(Radiology. 1999;211:257-263.)
© RSNA, 1999
Brain: Gadolinium-enhanced Fast Fluid-attenuated Inversion-Recovery MR Imaging1
Vincent P. Mathews, MD,
Karen S. Caldemeyer, MD,
Mark J. Lowe, PhD,
Stacy L. Greenspan, DO,
David M. Weber, PhD and
John L. Ulmer, MD
1 From the Department of Radiology, Indiana University School of Medicine, University Hospital, 550 N University Blvd, Rm 0279, Indianapolis, IN 46202-5253 (V.P.M., K.S.C., M.J.L., S.L.G.); GE Medical Systems, Milwaukee, Wis (D.M.W.); and the Department of Radiology, Medical College of Wisconsin, Milwaukee (J.L.U.). From the 1997 RSNA scientific assembly. Received March 3, 1998; revision requested April 6; final revision received July 30; accepted October 13. Address reprint requests to V.P.M.
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Abstract
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PURPOSE: To determine the clinical utility of gadolinium-enhanced fluid-attenuated inversion-recovery (FLAIR) magnetic resonance (MR) imaging of the brain by comparing results with those at gadolinium-enhanced T1-weighted MR imaging with magnetization transfer (MT) saturation.
MATERIALS AND METHODS: In 105 consecutive patients referred for gadolinium-enhanced brain imaging, FLAIR and T1-weighted MR imaging with MT saturation were performed before and after administration of gadopentetate dimeglumine (0.1 mmol per kilogram of body weight). Pre- and postcontrast images were evaluated to determine the presence of abnormal contrast enhancement and whether enhancement was more conspicuous with the FLAIR or T1-weighted sequences.
RESULTS: Thirty-nine studies showed intracranial contrast enhancement. Postcontrast T1-weighted images with MT saturation showed superior enhancement in 14 studies, whereas postcontrast fast FLAIR images showed superior enhancement in 15 studies. Four cases demonstrated approximately equal contrast enhancement with both sequences. Six cases showed some areas of enhancement better with T1-weighted imaging with MT saturation and other areas better with postcontrast fast FLAIR imaging. Superficial enhancement was typically better seen with postcontrast fast FLAIR imaging.
CONCLUSION: Fast FLAIR images have noticeable T1 contrast making gadolinium-induced enhancement visible. Gadolinium enhancement in lesions that are hyperintense on precontrast FLAIR images, such as intraparenchymal tumors, may be better seen on T1-weighted images than on postcontrast fast FLAIR images. However, postcontrast fast FLAIR images may be useful for detecting superficial abnormalities, such as meningeal disease, because they do not demonstrate contrast enhancement of vessels with slow flow as do T1-weighted images.
Index terms: Brain, MR, 10.12141 Magnetic resonance (MR), comparative studies, 10.12141 Magnetic resonance (MR), contrast enhancement, 10.12143 Magnetic resonance (MR), inversion recovery, 10.121413 Magnetic resonance (MR), magnetization transfer contrast, 10.121417 Magnetic resonance (MR), pulse sequences
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Introduction
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Intravenous magnetic resonance (MR) contrast agents are frequently used to evaluate patients with central nervous system complaints. Commonly used contrast agents employ the paramagnetic ion, gadolinium, which shortens both T1 and T2 of tissues in which it has accumulated. However, T1 shortening is the predominant effect at customary doses and is the phenomenon that is exploited to detect "contrast enhancement" of a lesion on clinical MR images. Therefore, T1-weighted spin-echo sequences are typically used for gadolinium-enhanced MR imaging (1,2).
Although T1-weighted sequences are primarily used for gadolinium-enhanced brain MR imaging, others such as proton-density and T2-weighted sequences may result in positive contrast enhancement (3). Attempts have been made to use the T1 contrast of fluid-attenuated inversion-recovery (FLAIR) imaging to evaluate the gadolinium-enhanced FLAIR sequence (4). However, initial clinical evaluations of gadolinium-enhanced fast FLAIR imaging of brain tumors reported that this technique did not offer information not available on gadolinium-enhanced T1-weighted images (5,6). The purpose of this study was to define instances of clinical utility of gadolinium-enhanced fast FLAIR imaging by comparing results to those with gadolinium-enhanced T1-weighted imaging with magnetization transfer (MT) saturation in patients with a broad spectrum of neurologic diseases.
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MATERIALS AND METHODS
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One hundred five consecutive patients (61 women, 44 men; mean age, 45 years; age range, 379 years) referred for gadolinium-enhanced brain imaging over a 3-month period (from August 1996 through November 1996) were evaluated on a 1.5-T clinical MR imager (Signa; GE Medical Systems; Milwaukee, Wis). This study was approved by the local institutional review board, and informed consent was obtained for the MR study from each person. Fast FLAIR and T1-weighted imaging were performed before and after administration of gadopentetate dimeglumine (Magnevist, 0.1 mmol per kilogram of body weight; Berlex Laboratories, Wayne, NJ). MT saturation at a frequency offset of 600 kHz was used in the gadolinium-enhanced T1-weighted sequence as previously described (7). Imaging parameters for fast FLAIR imaging included repetition time of 10,000 msec, effective echo time of 142 msec, inversion time of 2,200 msec, echo train length of 22, and imaging time of 3 minutes 40 seconds. Imaging parameters for T1-weighted imaging with MT saturation included repetition time of 650 msec, echo time of 25 msec, and imaging time of 4 minutes 28 seconds. All images were acquired at the same section locations with section thickness of 5 mm, intersection gap of 2.5 mm, field of view of 22 cm, matrix of 256 x 192, and one signal acquired. T1-weighted and FLAIR were used alternately as the first gadolinium-enhanced sequence.
The precontrast and postcontrast images were evaluated by two experienced neuroradiologists (V.P.M., K.S.C.) to determine the presence or absence and location of abnormal contrast enhancement. The readers then made a consensus determination of whether enhancement was more conspicuous on the postcontrast fast FLAIR images or the T1-weighted images with MT saturation or whether enhancement was equally obvious with both sequences.
In an attempt to determine the underlying mechanisms of image contrast demonstrated on the postcontrast FLAIR and T1-weighted images with and without MT saturation, glass tube phantoms filled with solutions of varying concentrations of gadopentetate dimeglumine were placed adjacent to the head of a volunteer (S.L.G.) and imaged with the same FLAIR and T1-weighted imaging parameters as were used with the patients. T1-weighted imaging was performed both with and without MT saturation. The concentrations of gadolinium ranged from 0.01 to 3 mmol/L.
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RESULTS
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Thirty-nine of the 105 studies showed intracranial contrast enhancement. Four cases were judged to have equal contrast enhancement on T1-weighted images with MT saturation and postcontrast fast FLAIR images. Postcontrast fast FLAIR images showed superior contrast enhancement in 15 studies (Figs 1, 2); in six of the 15, enhancement was seen on only the postcontrast fast FLAIR images. T1-weighted images with MT saturation showed superior contrast enhancement in 14 studies (Fig 3); in three of the 14, enhancement was seen on only T1-weighted images with MT saturation. Six cases demonstrated some areas of enhancement better on T1-weighted images with MT saturation and other areas better on postcontrast fast FLAIR images (Fig 4). Studies that showed superior enhancement on T1-weighted images with MT saturation did not differ from those that showed superior enhancement on FLAIR images in terms of which sequence was performed first or second after administration of gadopentetate dimeglumine. Specifically, among the 15 studies in which postcontrast fast FLAIR images were superior to T1-weighted images with MT saturation, the latter were obtained first in 12. Similarly, among the 14 studies in which T1-weighted images with MT saturation were superior to postcontrast fast FLAIR images, the former were obtained first in 11.

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Figure 1a. Images in a 51-year-old woman with a 3-day history of acute left hemiparesis due to right hemispheric cortical infarction. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle intravascular and cortical enhancement (arrows in b) in the area of infarction. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the infarction as focal cortical hyperintensity (arrows in c) and as obvious pial and gyral enhancement (arrows in d).
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Figure 1b. Images in a 51-year-old woman with a 3-day history of acute left hemiparesis due to right hemispheric cortical infarction. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle intravascular and cortical enhancement (arrows in b) in the area of infarction. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the infarction as focal cortical hyperintensity (arrows in c) and as obvious pial and gyral enhancement (arrows in d).
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Figure 1c. Images in a 51-year-old woman with a 3-day history of acute left hemiparesis due to right hemispheric cortical infarction. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle intravascular and cortical enhancement (arrows in b) in the area of infarction. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the infarction as focal cortical hyperintensity (arrows in c) and as obvious pial and gyral enhancement (arrows in d).
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Figure 1d. Images in a 51-year-old woman with a 3-day history of acute left hemiparesis due to right hemispheric cortical infarction. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle intravascular and cortical enhancement (arrows in b) in the area of infarction. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the infarction as focal cortical hyperintensity (arrows in c) and as obvious pial and gyral enhancement (arrows in d).
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Figure 2a. Images in a 60-year-old woman with a 2-day history of nausea, vomiting, and clumsiness due to medullary infarction. (a) Postcontrast T1-weighted image with MT saturation, (b) T2-weighted image, and (c) precontrast fast FLAIR image obtained at presentation were normal. (d) Postcontrast fast FLAIR image obtained at presentation depicts an abnormality in the area of infarction (arrow). (e) T2-weighted image obtained 4 days later depicts the medullary infarction (arrow).
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Figure 2b. Images in a 60-year-old woman with a 2-day history of nausea, vomiting, and clumsiness due to medullary infarction. (a) Postcontrast T1-weighted image with MT saturation, (b) T2-weighted image, and (c) precontrast fast FLAIR image obtained at presentation were normal. (d) Postcontrast fast FLAIR image obtained at presentation depicts an abnormality in the area of infarction (arrow). (e) T2-weighted image obtained 4 days later depicts the medullary infarction (arrow).
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Figure 2c. Images in a 60-year-old woman with a 2-day history of nausea, vomiting, and clumsiness due to medullary infarction. (a) Postcontrast T1-weighted image with MT saturation, (b) T2-weighted image, and (c) precontrast fast FLAIR image obtained at presentation were normal. (d) Postcontrast fast FLAIR image obtained at presentation depicts an abnormality in the area of infarction (arrow). (e) T2-weighted image obtained 4 days later depicts the medullary infarction (arrow).
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Figure 2d. Images in a 60-year-old woman with a 2-day history of nausea, vomiting, and clumsiness due to medullary infarction. (a) Postcontrast T1-weighted image with MT saturation, (b) T2-weighted image, and (c) precontrast fast FLAIR image obtained at presentation were normal. (d) Postcontrast fast FLAIR image obtained at presentation depicts an abnormality in the area of infarction (arrow). (e) T2-weighted image obtained 4 days later depicts the medullary infarction (arrow).
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Figure 2e. Images in a 60-year-old woman with a 2-day history of nausea, vomiting, and clumsiness due to medullary infarction. (a) Postcontrast T1-weighted image with MT saturation, (b) T2-weighted image, and (c) precontrast fast FLAIR image obtained at presentation were normal. (d) Postcontrast fast FLAIR image obtained at presentation depicts an abnormality in the area of infarction (arrow). (e) T2-weighted image obtained 4 days later depicts the medullary infarction (arrow).
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Figure 3a. Images in a 58-year-old man with metastatic adenocarcinoma of unknown primary origin illustrate the limitations of FLAIR MR imaging in instances of enhancing lesions with prominent surrounding edema. (a) Postcontrast T1-weighted image with MT saturation depicts the enhancing lesions (straight arrows) more clearly because the surrounding edema is hypointense. (b) Precontrast and (c) postcontrast fast FLAIR images depict the edema (arrowheads) as hyperintense, which reduces the lesion-to-background contrast of the metastases (large and small arrows in c). Also note the central portion of the temporal lobe lesion is not enhanced in a (curved arrow) but is enhanced in c possibly because there is a lower concentration of gadolinium centrally (see Discussion). The basal ganglia lesion appears smaller in c (small arrow) than in a possibly because the enhancing margin of the lesion blends with edema in c.
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Figure 3b. Images in a 58-year-old man with metastatic adenocarcinoma of unknown primary origin illustrate the limitations of FLAIR MR imaging in instances of enhancing lesions with prominent surrounding edema. (a) Postcontrast T1-weighted image with MT saturation depicts the enhancing lesions (straight arrows) more clearly because the surrounding edema is hypointense. (b) Precontrast and (c) postcontrast fast FLAIR images depict the edema (arrowheads) as hyperintense, which reduces the lesion-to-background contrast of the metastases (large and small arrows in c). Also note the central portion of the temporal lobe lesion is not enhanced in a (curved arrow) but is enhanced in c possibly because there is a lower concentration of gadolinium centrally (see Discussion). The basal ganglia lesion appears smaller in c (small arrow) than in a possibly because the enhancing margin of the lesion blends with edema in c.
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Figure 3c. Images in a 58-year-old man with metastatic adenocarcinoma of unknown primary origin illustrate the limitations of FLAIR MR imaging in instances of enhancing lesions with prominent surrounding edema. (a) Postcontrast T1-weighted image with MT saturation depicts the enhancing lesions (straight arrows) more clearly because the surrounding edema is hypointense. (b) Precontrast and (c) postcontrast fast FLAIR images depict the edema (arrowheads) as hyperintense, which reduces the lesion-to-background contrast of the metastases (large and small arrows in c). Also note the central portion of the temporal lobe lesion is not enhanced in a (curved arrow) but is enhanced in c possibly because there is a lower concentration of gadolinium centrally (see Discussion). The basal ganglia lesion appears smaller in c (small arrow) than in a possibly because the enhancing margin of the lesion blends with edema in c.
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Figure 4a. Images in a 54-year-old woman with seizures and central nervous system sarcoidosis. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict dural enhancement (arrows in b). (c, d) FLAIR (c) precontrast and (d) postcontrast images do not depict the extent of the dural enhancement as well as in a and b but do depict parenchymal enhancement (arrows in d) not depicted in a and b.
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Figure 4b. Images in a 54-year-old woman with seizures and central nervous system sarcoidosis. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict dural enhancement (arrows in b). (c, d) FLAIR (c) precontrast and (d) postcontrast images do not depict the extent of the dural enhancement as well as in a and b but do depict parenchymal enhancement (arrows in d) not depicted in a and b.
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Figure 4c. Images in a 54-year-old woman with seizures and central nervous system sarcoidosis. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict dural enhancement (arrows in b). (c, d) FLAIR (c) precontrast and (d) postcontrast images do not depict the extent of the dural enhancement as well as in a and b but do depict parenchymal enhancement (arrows in d) not depicted in a and b.
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Figure 4d. Images in a 54-year-old woman with seizures and central nervous system sarcoidosis. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict dural enhancement (arrows in b). (c, d) FLAIR (c) precontrast and (d) postcontrast images do not depict the extent of the dural enhancement as well as in a and b but do depict parenchymal enhancement (arrows in d) not depicted in a and b.
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The intraaxial or extraaxial locations of the enhancing lesions also did not differ between cases in which superior enhancement was seen on T1-weighted images with MT saturation compared with postcontrast fast FLAIR images. On the former, intraaxial lesions were seen in nine cases and extraaxial lesions in five. In the latter, intraaxial lesions were seen in nine cases and extraaxial lesions in six. However, separation of extraaxial lesions into either masses or meningeal infection or inflammation demonstrated more meningeal infectious-inflammatory lesions in cases in which superior enhancement was seen on postcontrast fast FLAIR images compared to T1-weighted images with MT saturation (four cases vs one case, respectively) (Fig 5).

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Figure 5a. Images in a 64-year-old woman with confusion and laboratory evidence of viral meningoencephalitis that subsequently improved with acyclovir therapy. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle leptomeningeal enhancement (arrows in b) that was not detected prospectively. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the leptomeningeal enhancement (arrows in d) more definitively.
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Figure 5b. Images in a 64-year-old woman with confusion and laboratory evidence of viral meningoencephalitis that subsequently improved with acyclovir therapy. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle leptomeningeal enhancement (arrows in b) that was not detected prospectively. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the leptomeningeal enhancement (arrows in d) more definitively.
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Figure 5c. Images in a 64-year-old woman with confusion and laboratory evidence of viral meningoencephalitis that subsequently improved with acyclovir therapy. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle leptomeningeal enhancement (arrows in b) that was not detected prospectively. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the leptomeningeal enhancement (arrows in d) more definitively.
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Figure 5d. Images in a 64-year-old woman with confusion and laboratory evidence of viral meningoencephalitis that subsequently improved with acyclovir therapy. (a, b) T1-weighted (a) precontrast and (b) postcontrast with MT saturation images depict subtle leptomeningeal enhancement (arrows in b) that was not detected prospectively. (c, d) FLAIR (c) precontrast and (d) postcontrast images depict the leptomeningeal enhancement (arrows in d) more definitively.
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An additional 15 studies showed ocular enhancement on postcontrast fast FLAIR images (Fig 6); in only one of these studies was ocular enhancement also visible on postcontrast T1-weighted images with MT saturation. Ten of these patients had diabetes mellitus, known diabetic retinopathy, or both; one had glaucoma; one had undergone ocular surgery; and three had no known ocular disease.

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Figure 6a. Images in a 67-year-old woman with diabetic retinopathy. (a, b) FLAIR (a) precontrast and (b) postcontrast images depict obvious ocular enhancement (arrow in b). (c, d) T1-weighted(c) precontrast and (d) postcontrast with MT saturation images do not depict ocular enhancement. A limitation of this comparison is that dedicated high-spatial-resolution fat-saturated T1-weighted images of the orbit were not obtained.
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Figure 6b. Images in a 67-year-old woman with diabetic retinopathy. (a, b) FLAIR (a) precontrast and (b) postcontrast images depict obvious ocular enhancement (arrow in b). (c, d) T1-weighted(c) precontrast and (d) postcontrast with MT saturation images do not depict ocular enhancement. A limitation of this comparison is that dedicated high-spatial-resolution fat-saturated T1-weighted images of the orbit were not obtained.
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Figure 6c. Images in a 67-year-old woman with diabetic retinopathy. (a, b) FLAIR (a) precontrast and (b) postcontrast images depict obvious ocular enhancement (arrow in b). (c, d) T1-weighted(c) precontrast and (d) postcontrast with MT saturation images do not depict ocular enhancement. A limitation of this comparison is that dedicated high-spatial-resolution fat-saturated T1-weighted images of the orbit were not obtained.
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Figure 6d. Images in a 67-year-old woman with diabetic retinopathy. (a, b) FLAIR (a) precontrast and (b) postcontrast images depict obvious ocular enhancement (arrow in b). (c, d) T1-weighted(c) precontrast and (d) postcontrast with MT saturation images do not depict ocular enhancement. A limitation of this comparison is that dedicated high-spatial-resolution fat-saturated T1-weighted images of the orbit were not obtained.
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The results of the phantom study are shown in Figure 7. The signal intensity of the various gadopentetate dimeglumine solutions compared with that of normal brain with fast FLAIR, T1-weighted, and T1-weighted with MT saturation sequences is plotted versus gadopentetate dimeglumine concentration. The graph shows that solutions with lower concentrations of gadopentetate dimeglumine have higher signal intensity relative to normal brain on FLAIR compared to T1-weighted images with or without MT saturation (Appendix).

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Figure 7. Graph shows the relative signal intensity of a gadolinium solution versus gadolinium concentration with various pulse sequences. Lower concentrations of gadolinium have higher signal intensity relative to normal brain on FLAIR images (C) than on T1-weighted images with (A) or without (B) MT saturation.
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DISCUSSION
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Gadopentetate dimeglumine is frequently given as an intravenous MR contrast agent for brain imaging in order to improve lesion detection or characterization. Even though gadolinium shortens both T1 and T2 of tissues in which it has accumulated, T1 shortening is the predominant effect at commonly used doses, which produces contrast enhancement of a lesion on clinical MR images. Typically, T1-weighted images are acquired before and after the administration of gadopentetate dimeglumine. Areas that develop hyperintensity on postcontrast compared with precontrast studies are said to have "enhanced." Enhancement occurs because gadolinium accumulates in the extracellular space and influences the MR relaxation of nearby tissue protons. For intraaxial brain lesions, the blood-brain barrier must be disrupted in order for gadopentetate dimeglumine to enter the extracellular space. For extraaxial lesions, enhancement is observed in lesions with relatively high vascularity (2). Lesion detection is affected by a number of factors including lesion size, image contrast (lesion-to-background ratio), and lesion location. Lesion detection can be improved by administering larger doses of contrast material that increase the signal of the lesion (8) or by applying MT saturation pulses that reduce the background signal intensity (7). In this study, postcontrast fast FLAIR images were compared with T1-weighted images with MT saturation because several studies have shown that T1-weighted images with MT saturation are more sensitive for depicting contrast enhancement than are those without MT saturation (1,912).
Although T1-weighted sequences are primarily used for postcontrast brain MR imaging, images obtained with other sequences such as proton-density weighted and T2 weighted may demonstrate positive contrast enhancement (3,13,14). Images obtained with long repetition time spin-echo sequences have been shown to demonstrate contrast enhancement in the majority of lesions seen to enhance on T1-weighted images (13,14). Contrast enhancement on proton-densityweighted images was more intense than that seen on T2-weighted images but less than or sometimes equal to that seen on T1-weighted images. New enhancing lesions not detected on the postcontrast T1-weighted images were rarely seen on long repetition time images; the observation of new lesions was attributed to delayed enhancement because the postcontrast long repetition time images were obtained after the postcontrast T1-weighted images (14). The concern that delayed enhancement might affect our results led us to alternate performance of the FLAIR and T1-weighted sequences after administration of gadopentetate dimeglumine. Because images obtained in only about one-third of patients demonstrated contrast enhancement, we did not have equal numbers of patients with enhancing lesions in whom FLAIR was the first postcontrast sequence compared with those in whom T1 weighted was the first postcontrast sequence. However, this did not appear to bias our results because the group with superior enhancement on T1-weighted images with MT saturation did not differ from that with superior enhancement on FLAIR images in terms of which sequence was performed first or second after administration of gadopentetate dimeglumine.
Attempts have been made to use the T1 contrast of the fast FLAIR sequence to evaluate gadolinium enhancement (4). However, in a clinical evaluation of postcontrast fast FLAIR imaging of gliomas, this technique did not offer information that was not available on postcontrast T1-weighted images (5). In another preliminary report of postcontrast fast FLAIR imaging of brain metastases, results with FLAIR and T1-weighted imaging were not significantly different overall after administration of a double dose of gadopentetate dimeglumine; however, postcontrast fast FLAIR imaging was helpful in some lesions near sulci that could be confused with cortical veins on postcontrast T1-weighted images (6). Our results also showed an advantage for postcontrast fast FLAIR over T1-weighted images in some superficial parenchymal lesions but a more consistent advantage for meningeal processes.
The fact that slow-flowing blood is not usually hyperintense on postcontrast fast FLAIR images but frequently is hyperintense on postcontrast T1-weighted images accounts in part for the ability of FLAIR images to sometimes allow more clear distinction between enhancing meninges or superficial parenchyma and enhancing cortical veins. However, other contrast mechanisms may account for the ability to observe gadolinium-induced enhancement on FLAIR images. Even though FLAIR images are commonly thought of as T2-weighted images with dark cerebrospinal fluid, these images have observable T1 contrast (15); therefore, T1 shortening produced by gadopentetate dimeglumine can be seen as hyperintensity on these images.
Although postcontrast fast FLAIR images were particularly effective for showing meningeal lesions, some cortical, subcortical, and extraaxial mass lesions were also depicted more clearly on them. However, other cortical, subcortical, and extraaxial mass lesions were depicted more clearly on T1-weighted images with MT saturation. The reasons for these observations are not clear but may be related to the vascularity and the status of the blood-brain barrier of the individual lesions which affect the concentration of gadopentetate dimeglumine within the lesion at different imaging times. Findings in our phantom study suggest that fast FLAIR imaging may be more sensitive than T1-weighted imaging with or without MT saturation for demonstrating lower concentrations of gadolinium. This implies that faintly enhancing lesions might be depicted more clearly on fast FLAIR images provided the T1 effect of gadolinium is not obscured by the high signal intensity caused by the long T2 of vasogenic edema or the lesion itself (Fig 3). Although the FLAIR sequence appears to be sensitive to T1 shortening at low gadolinium concentrations, findings in the phantom study suggest that the FLAIR sequence is sensitive to T2 effects at high gadolinium concentrations. This implies that lesions accumulating larger amounts of gadopentetate dimeglumine may not demonstrate gadolinium enhancement on FLAIR images because the signal-reducing T2 effects will obscure the signal-enhancing T1 effects. These observations need to be confirmed with in vivo models.
A final factor that may influence the observation of gadolinium enhancement with the FLAIR sequence is MT saturation. Because the FLAIR sequence used in this study is a fast spin-echo sequence with a long echo train of 22, there is an expected MT saturation effect (16,17). Others have found the MT saturation effect of the fast spin-echo T1-weighted sequence improves the conspicuity of gadolinium enhancement (18), and a similar effect may occur with our fast FLAIR sequence. Attempts to measure the magnitude of the MT saturation effect of the fast FLAIR sequence were limited by the inability to perform single-section imaging effectively with the sequence.
The fact that hyperintensity on FLAIR images may be due to either T2 lengthening or T1 shortening limits the usefulness of the FLAIR sequence if it is performed only after administration of gadopentetate dimeglumine. In addition to being unable to ascertain the causes of hyperintensity with the FLAIR sequence if only postcontrast FLAIR imaging is performed, areas of increased signal intensity from T2 lengthening, such as those seen with vasogenic edema, may obscure areas of breakdown of the blood-brain barrier. Therefore, it is unlikely that postcontrast fast FLAIR imaging can replace postcontrast T1-weighted imaging. On the basis of our results, however, postcontrast fast FLAIR imaging is useful in the evaluation of meningeal abnormalities and sometimes is helpful in showing enhancement of parenchymal lesions. Therefore, performance of postcontrast FLAIR imaging should be considered when a meningeal process is evaluated or when postcontrast T1-weighted findings are inconclusive.
In addition to depicting intracranial lesions, postcontrast fast FLAIR images demonstrated ocular contrast enhancement that was most commonly associated with diabetes. A limitation of this observation is the fact that neither the FLAIR nor the T1-weighted sequence was optimized for orbital imaging. In particular, high-spatial-resolution T1-weighted imaging with fat saturation was not performed. Further investigation is being carried out to determine the clinical importance of this ocular enhancement and whether enhancement on postcontrast fast FLAIR images might correspond to development of diabetic retinopathy.
In conclusion, even though FLAIR images are commonly thought of as T2-weighted images with dark cerebrospinal fluid, they have additional T1 contrast (15), which accounts for the ability to see gadolinium-induced enhancement. Gadolinium enhancement on FLAIR images may be difficult to see in lesions such as intraparenchymal tumors that have long T2, which makes them hyperintense. In these cases, T1-weighted imaging is superior to postcontrast fast FLAIR imaging for detecting the breakdown of the blood-brain barrier. However, superficial abnormalities, particularly meningeal diseases, may be better seen or only seen on postcontrast fast FLAIR images compared with T1-weighted images because they do not demonstrate contrast enhancement in vessels with slow flow. Our results also suggest that postcontrast fast FLAIR images should be obtained when it is necessary to detect minimal amounts of contrast enhancement. Therefore, gadolinium-enhanced FLAIR MR imaging is a potentially useful tool for the radiologist and should be considered when findings at gadolinium-enhanced T1-weighted imaging of the brain are inconclusive.
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APPENDIX
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Further amplification of the phantom study results is made by means of the following examination of the steady-state solution of the Bloch equations.
For a T1-weighted image, the MR signal intensity in a pixel with a given T1 and T2 is given with the following equation (19):
where ST1 is signal intensity at the echo time (TE) for a T1-weighted sequence, TR is repetition time, S0 is the MR signal intensity of the pixel immediately after the first excitation pulse, T1 is the T1 relaxation time, and T2 is the T2 relaxation time.
Similarly, for a fast FLAIR image, the MR signal intensity in a given pixel can be given with the following equation (19):
where SIR is the signal intensity at the echo time for an inversion-recovery sequence and TI is the inversion time.
Approximating the signal intensity in a fast FLAIR acquisition with that in an inversion-recovery sequence, Equation (2) shows that in the former a phantom with T1 = T2 = 4,000 msec (as for weakly doped water) will show a 20% signal intensity increase over that for a phantom with T1 = T2 = 5,000 msec (as for undoped water) (ie, SIRdoped/SIRundoped
1.2). A phantom with T1 = T2 = 100 msec (as for highly doped water) will show a 20% signal intensity decrease below that for an undoped phantom (ie, SIRdoped/SIRundoped
0.8). Thus, the fast FLAIR sequence will be sensitive to the T1 shortening at low gadolinium concentrations and the T2 effects at high gadolinium concentrations. Equation (1) shows that if TE << T2, the T1-weighted MR signal will be dominated by the T1 effects of gadolinium at both high and low concentrations. Because a short echo time is used in the MT saturation sequence, it will be relatively insensitive to T2 effects at both high and low gadolinium concentrations. (For a more thorough discussion of contrast mechanisms for MT saturation sequences, see reference 7.)
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Footnotes
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Abbreviations: FLAIR = fluid-attenuated inversion recovery
MT = magnetization transfer
Author contributions: Guarantor of integrity of entire study, V.P.M.; study concepts and design, all authors; definition of intellectual content, all authors; literature research, V.P.M., S.L.G., M.J.L.; clinical studies, V.P.M., K.S.C., S.L.G.; experimental studies, D.M.W., J.L.U., V.P.M., M.J.L.; data acquisition, V.P.M., K.S.C., S.L.G.; data analysis, V.P.M., K.S.C., M.J.L., J.L.U., D.M.W.; statistical analysis, V.P.M., M.J.L.; manuscript preparation, V.P.M.; manuscript editing and review, all authors.
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