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DOI: 10.1148/rg.262055063
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MR Pulse Sequences: What Every Radiologist Wants to Know but Is Afraid to Ask1

Richard Bitar, MD, MSc, General Leung, MSc, Richard Perng, MD, Sameh Tadros, MD, Alan R. Moody, FRCR, FRCP, Josee Sarrazin, MD, FRCP, Caitlin McGregor, MD, FRCP, Monique Christakis, MD, FRCP, Sean Symons, MD, FRCP, Andrew Nelson, RTR, RTMR and Timothy P. Roberts, PhD

1 From the Department of Medical Imaging, University of Toronto, Fitzgerald Building, 150 College St, Room 112, Toronto, Ontario, Canada M5S 3E2 (R.B., A.R.M., J.S., C.M., M.C., S.S., T.P.R.); and Department of Medical Imaging, Sunnybrook and Women’s College Health Sciences Centre, Toronto, Ontario, Canada (R.B., G.L., R.P., S.T., A.R.M., J.S., C.M., M.C., S.S., A.N.). Recipient of an Excellence in Design award for an education exhibit at the 2004 RSNA Annual Meeting. Received March 24, 2005; revision requested May 12 and received June 7; accepted July 6. All authors have no financial relationships to disclose.

Figure 1
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  		Figure 1a.  Basic physics of the MR signal. (a) As 1H nuclei spin, they induce their own magnetic field (tan), the direction (magnetic axis) of which is depicted by an arrow (yellow). The 1H nuclei initially precess with a wobble at various angles (1–6), but when they are exposed to an external magnetic field (B0), they align with it. The sum of all magnetic moments is called the net magnetization vector (NMV). (b) When an RF pulse is applied, the net magnetization vector is flipped at an angle ({alpha}), which produces two magnetization components: longitudinal magnetization (Mz ) and transverse magnetization (Mxy ). As the transverse magnetization precesses around a receiver coil, it induces a current (i). When the RF generator is turned off, T1 recovery and T2 and T2* decay occur.

 

Figure 1
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  		Figure 1b.  Basic physics of the MR signal. (a) As 1H nuclei spin, they induce their own magnetic field (tan), the direction (magnetic axis) of which is depicted by an arrow (yellow). The 1H nuclei initially precess with a wobble at various angles (1–6), but when they are exposed to an external magnetic field (B0), they align with it. The sum of all magnetic moments is called the net magnetization vector (NMV). (b) When an RF pulse is applied, the net magnetization vector is flipped at an angle ({alpha}), which produces two magnetization components: longitudinal magnetization (Mz ) and transverse magnetization (Mxy ). As the transverse magnetization precesses around a receiver coil, it induces a current (i). When the RF generator is turned off, T1 recovery and T2 and T2* decay occur.

 

Figure 2
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  		Figure 2a.  Magnetization relaxation and decay. (a) T1 recovery (spin-lattice relaxation) involves recovery of the longitudinal magnetization (yellow) because of the release of energy (green) into the environment. The lattice is indicated in tan. (b) T2 decay (spin-spin relaxation) is decay of the transverse magnetization because of the interaction of the individual magnetic fields of spinning nuclei. Note that all nuclei initially spin in phase (as indicated by the similar position of the red bands at the bottom of each circle), then move out of phase (with red bands in different positions). (c) T2* decay is decay of the transverse magnetization because of magnetic field inhomogeneities (Fi). {alpha} = flip angle, B0 = external magnetic field.

 

Figure 2
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  		Figure 2b.  Magnetization relaxation and decay. (a) T1 recovery (spin-lattice relaxation) involves recovery of the longitudinal magnetization (yellow) because of the release of energy (green) into the environment. The lattice is indicated in tan. (b) T2 decay (spin-spin relaxation) is decay of the transverse magnetization because of the interaction of the individual magnetic fields of spinning nuclei. Note that all nuclei initially spin in phase (as indicated by the similar position of the red bands at the bottom of each circle), then move out of phase (with red bands in different positions). (c) T2* decay is decay of the transverse magnetization because of magnetic field inhomogeneities (Fi). {alpha} = flip angle, B0 = external magnetic field.

 

Figure 2
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  		Figure 2c.  Magnetization relaxation and decay. (a) T1 recovery (spin-lattice relaxation) involves recovery of the longitudinal magnetization (yellow) because of the release of energy (green) into the environment. The lattice is indicated in tan. (b) T2 decay (spin-spin relaxation) is decay of the transverse magnetization because of the interaction of the individual magnetic fields of spinning nuclei. Note that all nuclei initially spin in phase (as indicated by the similar position of the red bands at the bottom of each circle), then move out of phase (with red bands in different positions). (c) T2* decay is decay of the transverse magnetization because of magnetic field inhomogeneities (Fi). {alpha} = flip angle, B0 = external magnetic field.

 

Figure 3
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  		Figure 3.  Definitions of common symbols used in pulse sequence diagrams.

 

Figure 4
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  		Figure 4a.  (a) Schematic representation of TR and TE. (b) Graphs show the effects of short and long TR (left) and short and long TE (right) on T1 recovery and T2 decay in fat and water: TR relates to T1 and affects T1 weighting, whereas TE relates to T2 and affects T2 weighting. msc = milliseconds, Mxy = transverse magnetization, Mz = longitudinal magnetization.

 

Figure 4
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  		Figure 4b.  (a) Schematic representation of TR and TE. (b) Graphs show the effects of short and long TR (left) and short and long TE (right) on T1 recovery and T2 decay in fat and water: TR relates to T1 and affects T1 weighting, whereas TE relates to T2 and affects T2 weighting. msc = milliseconds, Mxy = transverse magnetization, Mz = longitudinal magnetization.

 

Figure 5
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  		Figure 5.  Diagram shows the signal intensity of various tissues at T1- and T2-weighted imaging. However, note that the signal characteristics of proteinaceous tissues vary according to the amount of protein content: Tissues with high concentrations of protein may have high signal intensity on T1-weighted images (T1WI) and low signal intensity on T2-weighted images (T2WI). CSF = cerebrospinal fluid. (Sources: References 1, 3, and 4.)

 

Figure 6
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  		Figure 6.  Schematic and table show the x-, y-, and z-axis gradients (Gx, Gy, and Gz, respectively) that are used for section selection and for phase and frequency encoding during acquisitions in the most common imaging planes.

 

Figure 7
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  		Figure 7.  Schematic and corresponding MR images show the characteristics determined by data at the periphery of k-space (ie, spatial resolution, or definition of edges) and those determined by data at the center of k-space (ie, gross form and image contrast).

 

Figure 8
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  		Figure 8a.  Application of an SE pulse sequence. (a) Diagram shows the application of an initial pulse at a 90° flip angle to redirect the net magnetization vector into the transverse plane; a subsequent interval of T1, T2, and T2* relaxation, accompanied by the gradual dephasing of the transverse magnetization; and a second pulse applied at a flip angle of 180° to bring the spinning nuclei again into phase so that an echo is produced. Note the locations of the section-selective (Slice) and phase- and frequency-encoding (Readout) gradients (G). (b, c) Coronal T1-weighted (b) and axial T2-weighted (c) SE images of the brain. (d) Sagittal proton-density weighted SE image of the knee.

 

Figure 8
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  		Figure 8b.  Application of an SE pulse sequence. (a) Diagram shows the application of an initial pulse at a 90° flip angle to redirect the net magnetization vector into the transverse plane; a subsequent interval of T1, T2, and T2* relaxation, accompanied by the gradual dephasing of the transverse magnetization; and a second pulse applied at a flip angle of 180° to bring the spinning nuclei again into phase so that an echo is produced. Note the locations of the section-selective (Slice) and phase- and frequency-encoding (Readout) gradients (G). (b, c) Coronal T1-weighted (b) and axial T2-weighted (c) SE images of the brain. (d) Sagittal proton-density weighted SE image of the knee.

 

Figure 8
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  		Figure 8c.  Application of an SE pulse sequence. (a) Diagram shows the application of an initial pulse at a 90° flip angle to redirect the net magnetization vector into the transverse plane; a subsequent interval of T1, T2, and T2* relaxation, accompanied by the gradual dephasing of the transverse magnetization; and a second pulse applied at a flip angle of 180° to bring the spinning nuclei again into phase so that an echo is produced. Note the locations of the section-selective (Slice) and phase- and frequency-encoding (Readout) gradients (G). (b, c) Coronal T1-weighted (b) and axial T2-weighted (c) SE images of the brain. (d) Sagittal proton-density weighted SE image of the knee.

 

Figure 8
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  		Figure 8d.  Application of an SE pulse sequence. (a) Diagram shows the application of an initial pulse at a 90° flip angle to redirect the net magnetization vector into the transverse plane; a subsequent interval of T1, T2, and T2* relaxation, accompanied by the gradual dephasing of the transverse magnetization; and a second pulse applied at a flip angle of 180° to bring the spinning nuclei again into phase so that an echo is produced. Note the locations of the section-selective (Slice) and phase- and frequency-encoding (Readout) gradients (G). (b, c) Coronal T1-weighted (b) and axial T2-weighted (c) SE images of the brain. (d) Sagittal proton-density weighted SE image of the knee.

 

Figure 9
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  		Figure 9.  MR cholangiopancreatography. Sagittal fast SE image obtained with a heavily T2-weighted sequence (TE = 650) shows the common hepatic duct (arrowhead) and common bile duct (arrow).

 

Figure 10
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  		Figure 10a.  Clinical examples of SE and fast SE sequences. (a, b) Liver hemangioma. (a) Axial T2-weighted fast SE image (TE = 82.9) shows a high-signal-intensity lesion (arrow) in the right lobe of the liver. (b) Axial T2-weighted fast SE image (TE = 180), obtained with heavier T2 weighting than a, shows retention of high signal intensity in the lesion (arrow), a feature that indicates a cyst or hemangioma. (c) Polycystic kidney disease. Axial T2-weighted fast SE image provides excellent depiction of cysts, which appear as areas of high signal intensity in the liver and kidney. Differences in signal intensity among the cysts are due to different protein concentrations.

 

Figure 10
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  		Figure 10b.  Clinical examples of SE and fast SE sequences. (a, b) Liver hemangioma. (a) Axial T2-weighted fast SE image (TE = 82.9) shows a high-signal-intensity lesion (arrow) in the right lobe of the liver. (b) Axial T2-weighted fast SE image (TE = 180), obtained with heavier T2 weighting than a, shows retention of high signal intensity in the lesion (arrow), a feature that indicates a cyst or hemangioma. (c) Polycystic kidney disease. Axial T2-weighted fast SE image provides excellent depiction of cysts, which appear as areas of high signal intensity in the liver and kidney. Differences in signal intensity among the cysts are due to different protein concentrations.

 

Figure 10
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  		Figure 10c.  Clinical examples of SE and fast SE sequences. (a, b) Liver hemangioma. (a) Axial T2-weighted fast SE image (TE = 82.9) shows a high-signal-intensity lesion (arrow) in the right lobe of the liver. (b) Axial T2-weighted fast SE image (TE = 180), obtained with heavier T2 weighting than a, shows retention of high signal intensity in the lesion (arrow), a feature that indicates a cyst or hemangioma. (c) Polycystic kidney disease. Axial T2-weighted fast SE image provides excellent depiction of cysts, which appear as areas of high signal intensity in the liver and kidney. Differences in signal intensity among the cysts are due to different protein concentrations.

 

Figure 11
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  		Figure 11a.  Axial T1-weighted (a) and T2-weighted (b) fast SE images show a low-grade glioma. Because of hypercellularity, the tumor appears with hypointense signal in a and hyperintense signal in b. The cystic components and edema are better depicted in b than in a.

 

Figure 11
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  		Figure 11b.  Axial T1-weighted (a) and T2-weighted (b) fast SE images show a low-grade glioma. Because of hypercellularity, the tumor appears with hypointense signal in a and hyperintense signal in b. The cystic components and edema are better depicted in b than in a.

 

Figure 12
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  		Figure 12a.  Fast SE pulse sequence. (a) Pulse sequence diagram shows the fast SE sequence used to obtain the image in b. G = gradient, n = number of repetitions. (b, c) Axial T2-weighted fast SE image (b) and conventional SE image (c) provide comparable depiction of a brain tumor. The acquisition time for conventional SE imaging was 7 minutes 17 seconds, whereas that for fast SE imaging with an echo train length of 16 was 34 seconds.

 

Figure 12
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  		Figure 12b.  Fast SE pulse sequence. (a) Pulse sequence diagram shows the fast SE sequence used to obtain the image in b. G = gradient, n = number of repetitions. (b, c) Axial T2-weighted fast SE image (b) and conventional SE image (c) provide comparable depiction of a brain tumor. The acquisition time for conventional SE imaging was 7 minutes 17 seconds, whereas that for fast SE imaging with an echo train length of 16 was 34 seconds.

 

Figure 12
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  		Figure 12c.  Fast SE pulse sequence. (a) Pulse sequence diagram shows the fast SE sequence used to obtain the image in b. G = gradient, n = number of repetitions. (b, c) Axial T2-weighted fast SE image (b) and conventional SE image (c) provide comparable depiction of a brain tumor. The acquisition time for conventional SE imaging was 7 minutes 17 seconds, whereas that for fast SE imaging with an echo train length of 16 was 34 seconds.

 

Figure 13
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  		Figure 13a.   (a) Conventional inversion-recovery sequence diagram shows a 180° preparatory pulse applied to null the signal from either fat or water. At a predetermined inversion time (TI), a 90° pulse is applied, and the SE sequence is continued. G = gradient. (b) Coronal STIR image shows an insufficiency fracture of the distal tibia, with an extensive area of high signal intensity in bone marrow near the site of the fracture (arrow).

 

Figure 13
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  		Figure 13b.   (a) Conventional inversion-recovery sequence diagram shows a 180° preparatory pulse applied to null the signal from either fat or water. At a predetermined inversion time (TI), a 90° pulse is applied, and the SE sequence is continued. G = gradient. (b) Coronal STIR image shows an insufficiency fracture of the distal tibia, with an extensive area of high signal intensity in bone marrow near the site of the fracture (arrow).

 

Figure 14
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  		Figure 14.  Diagrams show T1 recovery in water and in tissue with use of a conventional inversion-recovery sequence. Nulling of the water signal is seen at TI, when there is virtually no net magnetization vector (NMV) in water. When the 90° pulse flips the net magnetization vector into the transverse plane, little or no transverse magnetization (Tm) is present, and, therefore, no signal is detected in water. Lm = longitudinal magnetization.

 

Figure 15
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  		Figure 15a.  Comparison of fast SE and STIR sequences for depiction of bone marrow edema. (a) Diagram of the STIR sequence (TI = 100–180 msec for fat). (b, c) Coronal T1-weighted fast SE image (b) and coronal STIR image (c) both show pancarpal rheumatoid arthritis; however, the extent of bone marrow edema throughout the carpal bones, distal radius, and ulna is better depicted in c than in b.

 

Figure 15
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  		Figure 15b.  Comparison of fast SE and STIR sequences for depiction of bone marrow edema. (a) Diagram of the STIR sequence (TI = 100–180 msec for fat). (b, c) Coronal T1-weighted fast SE image (b) and coronal STIR image (c) both show pancarpal rheumatoid arthritis; however, the extent of bone marrow edema throughout the carpal bones, distal radius, and ulna is better depicted in c than in b.

 

Figure 15
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  		Figure 15c.  Comparison of fast SE and STIR sequences for depiction of bone marrow edema. (a) Diagram of the STIR sequence (TI = 100–180 msec for fat). (b, c) Coronal T1-weighted fast SE image (b) and coronal STIR image (c) both show pancarpal rheumatoid arthritis; however, the extent of bone marrow edema throughout the carpal bones, distal radius, and ulna is better depicted in c than in b.

 

Figure 16
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  		Figure 16a.  Comparison of magnetic field inhomogeneities with fast SE versus STIR sequences. (a) Sagittal T2-weighted fast SE image obtained with spectral fat suppression, which requires a uniform magnetic field, shows incomplete fat saturation in regions where there is field inhomogeneity, such as at the irregular air–soft tissue interfaces of the toes (arrow). (b) Sagittal image obtained with STIR, which is less susceptible than fast SE sequences to magnetic field inhomogeneities, provides more uniform and more complete fat saturation (arrow). Bone infarcts in the distal tibia and heel appear as areas of high signal intensity on both images.

 

Figure 16
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  		Figure 16b.  Comparison of magnetic field inhomogeneities with fast SE versus STIR sequences. (a) Sagittal T2-weighted fast SE image obtained with spectral fat suppression, which requires a uniform magnetic field, shows incomplete fat saturation in regions where there is field inhomogeneity, such as at the irregular air–soft tissue interfaces of the toes (arrow). (b) Sagittal image obtained with STIR, which is less susceptible than fast SE sequences to magnetic field inhomogeneities, provides more uniform and more complete fat saturation (arrow). Bone infarcts in the distal tibia and heel appear as areas of high signal intensity on both images.

 

Figure 17
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  		Figure 17a.  Comparison of fast SE and FLAIR sequences for depiction of lung cancer metastases to brain. (a) Diagram of the FLAIR sequence shows a TI of 1700–2200 msec for cerebrospinal fluid. (b) Axial T2-weighted fast SE image shows white matter abnormalities in the left temporal lobe. (c) Axial T2-weighted FLAIR image obtained with nulling of the signal from cerebrospinal fluid shows the metastatic lesions more clearly.

 

Figure 17
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  		Figure 17b.  Comparison of fast SE and FLAIR sequences for depiction of lung cancer metastases to brain. (a) Diagram of the FLAIR sequence shows a TI of 1700–2200 msec for cerebrospinal fluid. (b) Axial T2-weighted fast SE image shows white matter abnormalities in the left temporal lobe. (c) Axial T2-weighted FLAIR image obtained with nulling of the signal from cerebrospinal fluid shows the metastatic lesions more clearly.

 

Figure 17
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  		Figure 17c.  Comparison of fast SE and FLAIR sequences for depiction of lung cancer metastases to brain. (a) Diagram of the FLAIR sequence shows a TI of 1700–2200 msec for cerebrospinal fluid. (b) Axial T2-weighted fast SE image shows white matter abnormalities in the left temporal lobe. (c) Axial T2-weighted FLAIR image obtained with nulling of the signal from cerebrospinal fluid shows the metastatic lesions more clearly.

 

Figure 18
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  		Figure 18a.  Comparison of T1-weighted and T2-weighted GRE pulse sequences. (a) GRE pulse sequence diagram shows a variable flip angle and the gradients used to dephase (negative) and rephase (positive) transverse magnetization. Note the locations of the section-selective (Gslice ), phase-encoding (Gphase ), and frequency-encoding (Gfreq/read ) gradients. (b–d) Axial T1-weighted GRE images of the brain (b) and upper abdomen (c), and axial T2*-weighted GRE image of the brain (d), obtained with the pulse sequence in a.

 

Figure 18
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  		Figure 18b.  Comparison of T1-weighted and T2-weighted GRE pulse sequences. (a) GRE pulse sequence diagram shows a variable flip angle and the gradients used to dephase (negative) and rephase (positive) transverse magnetization. Note the locations of the section-selective (Gslice ), phase-encoding (Gphase ), and frequency-encoding (Gfreq/read ) gradients. (b–d) Axial T1-weighted GRE images of the brain (b) and upper abdomen (c), and axial T2*-weighted GRE image of the brain (d), obtained with the pulse sequence in a.

 

Figure 18
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  		Figure 18c.  Comparison of T1-weighted and T2-weighted GRE pulse sequences. (a) GRE pulse sequence diagram shows a variable flip angle and the gradients used to dephase (negative) and rephase (positive) transverse magnetization. Note the locations of the section-selective (Gslice ), phase-encoding (Gphase ), and frequency-encoding (Gfreq/read ) gradients. (b–d) Axial T1-weighted GRE images of the brain (b) and upper abdomen (c), and axial T2*-weighted GRE image of the brain (d), obtained with the pulse sequence in a.

 

Figure 18
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  		Figure 18d.  Comparison of T1-weighted and T2-weighted GRE pulse sequences. (a) GRE pulse sequence diagram shows a variable flip angle and the gradients used to dephase (negative) and rephase (positive) transverse magnetization. Note the locations of the section-selective (Gslice ), phase-encoding (Gphase ), and frequency-encoding (Gfreq/read ) gradients. (b–d) Axial T1-weighted GRE images of the brain (b) and upper abdomen (c), and axial T2*-weighted GRE image of the brain (d), obtained with the pulse sequence in a.

 

Figure 19
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  		Figure 19a.  Comparison of FLAIR and GRE sequences for the depiction of hemorrhage. (a) Axial T2-weighted FLAIR image shows an area of high signal intensity in the right parietal lobe, a finding indicative of hemorrhage. (b) Axial T2-weighted GRE image shows signal loss due to the magnetic susceptibility of hemoglobin in the area of hemorrhage.

 

Figure 19
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  		Figure 19b.  Comparison of FLAIR and GRE sequences for the depiction of hemorrhage. (a) Axial T2-weighted FLAIR image shows an area of high signal intensity in the right parietal lobe, a finding indicative of hemorrhage. (b) Axial T2-weighted GRE image shows signal loss due to the magnetic susceptibility of hemoglobin in the area of hemorrhage.

 

Figure 20
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  		Figure 20a.  Pigmented villonodular synovitis. (a) Coronal protondensity weighted fast SE image obtained with fat saturation shows a large parameniscal cyst that contains punctate low-signal-intensity foci (arrow). (b) Coronal T2*-weighted GRE image depicts the punctate foci (arrow) much more prominently, with a visual effect (blooming artifact) that is related to the magnetic susceptibility of hemosiderin in the area affected by pigmented villonodular synovitis.

 

Figure 20
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  		Figure 20b.  Pigmented villonodular synovitis. (a) Coronal protondensity weighted fast SE image obtained with fat saturation shows a large parameniscal cyst that contains punctate low-signal-intensity foci (arrow). (b) Coronal T2*-weighted GRE image depicts the punctate foci (arrow) much more prominently, with a visual effect (blooming artifact) that is related to the magnetic susceptibility of hemosiderin in the area affected by pigmented villonodular synovitis.

 

Figure 21
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  		Figure 21a.  MR cerebral perfusion study with normal findings. (a) Axial T1-weighted SE image. (b, c) Corresponding perfusion images show negative enhancement (b) and the maximum enhancement slope (c).

 

Figure 21
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  		Figure 21b.  MR cerebral perfusion study with normal findings. (a) Axial T1-weighted SE image. (b, c) Corresponding perfusion images show negative enhancement (b) and the maximum enhancement slope (c).

 

Figure 21
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  		Figure 21c.  MR cerebral perfusion study with normal findings. (a) Axial T1-weighted SE image. (b, c) Corresponding perfusion images show negative enhancement (b) and the maximum enhancement slope (c).

 

Figure 22
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  		Figure 22a.  Spoiled and refocused GRE sequences. (a) Axial T2-weighted partially refocused (coherent) GRE image of the internal auditory canal. (b) Oblique sagittal T2-weighted SSFP image of the heart. (c) Axial T1-weighted spoiled (incoherent) GRE image of the brain.

 

Figure 22
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  		Figure 22b.  Spoiled and refocused GRE sequences. (a) Axial T2-weighted partially refocused (coherent) GRE image of the internal auditory canal. (b) Oblique sagittal T2-weighted SSFP image of the heart. (c) Axial T1-weighted spoiled (incoherent) GRE image of the brain.

 

Figure 22
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  		Figure 22c.  Spoiled and refocused GRE sequences. (a) Axial T2-weighted partially refocused (coherent) GRE image of the internal auditory canal. (b) Oblique sagittal T2-weighted SSFP image of the heart. (c) Axial T1-weighted spoiled (incoherent) GRE image of the brain.

 

Figure 23
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  		Figure 23a.  Spoiled GRE sequences for detection of liver hemangioma. (a) Axial T1-weighted spoiled GRE image obtained with fat saturation shows a low-signal-intensity lesion in the right lobe of the liver. (b, c) Axial multiphase T1-weighted spoiled GRE images obtained with gadolinium show nodular discontinuous peripheral enhancement immediately after intravenous contrast material injection and in the arterial phase (b), with gradual filling over time in the venous phase (c), features that help confirm the presence of a hemangioma.

 

Figure 23
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  		Figure 23b.  Spoiled GRE sequences for detection of liver hemangioma. (a) Axial T1-weighted spoiled GRE image obtained with fat saturation shows a low-signal-intensity lesion in the right lobe of the liver. (b, c) Axial multiphase T1-weighted spoiled GRE images obtained with gadolinium show nodular discontinuous peripheral enhancement immediately after intravenous contrast material injection and in the arterial phase (b), with gradual filling over time in the venous phase (c), features that help confirm the presence of a hemangioma.

 

Figure 23
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  		Figure 23c.  Spoiled GRE sequences for detection of liver hemangioma. (a) Axial T1-weighted spoiled GRE image obtained with fat saturation shows a low-signal-intensity lesion in the right lobe of the liver. (b, c) Axial multiphase T1-weighted spoiled GRE images obtained with gadolinium show nodular discontinuous peripheral enhancement immediately after intravenous contrast material injection and in the arterial phase (b), with gradual filling over time in the venous phase (c), features that help confirm the presence of a hemangioma.

 

Figure 24
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  		Figure 24a.  (a) Echo-planar imaging sequence diagram. (b) Axial T2-weighted echo-planar image (EPI) of the brain, obtained with the pulse sequence shown in a.

 

Figure 24
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  		Figure 24b.  (a) Echo-planar imaging sequence diagram. (b) Axial T2-weighted echo-planar image (EPI) of the brain, obtained with the pulse sequence shown in a.

 

Figure 25
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  		Figure 25a.  (a) Diffusion-weighted imaging sequence diagram. (b) Axial diffusion-weighted brain image shows areas of restricted diffusion with high signal intensity.

 

Figure 25
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  		Figure 25b.  (a) Diffusion-weighted imaging sequence diagram. (b) Axial diffusion-weighted brain image shows areas of restricted diffusion with high signal intensity.

 

Figure 26
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  		Figure 26.  Schematics and corresponding diffusion-weighted brain image show areas of restricted (left) and unrestricted (right) diffusion.

 

Figure 27
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  		Figure 27a.  Combination of FLAIR and diffusion-weighted imaging with ADC mapping for depiction of effects of multiple strokes. (a) Axial T2-weighted FLAIR image shows three areas affected by strokes (arrows). (b, c) Axial diffusion-weighted echo-planar image (b) and ADC map (c) allow determination of the age of the strokes: The affected areas of the right frontal operculum and left frontal lobe (single arrows) show no evidence of restricted diffusion; this finding indicates that the stroke is old. In contrast, the affected area of the left parietal lobe (double arrows) appears bright in b and dark in c, evidence of restricted diffusion indicative of the most recent stroke. The area of the second most recent stroke, that in the left frontal lobe (single arrow), appears bright in both b and c; and the area of the oldest stroke, that in the right frontal operculum (single arrow), appears dark in b and bright in c.

 

Figure 27
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  		Figure 27b.  Combination of FLAIR and diffusion-weighted imaging with ADC mapping for depiction of effects of multiple strokes. (a) Axial T2-weighted FLAIR image shows three areas affected by strokes (arrows). (b, c) Axial diffusion-weighted echo-planar image (b) and ADC map (c) allow determination of the age of the strokes: The affected areas of the right frontal operculum and left frontal lobe (single arrows) show no evidence of restricted diffusion; this finding indicates that the stroke is old. In contrast, the affected area of the left parietal lobe (double arrows) appears bright in b and dark in c, evidence of restricted diffusion indicative of the most recent stroke. The area of the second most recent stroke, that in the left frontal lobe (single arrow), appears bright in both b and c; and the area of the oldest stroke, that in the right frontal operculum (single arrow), appears dark in b and bright in c.

 

Figure 27
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  		Figure 27c.  Combination of FLAIR and diffusion-weighted imaging with ADC mapping for depiction of effects of multiple strokes. (a) Axial T2-weighted FLAIR image shows three areas affected by strokes (arrows). (b, c) Axial diffusion-weighted echo-planar image (b) and ADC map (c) allow determination of the age of the strokes: The affected areas of the right frontal operculum and left frontal lobe (single arrows) show no evidence of restricted diffusion; this finding indicates that the stroke is old. In contrast, the affected area of the left parietal lobe (double arrows) appears bright in b and dark in c, evidence of restricted diffusion indicative of the most recent stroke. The area of the second most recent stroke, that in the left frontal lobe (single arrow), appears bright in both b and c; and the area of the oldest stroke, that in the right frontal operculum (single arrow), appears dark in b and bright in c.

 

Figure 28
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  		Figure 28a.  Comparison of MR angiographic images obtained with different sequences. (a) Maximum intensity projection from 2D time-of-flight imaging of the cerebral veins. (b) Axial image obtained with MOTSA. (c) Maximum intensity projection from MOTSA data (same examination as b). (d) Phase-contrast image shows left subclavian steal syndrome. In this example, caudal-to-cranial flow appears dark, and cranial-to-caudal flow appears bright. The left vertebral artery appears bright (arrow), a feature that indicates subclavian steal. (e) Maximum intensity projection from contrast-enhanced MR angiography at the level of the heart, aorta, and vessels of the aortic arch.

 

Figure 28
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  		Figure 28b.  Comparison of MR angiographic images obtained with different sequences. (a) Maximum intensity projection from 2D time-of-flight imaging of the cerebral veins. (b) Axial image obtained with MOTSA. (c) Maximum intensity projection from MOTSA data (same examination as b). (d) Phase-contrast image shows left subclavian steal syndrome. In this example, caudal-to-cranial flow appears dark, and cranial-to-caudal flow appears bright. The left vertebral artery appears bright (arrow), a feature that indicates subclavian steal. (e) Maximum intensity projection from contrast-enhanced MR angiography at the level of the heart, aorta, and vessels of the aortic arch.

 

Figure 28
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  		Figure 28c.  Comparison of MR angiographic images obtained with different sequences. (a) Maximum intensity projection from 2D time-of-flight imaging of the cerebral veins. (b) Axial image obtained with MOTSA. (c) Maximum intensity projection from MOTSA data (same examination as b). (d) Phase-contrast image shows left subclavian steal syndrome. In this example, caudal-to-cranial flow appears dark, and cranial-to-caudal flow appears bright. The left vertebral artery appears bright (arrow), a feature that indicates subclavian steal. (e) Maximum intensity projection from contrast-enhanced MR angiography at the level of the heart, aorta, and vessels of the aortic arch.

 

Figure 28
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  		Figure 28d.  Comparison of MR angiographic images obtained with different sequences. (a) Maximum intensity projection from 2D time-of-flight imaging of the cerebral veins. (b) Axial image obtained with MOTSA. (c) Maximum intensity projection from MOTSA data (same examination as b). (d) Phase-contrast image shows left subclavian steal syndrome. In this example, caudal-to-cranial flow appears dark, and cranial-to-caudal flow appears bright. The left vertebral artery appears bright (arrow), a feature that indicates subclavian steal. (e) Maximum intensity projection from contrast-enhanced MR angiography at the level of the heart, aorta, and vessels of the aortic arch.

 

Figure 28
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  		Figure 28e.  Comparison of MR angiographic images obtained with different sequences. (a) Maximum intensity projection from 2D time-of-flight imaging of the cerebral veins. (b) Axial image obtained with MOTSA. (c) Maximum intensity projection from MOTSA data (same examination as b). (d) Phase-contrast image shows left subclavian steal syndrome. In this example, caudal-to-cranial flow appears dark, and cranial-to-caudal flow appears bright. The left vertebral artery appears bright (arrow), a feature that indicates subclavian steal. (e) Maximum intensity projection from contrast-enhanced MR angiography at the level of the heart, aorta, and vessels of the aortic arch.

 

Figure 29
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  		Figure 29a.  Comparison of GRE and contrast-enhanced MR angiographic sequences for depiction of type B aortic dissection. (a) Coronal T1-weighted spoiled GRE image does not clearly depict aortic dissection. (b, c) Coronal contrast-enhanced MR angiogram (b) and maximum intensity projection (c) obtained with a gadolinium-based contrast agent elegantly demonstrate the true lumen (single arrow) and false lumen (double arrows).

 

Figure 29
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  		Figure 29b.  Comparison of GRE and contrast-enhanced MR angiographic sequences for depiction of type B aortic dissection. (a) Coronal T1-weighted spoiled GRE image does not clearly depict aortic dissection. (b, c) Coronal contrast-enhanced MR angiogram (b) and maximum intensity projection (c) obtained with a gadolinium-based contrast agent elegantly demonstrate the true lumen (single arrow) and false lumen (double arrows).

 

Figure 29
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  		Figure 29c.  Comparison of GRE and contrast-enhanced MR angiographic sequences for depiction of type B aortic dissection. (a) Coronal T1-weighted spoiled GRE image does not clearly depict aortic dissection. (b, c) Coronal contrast-enhanced MR angiogram (b) and maximum intensity projection (c) obtained with a gadolinium-based contrast agent elegantly demonstrate the true lumen (single arrow) and false lumen (double arrows).

 

Figure 30
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  		Figure 30a.  Comparison of fat-saturation and water-excitation sequences at MR imaging. (a) Axial T1-weighted image of the neck obtained with a double inversion-recovery pulse sequence with fat saturation. (b) Coronal STIR image of the knee. (c) Axial T1-weighted GRE image of the neck, obtained with a water-excitation sequence.

 

Figure 30
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  		Figure 30b.  Comparison of fat-saturation and water-excitation sequences at MR imaging. (a) Axial T1-weighted image of the neck obtained with a double inversion-recovery pulse sequence with fat saturation. (b) Coronal STIR image of the knee. (c) Axial T1-weighted GRE image of the neck, obtained with a water-excitation sequence.

 

Figure 30
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  		Figure 30c.  Comparison of fat-saturation and water-excitation sequences at MR imaging. (a) Axial T1-weighted image of the neck obtained with a double inversion-recovery pulse sequence with fat saturation. (b) Coronal STIR image of the knee. (c) Axial T1-weighted GRE image of the neck, obtained with a water-excitation sequence.

 

Figure 31
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  		Figure 31a.  Use of fat suppression for detection of simple lipoma. (a, b) Coronal (a) and axial (b) T1-weighted SE images show a large ovoid lesion in the palm of the hand with signal intensity paralleling that of subcutaneous fat. (c) Axial T2-weighted fast SE image obtained with fat saturation shows uniform suppression of signal throughout the lesion, an indication that the lesion is composed entirely of fat.

 

Figure 31
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  		Figure 31b.  Use of fat suppression for detection of simple lipoma. (a, b) Coronal (a) and axial (b) T1-weighted SE images show a large ovoid lesion in the palm of the hand with signal intensity paralleling that of subcutaneous fat. (c) Axial T2-weighted fast SE image obtained with fat saturation shows uniform suppression of signal throughout the lesion, an indication that the lesion is composed entirely of fat.

 

Figure 31
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  		Figure 31c.  Use of fat suppression for detection of simple lipoma. (a, b) Coronal (a) and axial (b) T1-weighted SE images show a large ovoid lesion in the palm of the hand with signal intensity paralleling that of subcutaneous fat. (c) Axial T2-weighted fast SE image obtained with fat saturation shows uniform suppression of signal throughout the lesion, an indication that the lesion is composed entirely of fat.

 

Figure 32
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  		Figure 32a.  Comparison of axial T1-weighted spoiled GRE images obtained at 1.5 T with in-phase imaging (TE = 4.2 msec) (a) and with out-of-phase imaging (TE = 2.1 msec) (b) shows an adrenal adenoma (arrow), which appears in b as an area of signal void due to cancellation of the signal from microscopic fat.