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(Radiology. 2000;215:476-482.)
© RSNA, 2000

Neuroradiology

Middle Cerebral Artery (MCA) Susceptibility Sign at Susceptibility-based Perfusion MR Imaging: Clinical Importance and Comparison with Hyperdense MCA Sign at CT 1

Sebastian Flacke, MD, Horst Urbach, MD, Ewald Keller, MD, Frank Träber, PhD, Alexander Hartmann, MD, Jochen Textor, MD, Juergen Gieseke, PhD, Wolfgang Block, PhD, Paul J. M. Folkers, PhD and Hans H. Schild, MD

1 From the Departments of Radiology (S.F., H.U., E.K., F.T., J.T., W.B., H.H.S.) and Neurology (A.H.), University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany, and Philips Medical Systems, Best, the Netherlands (J.G., P.J.M.F.). Received March 9, 1999; revision requested May 6; final revision received August 16; accepted September 9. Address correspondence to S.F. (e-mail: flacke@uni-bonn.de).


   Abstract
TOP
 Abstract
Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To describe the radiologic findings of susceptibility changes in acute middle cerebral artery (MCA) thromboembolism detected with three-dimensional (3D) susceptibility-based perfusion magnetic resonance (MR) imaging and to compare the detectability and clinical value of this sign with those of the hyperdense MCA sign at computed tomography (CT).

MATERIALS AND METHODS: Twenty-three patients (mean age, 55 years) underwent CT and MR imaging within the first 6 hours after the onset of acute MCA stroke. The hyperdense MCA sign at CT and the presence of susceptibility changes in acute thromboembolism as depicted on T2*-weighted 3D perfusion MR images were assessed. The presence of each sign was correlated with clinical presentation.

RESULTS: The sensitivity of the hyperdense MCA sign at CT was 54% (negative predictive value, 71%) compared with 82% (negative predictive value, 86%) for the susceptibility changes at MR imaging. There were no false-positive CT or MR readings. The presence of the MCA susceptibility sign correlated positively with the initial clinical presentation ({chi}2 = 7.987, P = .009, Spearman {rho} = 0.589). However, neither of the signs was a predictor for clinical outcome in cases of spontaneous MCA stroke.

CONCLUSION: In addition to the information traditionally provided with reconstructed perfusion parameter maps, 3D susceptibility-based perfusion MR images allow the identification of acute MCA thromboembolism with a sensitivity higher than that of CT.

Index terms: Blood vessels, MR, 17.12144, 174.12144 • Brain, CT, 10.1211 • Brain, infarction, 10.78, 17.78, 174.78 • Brain, MR, 10.12144 • Computed tomography (CT), comparative studies, 10.1211 • Embolism, 17.77 • Magnetic resonance (MR), comparative studies • Magnetic resonance (MR), diffusion study, 10.12144 • Magnetic resonance (MR), vascular studies, 17.12144, 174.12144


   Introduction
TOP
 Abstract
 Introduction
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Modern approaches to patients with acute ischemic stroke emphasize early diagnosis and management (1). With their high sensitivity to acute cerebral infarction, the new magnetic resonance (MR) imaging techniques with echo-planar, diffusion-weighted, and perfusion MR imaging integrated in the initial imaging protocol are gaining an increasingly important role (2–5).

Diffusion MR imaging depicts early diffusion changes associated with cytotoxic edema following energy metabolism failure and disruption of ion homeostasis (6). Perfusion MR imaging, which maps the relative regional blood volume, has the potential to characterize the degree of regional hypoperfusion, which seems to be an important prognostic factor to determine final infarct extension (7). The most commonly used method to assess perfusion in the brain with MR imaging is dynamic susceptibility-based MR imaging in which contrast is generated by means of the T2* effect of the contrast agent (8,9). Relative regional cerebral blood volume (RCBV), time of bolus arrival, and time to bolus peak can be derived in a straightforward manner on the basis of tracer kinetic theory, assuming that the relaxation rate is roughly proportional to the concentration of the contrast agent in the image voxel (10–12). However, this technique is sensitive not only to susceptibility changes following administration of contrast agent but also to susceptibility variation of paramagnetic deoxygenated hemoglobin, which is encountered in high concentration in acute thromboembolism (13,14). Thus, without imaging other than the standard T2*-weighted perfusion MR imaging, susceptibility changes associated with acute thromboembolism may be detectable.

In this study, we evaluated the radiologic findings of thromboembolism-related susceptibility changes in acute middle cerebral artery (MCA) occlusion as detected with three-dimensional (3D) susceptibility-based perfusion MR imaging. We named this radiologic finding the MCA susceptibility sign. The detectability and clinical value of this sign were assessed and compared with those of the well-known hyperdense MCA sign at computed tomography (CT) (15–18).


   MATERIALS AND METHODS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Patients
From November 1997 to November 1998, 28 patients with acute supratentorial neurologic deficit were referred to our department for CT and MR imaging evaluation within 6 hours after the onset of symptoms, according to the guidelines for clinical investigations of the hospital. Prior to all examinations and interventional procedures, written informed consent was obtained from the patient or his or her relatives after the nature of the procedure had been fully explained. Inclusion criteria for this study were (a) a precisely defined and witnessed onset of symptoms; (b) no evidence of cerebral hemorrhage; (c) a stroke within the MCA territory proved at follow-up imaging or a transient neurologic deficit clearly related to the MCA territory; (d) an assessment of patency or occlusion of the MCA with digital subtraction angiography, MR imaging (MR angiography, perfusion MR imaging), or Doppler flow measurements.

Intracranial hemorrhage was found in one patient. Another four patients were excluded because a vascular territory involvement different from the MCA was seen at MR imaging. Therefore, the data refer to 23 patients (nine women and 14 men; age range, 18–79 years; median age, 57 years; mean age, 55 years) (Table 1). A subset of 10 patients underwent selective intracarotid digital subtraction angiography via the transfemoral route, as these patients were thought to possibly benefit from intraarterial thrombolytic therapy. On the basis of all diagnostic information, thrombolysis was performed in one of these patients, but recanalization of the MCA was not achieved. Therefore, all observations are on the basis of spontaneous stroke evolution after treatment with a full dose of heparin.


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  		TABLE 1. Summary of Patient Data
 
Occlusion of the MCA as delineated at digital subtraction angiography or MR angiography was classified as follows: type 1, proximal to and along the origin of the lenticulostriate branches; type 2, distal to the lenticulostriate origins; type 3, distal to the divisional bifurcation; type 4, individual branch involvement; and type 0, no occlusion (19,20). All surviving patients were reexamined between 4 weeks and 3 months after ictus. Clinical findings were scored according to the Rankin stroke scale (21).

Imaging Examinations
The initial imaging examination was CT in 20 patients and MR in three patients. The interval between CT and diffusion-weighted MR imaging ranged from 20 to 190 minutes (mean, 81 minutes). Nonenhanced CT scans were obtained with section thickness of 4 mm infratentorially and 8 mm supratentorially (Somatom Plus; Siemens Medical Systems; Erlangen, Germany).

All MR studies were performed with a standard 1.5-T clinical imager (Gyroscan ACS-NT Compact Plus [23 mT/m with 0.2-msec rise time]; Philips Medical Systems, Best, the Netherlands) with a standard quadrature head coil. The imaging protocol is listed in Table 2. The susceptibility-based perfusion MR pulse sequence was a 3D segmented echo-planar imaging technique with echo sampling shifted to the next repetition time, which results in echo time greater than repetition time (22–24). Echo shifting was accomplished by means of additional gradients that were placed in all three principal gradient directions. The bolus of 0.2 mmol of gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) per kilogram of body weight was injected in the antecubital fossa by using a power injector (Spectris; Medrad Europe, Maastricht, the Netherlands) and an injection speed of 8 mL/sec. The bolus perfusion data were processed; converted into parameter maps for RCBV, mean transit time, and time to bolus peak; and analyzed as previously described (5).


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  		TABLE 2. MR Imaging Examination Protocol
 
Image Analysis
In a consensus reading, three experienced neuroradiologists (H.U., E.K., J.T.) blinded to the patient's symptoms assessed the presence and location of a susceptibility change related to acute thromboembolism on pre- and postcontrast T2*-weighted images of the perfusion data set and on reconstructed perfusion parameter maps. MR imaging criteria for the MCA susceptibility sign are defined in Table 3. In a second consensus reading, the interpreters were aware of the patient's symptoms and determined the presence and location of the hyperdense MCA sign on the initial CT scans (Table 3). The signs were judged to be present on the basis of only unanimous decision, which was obtained in all cases. If a disagreement had occurred, the sign would have been judged as absent. The location of the hyperdense MCA sign or its MR correlate was classified as follows: (a) proximal MCA trunk, (b) distal MCA trunk, (c) insular branches, or (d) not present.


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  		TABLE 3. Image Criteria of the Hyperdense MCA Sign at CT and the MCA Susceptibility Sign at MR Imaging
 
The extension of relative RCBV less than 20% of that in the contralateral unaffected hemisphere, including areas where signal intensity could not be fitted to a gamma-variate function owing to complete signal dropout, was grouped into five categories: (a) no RCBV deficit, (b) RCBV deficit limited to the basal ganglia, (c) RCBV deficit in less than one-third of the MCA territory, (d) RCBV deficit in less than two-thirds of the MCA territory, (e) RCBV deficit in more than two-thirds of the MCA territory.

Statistical Analysis
Data analysis included descriptive statistics, Fisher exact test for 2 x 2 tables, and Spearman rank correlation ({rho}). Forward and backward unconditioned linear regression analysis was performed to assess the influence on clinical outcome of age, sex, presence of the hyperdense MCA sign at CT, presence of the MCA susceptibility sign at MR, location of the thromboembolism as depicted on T2*-weighted MR images, size of the initial RCBV deficit, and location of the thromboembolism as depicted at digital subtraction angiography or MR angiography.

At 3-month follow-up, clinical outcome was scored according to the Rankin scale. Age was included as a continuous variable; sex and presence of embolus were binary variables. Location of the embolus and size of initial perfusion deficit were categorical variables divided into four or five groups, respectively. For all statistical analysis, the significance level for differences was set at P less than or equal to .05.


   RESULTS
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
A territorial MCA infarct was found on initial and follow-up imaging studies in 20 of 23 patients. No lesions were found on initial and follow-up MR imaging and CT studies in three patients in whom neurologic symptoms resolved completely within the first 24 hours; the clinical diagnosis of transient ischemic attack was established in all three.

In 11 of the 23 patients, types 1–3 MCA occlusions were proved at digital subtraction angiography (n = 6) or MR angiography and Doppler flow measurement (n = 5). In nine of the 23 patients, type 4 MCA occlusion was present on the basis of digital subtraction angiography (n = 4) or MR angiography, perfusion deficits on reconstructed parameter maps, and final infarct extension (n = 5).

In all 23 patients, the hyperdense MCA sign as detected at CT and its MR correlate were ipsilateral to the clinically involved hemisphere. In nine of the 11 patients with angiographically proved types 1–3 MCA occlusions, the thromboembolism-related susceptibility changes could be readily visualized (Fig 1). Sensitivity, specificity, and predictive values are listed in Table 4. None of the CT and MR readings were false-positive. In six of the 11 patients, all hyperdense MCA signs depicted at CT were also detected on the T2*-weighted images of the perfusion data set acquired in the same location (Fig 2). The MCA susceptibility sign was depicted in the proximal horizontal part of the MCA in one patient (Fig 3), in the complete horizontal part of the MCA in five patients, in the distal horizontal part in two patients, and in one of the insular branches in one patient (Fig 4). In patients 3 and 8, the thromboembolism was not detected at MR imaging. In patient 3, the cross section of an angiographically proved thrombus that was mainly within the distal internal carotid artery, or carotid T, was displayed on transverse views, which led to underestimation of the thromboembolism-related susceptibility changes. In patient 8, a dental implant was the source of extensive susceptibility artifacts at the skull base, which obscured the area of the MCA trunk.



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  		Figure 1a. Patient 4. (a) Transverse T2*-weighted MR image (repetition time msec/echo time msec = 13/26, flip angle of 8°) shows the susceptibility artifact of acute thromboembolism in the left MCA (wide arrow) in a patient with acute right-sided hemiparesis. The susceptibility changes clearly exceed the vessel diameter, which can be estimated from the contralateral unaffected side (thin arrow). (b) Corresponding transverse CT scan does not depict a hyperdense MCA sign (arrow). (c) Anteroposterior angiogram displays acute MCA occlusion (arrow).

 


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  		Figure 1b. Patient 4. (a) Transverse T2*-weighted MR image (repetition time msec/echo time msec = 13/26, flip angle of 8°) shows the susceptibility artifact of acute thromboembolism in the left MCA (wide arrow) in a patient with acute right-sided hemiparesis. The susceptibility changes clearly exceed the vessel diameter, which can be estimated from the contralateral unaffected side (thin arrow). (b) Corresponding transverse CT scan does not depict a hyperdense MCA sign (arrow). (c) Anteroposterior angiogram displays acute MCA occlusion (arrow).

 


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  		Figure 1c. Patient 4. (a) Transverse T2*-weighted MR image (repetition time msec/echo time msec = 13/26, flip angle of 8°) shows the susceptibility artifact of acute thromboembolism in the left MCA (wide arrow) in a patient with acute right-sided hemiparesis. The susceptibility changes clearly exceed the vessel diameter, which can be estimated from the contralateral unaffected side (thin arrow). (b) Corresponding transverse CT scan does not depict a hyperdense MCA sign (arrow). (c) Anteroposterior angiogram displays acute MCA occlusion (arrow).

 

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  		TABLE 4. Diagnostic Value of Hyperdense MCA Sign at CT and MCA Susceptibility Sign at MR Imaging in 23 Patients
 


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  		Figure 2a. Patient 2. (a) Transverse CT scan shows a hyperdense MCA sign (arrows) of the left MCA in a patient with acute right-sided hemiparesis. (b) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrows) in the same location.

 


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  		Figure 2b. Patient 2. (a) Transverse CT scan shows a hyperdense MCA sign (arrows) of the left MCA in a patient with acute right-sided hemiparesis. (b) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrows) in the same location.

 


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  		Figure 3a. Patient 9. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) depicts an MCA susceptibility sign (arrow) in the proximal horizontal part of the MCA in a patient with acute right-sided hemiparesis. (b) Corresponding transverse CT scan does not show a hyperdense MCA sign (arrow). (c) Coronal maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) demonstrates the proximal MCA occlusion (arrow).

 


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  		Figure 3b. Patient 9. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) depicts an MCA susceptibility sign (arrow) in the proximal horizontal part of the MCA in a patient with acute right-sided hemiparesis. (b) Corresponding transverse CT scan does not show a hyperdense MCA sign (arrow). (c) Coronal maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) demonstrates the proximal MCA occlusion (arrow).

 


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  		Figure 3c. Patient 9. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) depicts an MCA susceptibility sign (arrow) in the proximal horizontal part of the MCA in a patient with acute right-sided hemiparesis. (b) Corresponding transverse CT scan does not show a hyperdense MCA sign (arrow). (c) Coronal maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) demonstrates the proximal MCA occlusion (arrow).

 


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  		Figure 4a. Patient 11. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrow) within the sylvian fissure in a patient with right-sided hemiparesis and aphasia. (b) Transverse maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) displays the occlusion of an insular branch (arrow). (c, d) Reconstructed transverse parameter maps of the 3D perfusion data set show a corresponding perfusion deficit in (c) axial RCBV (arrow) and (d) time to bolus peak (arrows).

 


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  		Figure 4b. Patient 11. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrow) within the sylvian fissure in a patient with right-sided hemiparesis and aphasia. (b) Transverse maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) displays the occlusion of an insular branch (arrow). (c, d) Reconstructed transverse parameter maps of the 3D perfusion data set show a corresponding perfusion deficit in (c) axial RCBV (arrow) and (d) time to bolus peak (arrows).

 


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  		Figure 4c. Patient 11. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrow) within the sylvian fissure in a patient with right-sided hemiparesis and aphasia. (b) Transverse maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) displays the occlusion of an insular branch (arrow). (c, d) Reconstructed transverse parameter maps of the 3D perfusion data set show a corresponding perfusion deficit in (c) axial RCBV (arrow) and (d) time to bolus peak (arrows).

 


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  		Figure 4d. Patient 11. (a) Transverse T2*-weighted MR image (18/26 with flip angle of 8°) shows an MCA susceptibility sign (arrow) within the sylvian fissure in a patient with right-sided hemiparesis and aphasia. (b) Transverse maximum intensity projection image of the 3D time-of-flight MR angiogram (22/2.8 with flip angle of 20°) displays the occlusion of an insular branch (arrow). (c, d) Reconstructed transverse parameter maps of the 3D perfusion data set show a corresponding perfusion deficit in (c) axial RCBV (arrow) and (d) time to bolus peak (arrows).

 
There was no correlation between the time of examination (grouped into hours after onset of symptoms) and the presence of the hyperdense MCA sign at CT ({chi}2 = 8.306, P = .140, df = 5) or its MR correlate ({chi}2 = 7.186, P = .126, df = 5) during the first 6 hours after the onset of symptoms. The initial clinical symptoms were independent of the presence or absence of the hyperdense MCA sign at CT. Conversely, detection of the MCA susceptibility sign correlated with a higher initial Rankin score ({chi}2 = 7.987, P = .009, {rho} = 0.589).

We found no influence on clinical outcome for sex, presence of the hyperdense MCA sign, or presence and location of the MCA susceptibility sign. A weak correlation was found between the location of the thromboembolism (standardized regression coefficient ß = -0.300, t = -2.175, P = .042) as detected at early angiography and the Rankin score at 3-month follow-up. The age of the patient (ß = 0.344, t = 3.633, P = .002) and the initial perfusion deficit as displayed on reconstructed RCBV maps (ß = 0.548, t = 3.900, P = .001) correlated best with the final clinical outcome in spontaneous MCA stroke.


   DISCUSSION
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
Susceptibility-based brain perfusion MR imaging has become a widespread tool for the assessment of microscopic motion of water and cellular material through the brain. This technique provides qualitative information about the distribution of perfusion over the brain and has been shown to be an important functional MR imaging technique in the assessment of acute stroke, particularly in combination with diffusion-weighted MR imaging (2,3,25,26). Although findings in experimental studies (13,14,27) indicate the potential of susceptibility-weighted MR imaging in detection of thromboembolism, the possibility of detecting susceptibility changes in hyperacute human MCA stroke has not been considered previously in the literature, to our knowledge.

We recognized two important aspects that enable detection of thromboembolism-related susceptibility changes within the MCA trunk: (a) 3D whole-brain coverage is needed to ensure inclusion of the MCA in the field of view, and (b) a good compromise has to be found between T2* sensitivity on the one hand and magnetic field distortions on the other to allow visualization of the MCA near the skull base. In this study, we considered both aspects by using a 3D perfusion MR imaging technique based on the principles of echo shifting (22,23). This technique has good T2* sensitivity without imposing a time penalty because the echo time is longer than the repetition time. Whole-brain coverage is achieved with a dynamic time resolution of less than 2 seconds. This fast acquisition reduces artifacts due to patient movement for a single dynamic image. Furthermore, since the echo train is short, there are only minor image distortions due to T2* decay as a consequence of increased susceptibility near the sinuses and posterior fossa (24).

If standard perfusion MR imaging is performed, detection of the MCA susceptibility sign on T2*-weighted images provides additional information about the location and, to some extent, the size of the thromboembolism. In principle, other imaging techniques sensitive for susceptibility changes may provide similar information. However, additional imaging would be needed that would prolong the total examination time. Therefore, we consider the MCA susceptibility sign to be an additional benefit from perfusion MR imaging rather than a primary and necessary target for imaging.

In our patient group, the sensitivity of MR imaging was higher than that of CT in the detection of an MCA thromboembolism, although the perfusion data were interpreted without knowledge of the clinically affected hemisphere. The sensitivity of the hyperdense MCA sign at CT was 54%, which is in line with data from other studies (19,28,29) that also attest to its clinical value.

Although the sensitivity of the hyperdense MCA sign and its MR correlate may depend on the time of examination, we found no correlation between the time of examination and the presence of both signs during the first 6 hours after the onset of symptoms (18,28). It may be of further interest to monitor the signal changes of the intraluminal blood clot at MR imaging during thrombus organization and recanalization, as methemoglobin-containing blood clots seem to be indistinguishable from flowing blood (13). We did not encounter this potential pitfall in this study of acute thromboembolism during the first 6 hours.

One limitation of these MR techniques was clearly demonstrated in the cases of the two patients in whom the thromboembolism could not be visualized. Field distortion due to dental implants may extend to the skull base and completely deteriorate MR images, especially T2*-weighted images. Also, susceptibility changes of small blood clots in the proximal part of the MCA and within the distal internal carotid artery may be underestimated as transverse views display them in only cross section. However, the associated perfusion deficit downstream from the occluded vessel would remain detectable and could be readily displayed on reconstructed perfusion parameter maps. With the inclusion of dynamic information in the diagnostic criteria for the MCA susceptibility sign, misinterpretation due to regional vessel wall abnormalities such as aneurysm is unlikely.

The clinical value of thromboembolism as detected at early CT has been controversial (30–35). Although we could not confirm that patients with a hyperdense MCA sign were admitted earlier than other patients with hyperacute infarction, there was a significant correlation between the presence of the MCA susceptibility sign and the initial clinical symptoms. On the basis of our observations, the presence of the hyperdense MCA sign or the MCA susceptibility sign as a single prognostic factor has no association with poor prognosis in spontaneous MCA stroke, as has been reported by various authors (30–33). In this study, the patients died who had an MCA susceptibility sign and an initial perfusion deficit of more than two-thirds of the MCA territory, as detected on reconstructed regional cerebral blood volume maps. However, the presence of the MCA susceptibility sign was also associated with small perfusion deficits within the MCA territory. This feature of MCA occlusion with good collateral blood supply was observed in the younger patients in this study group. Our data support findings that outcome may be better predicted by considering additional clinical and imaging findings than by considering only MCA occlusion or signs of MCA occlusion (2,29,34). In this study, the size of the perfusion deficit as detected at initial imaging was shown to be a good predictor of clinical outcome, which confirms the findings of Barber et al (2) and Tong et al (35).

Another limitation of this study is that the neurologic deficit was quantified by using the Rankin scale, which is reported (21) to be less sensitive than other scales. However, the simplicity and good reliability of this scale is appropriate for documenting the degree of handicap at follow-up examinations (21).

In conclusion, 3D susceptibility-based perfusion MR imaging allows the identification of MCA thromboembolism with higher sensitivity than does CT and provides additional information with reconstructed perfusion parameter maps. The location and approximate size of a thromboembolism can be readily depicted with a sensitivity of 82%. The MCA susceptibility sign is not a single predictor of clinical outcome in spontaneous MCA infarction. The description of the MCA susceptibility is an additional benefit from perfusion MR imaging and together with information derived from the perfusion parameter maps (ie, the RCBV deficit) may help identification of high-risk patients during initial imaging.


   Acknowledgments
 
We thank Edith Disput from the Department of Radiology, University of Bonn, Germany, for photographic work.


   Footnotes
 
Abbreviations: MCA = middle cerebral artery RCBV = regional cerebral blood volume 3D = three-dimensional

Author contributions: Guarantors of integrity of entire study, H.H.S., S.F.; study concepts, S.F.; study design, S.F., H.U.; definition of intellectual content, H.H.S.; literature research, S.F., H.U., E.K.; clinical studies, A.H., J.T., H.U.; data acquisition, S.F., H.U., E.K., J.T.; data analysis, J.T., S.F., H.U., E.K., J.G.; statistical analysis, S.F., W.B.; manuscript preparation, S.F., H.U.; manuscript editing, F.T.; manuscript review, J.G., P.J.M.F., H.H.S., F.T.


   References
TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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