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1 Department of Radiology, Stanford University, 300 Pasteur Dr., Grant Bldg.
S0-68B, Stanford, CA 94305-5105.
2 GE Applied Science Laboratory West, Menlo Park, CA.
3 Department of Medical Biophysics, University of Toronto, Toronto, ON,
Canada.
Received November 20, 2003;
accepted after revision February 21, 2004.
Address correspondence to G. E. Gold
(gold{at}stanford.edu).
Abstract
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MATERIALS AND METHODS. In the knees of five healthy volunteers, we measured the T1 and T2 relaxation times of cartilage, synovial fluid, muscle, marrow, and fat at 1.5 and 3.0 T. The T1 relaxation times were measured using a spiral Look-Locker sequence with eight samples along the T1 recovery curve. The T2 relaxation times were measured using a spiral T2 preparation sequence with six echoes. Accuracy and repeatability of the T1 and T2 measurement sequences were verified in phantoms.
RESULTS. T1 relaxation times in cartilage, muscle, synovial fluid, marrow, and subcutaneous fat at 3.0 T were consistently higher than those measured at 1.5 T. Measured T2 relaxation times were reduced at 3.0 T compared with 1.5 T. Relaxation time measurements in vivo were verified using calculated and measured signal-to-noise results. Relaxation times were used to develop a high-resolution protocol for T2-weighted imaging of the knee at 3.0 T.
CONCLUSION. MRI at 3.0 T can improve resolution and speed in musculoskeletal imaging; however, interactions between field strength and relaxation times need to be considered for optimal image contrast and signal-to-noise ratio. Scanning can be performed in shorter times at 3.0 T using single-average acquisitions. Efficient higher-resolution imaging at 3.0 T can be done by increasing the TR to account for increased T1 relaxation times and acquiring thinner slices than at 1.5 T.
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Prior measurements of relaxation times at 4.0 T showed increases in T1 relaxation time of 70–90% and decreases in T2 relaxation time of 10–20% compared with times at 1.5 T [3]. Although relaxation times at 3.0 T also change compared with those at 1.5 T, in vivo values have not been available in the literature to our knowledge. The changes in these parameters affect the choice of TR and TE that are appropriate for 3.0 T, and ultimately affect the contrast and SNR of the images produced. At 3.0 T, the chosen TR and TE must reflect the underlying tissues being imaged and the contrast desired.
Musculoskeletal imaging protocols typically consist of several 2D multisection scans, with or without fat saturation. At 3.0 T, because the T1 relaxation times have increased, the TR must be longer to maximize the SNR gain. At 3.0 T, TR must also be longer to achieve the same type of contrast on T1-weighted images as achieved with 1.5 T. Similarly, the TE should be slightly shorter to account for decreases in T2 relaxation times. The number of slices and the spatial resolution required may also influence the choice of TR and TE. We report the in vivo measurements of T1 and T2 for various musculoskeletal tissues at 3.0 T and illustrate the interactions of these parameters with the selection of TR and TE to achieve a given image contrast.
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Phantom Validation
The T1 and T2 relaxation time measurement techniques were validated using a
phantom of known relaxation times. Seven phantom components of known
relaxation times (Eurospin) were chosen to cover the expected range of
relaxation times in musculoskeletal tissue. Five separate T1 and T2 relaxation
time measurements were made at 1.5 and 3.0 T to determine the accuracy and
repeatability of the measurement techniques. The protocols and coils used for
the phantoms were the same as those used for the in vivo measurements.
T1 Relaxation Time Measurement Protocol
Images for the T1 measurements in our five volunteers were obtained using a
Look-Locker method [4]. Alpha
pulses of 10° were used to acquire eight images representing eight
equidistant samples along the T1 recovery curve. The sampling period was
tailored to provide sampling times with adequate coverage of the T1 recovery
curve for each tissue of interest (Table
1). Acquisitions with the inversion pulse are subtracted from
non–inversion recovery steady-state acquisitions, yielding an understood
asymptote of zero [5]. Because
the asymptote of the exponential is known, acquiring the last sample at a time
approximately equal to the T1 relaxation time of the tissue is sufficient. A
TR of 5,000 msec was selected to provide adequate longitudinal recovery.
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T2 Relaxation Time Measurement Protocol
Images for the T2 measurements in our five volunteers were obtained using a
T2 preparation sequence
[5–8].
The T2 preparation sequence consists of a 90° tip-down pulse, a train of
equally spaced 180° pulses, and a (–90°) tip-up pulse. Different
TEs are generated by varying the number of 180° pulses during the train of
180° pulses or by varying the space between those 180° pulses
(Table 1). Images were acquired
at six TEs with a TR of 3 sec.
Acquisition and Postprocessing
Both T1- and T2-weighted image sets were acquired using a spectral spatial
excitation with spiral readout consisting of 4,096 points and 8 arms. Other
imaging parameters included a field of view of 18 cm, slice thickness of 3 mm,
and 4 averages for T1-weighted and 2 averages for T2-weighted. In-plane
resolution was 0.5 mm. For fat and marrow measurements, the spectral spatial
excitation was centered on the lipid resonance. Using a custom software tool,
ROIs were placed on each tissue of interest and a monoexponential fit was
calculated for each ROI [9].
ROIs were placed in the patella cartilage, lateral gastrocnemius muscle,
femoral bone marrow, patellofemoral joint fluid, and medial subcutaneous fat;
ROIs in the fluid and cartilage were relatively small because of the smaller
volumes of tissue present. To preserve the integrity of the relaxation curve
fit, points below or near the noise floor were discarded. Relaxation times
were averaged across all subjects and the SDs of the measurements were
calculated. Values for p were calculated using a paired Student's
t test.
In Vivo Verification
Two of the original five volunteers were imaged at 1.5 and at 3.0 T to
verify T1 relaxation times of muscle and marrow fat. A spin-echo sequence was
used with a TE of 14 msec and TRs of 800, 2,000, 4,000, and 6,000 msec at 1.5
and 3.0 T. Pixel bandwidth was ± 16 kHz; field of view, 16 cm; and
matrix, 512 x 192. SNR values were measured from the images. Using the
MRI signal equation,
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One of the original five volunteers was imaged at both 1.5 and 3.0 T to verify SNR measurements and contrast-to-noise ratio (CNR) values. A sagittal proton density–weighted fast spin-echo sequence was used with a TR/minimum TE of 4,000/14. A coronal T1-weighted spin-echo sequence was used with a TR/minimum TE of 800/14. The imaging parameters were identical at each field strength. SNR was calculated as signal divided by the SD of the noise in each tissue in five locations. Significance of the SNR differences was determined using a paired Student's t test. CNR was calculated for cartilage and fluid at each TR for 1.5 and 3.0 T and compared.
Protocol Design Example
We used our relaxation time measurements to design a high-resolution
T2-weighted imaging protocol for 3.0 T. The goals of our 3.0-T protocol were
to achieve a higher spatial resolution than that achieved with 1.5 T with
comparable SNR of cartilage and muscle in a similar scanning time
(Table 2). Receiver bandwidth
was identical at both field strengths (± 16 kHz). Matrix size at both
field strengths was 512 x 192 to achieve a relatively high spatial
resolution with a total scanning time of less than 5 min.
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To increase resolution at 3.0 T, the TR was increased to account for increases in T1 relaxation times, the TE was slightly decreased to account for decreases in T2 relaxation times, and the slice thickness was decreased. In one 3.0-T protocol, the number of signal averages was decreased to keep imaging time constant, and in the other the echo-train length was increased. A T2-weighted protocol was chosen because it is part of most knee imaging protocols and, as a low-SNR sequence, it illustrates the SNR differences between 1.5 and 3.0 T.
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Our in vivo results show that T1 values increased when moving from 1.5 to 3.0 T (Table 3), and T2 values decreased slightly (Table 4). These results are statistically significant, as indicated by the calculated p values, and are consistent with results at other field strengths and using tissue samples [2, 3, 10]. The T2 relaxation time of synovial fluid decreased sharply from 1.5 to 3.0 T.
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To confirm the accuracy of the measured T1 relaxation times in vivo, we measured the signal levels of muscle and marrow fat in two volunteers using various TRs at 1.5 and 3.0 T (Figs. 3A, 3B and 4A, 4B, respectively). The signal levels predicted from the MR signal equation using the measured relaxation times compared well with measured signal levels in muscle and fat. Measured signal levels in cartilage and synovial fluid showed high variability, probably because of individual variation or partial volume effects.
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Using the measured relaxation times and values of the proton density from
the literature, we calculated the signal levels for various tissues at a fixed
TE (14 msec) versus TR (Figs.
5A and
5B). Signal levels were
divided by the square root of the TR to fix total scanning time and were
normalized to 1 for the maximum signal at 3.0 T. Values of proton density or
relative to water used for the calculated signal levels were taken from
the literature and were as follows: synovial fluid, 1.0
[11,
12]; marrow fat and
subcutaneous fat, 1.0 [13];
cartilage, 0.7 [3,
10]; and muscle, 0.6
[14–16].
Image contrast at a given TR is based on the signal difference between two
tissues.
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Knee images obtained at 1.5 and 3.0 T in a healthy volunteer show the changes in contrast indicated by our calculations (Figs. 6A, 6B, 6C, 6D and 7A, 7B). Measurements of the CNR show that the relative contrast between fluid and cartilage at a long TR of 4,000 msec is increased at 3.0 T compared with 1.5 T (CNR of 37.5 vs 16.2), which is predicted from the relaxation times. At a shorter TR of 800 msec, the cartilage-to-fluid CNR is also greater at 3.0 T than at 1.5 T (11.9 vs 4.8). SNR measurements also show the approximately twofold increase in SNR at 3.0 T, which accounts for much of the increase in contrast between fluid and cartilage at a long TR (Figs. 7A and 7B). The SNR gain was statistically significant for both a TR of 4,000 msec and a TR of 800 msec (p < 0.02), although generally less than twofold at a TR of 800 msec.
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Images from the 1.5 to 3.0 T comparison (Figs. 8A, 8B, 8C, and 8D) show that comparable SNR can be obtained at higher resolution at 3.0 T with a TE and TR that take the changes in relaxation times into account. The SNR of cartilage at 1.5 T with a slice thickness of 3.5 mm was 10.4, and at 3.0 T with a section thickness of 1.8 mm was 11.5. Using a section thickness of 2.2 mm at 3.0 T, the cartilage SNR was 15.7. Use of a thin section (1.8 mm) at 1.5 T resulted in a low cartilage SNR of 3.8. The muscle SNR at 3.0 T, using a section thickness of 1.8 mm, was more than twice the muscle SNR at 1.5 T (8.5 vs 3.0). The cartilage SNR was similarly increased at 3.0 T (11.5 vs 3.8), with more variability in the measurement. The greater-than-twofold increase here in SNR at 3.0 versus 1.5 T is caused by differences in the acquisition protocol and the increase in magnetization at 3.0 T.
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In our volunteers, measured T1 and T2 relaxation times were in the range of published values [2, 3, 10]. The sharp decrease of the measured T2 relaxation time for synovial fluid was also observed at 4 T [3]. The T2 relaxation times of fat and marrow are longer than the values reported by Duewell et al. [3] but similar to the values reported by Bottomley et al. [2]. Cartilage and synovial fluid relaxation times had relatively high SDs that may be the result of small ROIs, spatial or individual variations, or pathology [23–25]. Reported relaxation times in synovial fluid vary greatly [10–12].
We confirmed our measurements of T1 relaxation times by measuring signal levels in muscle and marrow fat in two volunteers. The predicted signal levels and the measured levels correlated well (Figs. 3A, 3B and 4A, 4B), indicating that our T1 relaxation times for these tissues are accurate in vivo. The results of this correlation with measured values in cartilage and synovial fluid are not as accurate, perhaps because of individual variability or small ROIs.
Image contrast at 3.0 T depends on the relaxation times of the various musculoskeletal tissues and the SNR gain. For example, cartilage and fluid have the same signal (zero contrast) at a TR of approximately 1,600 msec at 3.0 T, compared with a TR of approximately 1,200 msec at 1.5 T (Figs. 5A and 5B). This fact shows that contrast comparable to that of 1.5 T can be achieved with a longer TR at 3.0 T because of the increase in T1 relaxation times. The SNR gain at a short TR is also less than a factor of 2 because of the increase in T1 relaxation times, which was also found at 4.0 T [3]. Comparison of the maximum signal levels of fat at a short TR (Figs. 5A and 5B) shows that the signal increase at 3.0 T will be about 1.7 times that at 1.5 T. To achieve a similar image contrast to that at 1.5 T and maximize the SNR gain at 3.0 T, the TR should be longer for T1-weighted imaging at 3.0 T.
Image contrast between cartilage and fluid in proton density–weighted or T2-weighted imaging may be improved at 3.0 T. Contrast between cartilage and fluid is increased at 3.0 T (Figs. 5A and 5B), with the increase being greater at a longer TR because of the T1 recovery of the fluid. At a long TR, the twofold gain in SNR is achieved because of greater longitudinal relaxation. As with 4.0 T [3], we found no major qualitative differences in tissue contrast at 3.0 T compared with 1.5 T (Figs. 6A, 6B, 6C, and 6D). The impact of the decrease in T2 relaxation times at 3.0 T will be less significant for spin-echo imaging but may be more important for gradient echo imaging.
We did not measure relaxation times in ligaments and menisci. These tissues generally have short T2 relaxation times at 1.5 T [26] and have little signal on routine MRI sequences. With the shorter T2 relaxation times seen at 3.0 T, normal menisci and ligaments should have even less signal. Contrast between these tissues and synovial fluid will be important in the visualization of pathology at 3.0 T. On the basis of our results, contrast between fluid and tissues with little signal should be increased at 3.0 T compared with 1.5 T (Figs. 5A and 5B).
The resonance frequency at 3.0 T is twice that at 1.5 T, about 125 MHz, and the radiofrequency power for excitation at 3.0 T is four times higher than at 1.5 T [27, 28]. Because the radiofrequency power deposited is a function of tissue volume excited, radiofrequency power deposition is more a problem with large body areas (hips) than with smaller areas (knees) [28]. Radiofrequency power deposition was carefully monitored during our study. Pulse sequences that are particularly affected by increased radiofrequency power deposition are spin-echo sequences at a short TR (T1-weighted) or fast spin-echo sequences with multiple 180° refocusing pulses. For this reason, manufacturers have begun to offer the option of fast spin echo with refocusing pulses of less than 180° [29]. These sequences are less SNR-efficient than conventional fast spin echo but offer less power deposition.
Our study has three major limitations. First, we studied only healthy volunteers, so we do not have relaxation data on important pathology such as marrow edema. However, the imaging protocols designed for 3.0 T based on the relaxation measurements in our study have shown marrow edema in a few cases. Second, significant variation occurs in the T1 and T2 relaxation times of cartilage and synovial fluid in our data. However, the reported relaxation times of synovial fluid have considerable variability [10–12], and cartilage relaxation times are age-dependent [12, 23]. Finally, we studied only a limited number of subjects for our relaxation time measurements, in vivo verification of T1 measurements, and SNR measurements. However, the relaxation measurements we obtained are within expected ranges from prior studies at other field strengths [3] and show significant changes from 1.5 to 3.0 T. Our data give us the needed starting point to design musculoskeletal imaging protocols at 3.0 T.
Increased resolution may be helpful in several problem areas of musculoskeletal imaging [30]. On the basis of the measured changes in relaxation times, we designed two protocols for imaging at increased resolution at 3.0 T in the same imaging time as at 1.5 T (Table 2). In general, the principles behind the protocol design are as follows: First, decrease the TE to compensate for shorter T2 relaxation times; second, increase TR to compensate for longer T1 relaxation times; and third, decrease the number of signal averages or increases the echo-train length to keep the scanning time comparable. The images from these protocols (Figs. 8A, 8B, 8C, and 8D) show that the additional signal at 3.0 T allows the acquisition of more and thinner slices than 1.5 T at similar SNR and scanning times.
Similar principles will allow the use of the additional signal at 3.0 T to increase imaging speed compared with 1.5 T, while keeping SNR and spatial resolution equivalent. One way to improve imaging speed is to reduce signal averages. Because each additional signal average doubles the scanning time while providing an increase in SNR equal only to the square root of 2, the number of signal averages can be decreased by a factor of 2–4 at 3.0 T while maintaining comparable SNR to 1.5 T. In practice, other considerations, such as reducing phase wrap, may limit the reduction of signal averages. However, even with increasing the TR to account for T1 increases at 3.0 T, considerable saving in imaging time will be possible.
Relaxation times and contrast between normal tissues are not the only factors that go into designing a clinical MRI protocol. Other factors such as contrast resolution between abnormal tissues, the effect of artifacts, and clinical throughput are all critically important in everyday practice. Contrast between fluid and tissues such as menisci and ligaments should increase at 3.0 T, but this hypothesis needs to be proven clinically. Increased chemical shift artifacts on non–fat-saturated sequences may require the use of a higher receiver bandwidth at 3.0 T. The relaxation time measurements provided in this study give important information for designing clinical protocols at 3.0 T, but experience in the clinical setting is crucial to determine the best protocols for a given practice.
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| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
) and calculated (dotted
lines) signal levels in muscle (A) and marrow fat (B) were
normalized to 1 at TR of 6,000 msec. Note excellent agreement between
predicted and calculated values, indicating measured relaxation times are
accurate.
