–3 HU decrease in attenuation on CT scans (24). Thus, the CT attenuation of brain swelling caused by ischemic edema will decrease, but the CT attenuation of brain swelling due to cerebral hyperemia does not decrease; rather, it theoretically increases due to a relative increase in the blood content of tissue. Our study suggests that brain swelling without hypoattenuation is predominantly caused by cerebral hyperemia and not by ischemic edema. This result also supports the suggestion of von Kummer (10) and von Kummer et al (5) that brain swelling without hypoattenuation is an effect of compensatory vasodilation and is not closely associated with brain tissue damage. In our study, the relative CBF of the lesion was variable, whereas an increase in CBV was found consistently in most patients. This may be explained by the biphasic hemodynamics of CBV (21) and early postischemic hyperperfusion (22). Maximal vasodilation occurs before a significant CBF reduction to approximately 50% of that of normal tissue, and cerebral hyperemia can occur in both oligemic and penumbral tissue (20,21), which has also been shown with perfusion MR studies (25–30). Increased CBF in the lesion might be explained by early postischemic hyperperfusion, including spontaneous reperfusion or uncommon hyperperfusion during permanent artery occlusion, which may be caused by the opening up or widening of collateral circulation (22). According to the results of previous studies (29,30), the mean lesion volume on DW images was close to the lesion volume of ischemic tissue with TTP delay of more than 6–8 seconds, and TTP delay of 4 or more seconds was found to be associated with functional impairment (29). Thus, moderate TTP delay (<6–8 seconds) of the lesion with a CT sign of only gyral swelling may be consistent with TTP delay of oligemic or penumbral tissue.

The CT finding of brain swelling was found in 14% of patients during a National Institute of Neurological Disorders and Stroke trial and in 79% of patients during a European Cooperative Acute Stroke Study I trial (5,6). Although the incidence of brain swelling without concomitant hypoattenuation was not separately documented in those trials, the incidence of a CT sign showing brain swelling without hypoattenuation was low (occurring in 13% of patients) in our study. Although the reason for low incidence is unclear, brain swelling due to cerebral hyperemia might develop only during a short period of hemodynamic change selectively in the patients with proximal vessel occlusion and relatively good collateral flow. In this study, we included patients with obvious brain swelling, and some patients with mild brain swelling might have been missed because mild brain swelling is subtle on visual inspection.

Our study has limitations. First, the correlation between CT and MR imaging may have been influenced by the time interval between CT and MR imaging. Second, the manually drawn ROIs of gray matter may have included a portion of subcortical white matter. Third, the patient population is relatively small, and further investigations may be needed for verification and to determine the clinical importance.

In this study, we evaluated lesions only by using one image that showed the most obvious brain swelling to avoid the possible inclusion of false-positive lesions, as the CT finding investigated was subtle, and interobserver agreement was not high.

In conclusion, brain swelling without hypoattenuation on CT scans had no acute cytotoxic edema and was associated with a high CBV and no significant CBF decrease. This CT sign of early ischemic change does not represent severe ischemic damage, but it does suggest ischemic penumbral or oligemic tissue. Thus, brain swelling without concomitant hypoattenuation on CT scans should not be used as a CT exclusion criterion for the one-third rule when determining thrombolytic therapy in patients with acute ischemic stroke.


   FOOTNOTES
 
Abbreviations: ADC = apparent diffusion coefficient, CBF = cerebral blood flow, CBV = cerebral blood volume, DW = diffusion weighted, FLAIR = fluid-attenuated inversion recovery, PW = perfusion weighted, ROI = region of interest, TTP = time to peak

Authors stated no financial relationship to disclose.

Author contributions: Guarantor of integrity of entire study, D.G.N.; study concepts, D.G.N., E.Y.K.; study design, D.G.N., E.Y.K., J.W.R.; literature research, D.G.N., E.Y.K.; clinical studies, D.G.N., E.Y.K., J.W.R., K.H.L., H.G.R., S.S.K.; data acquisition, J.W.R., K.H.L., H.G.R., S.S.K.; data analysis/interpretation, D.G.N., E.Y.K., I.C.S.; statistical analysis, D.G.N.; manuscript preparation, D.G.N., E.Y.K.; manuscript definition of intellectual content, D.G.N., K.H.C.; manuscript editing, D.G.N., E.Y.K., K.H.C.; manuscript revision/review and final version approval, all authors


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 

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