Susceptibility-Weighted Imaging in Patients with Pyogenic Brain Abscesses at 1.5T: Characteristics of the Abscess Capsule

Discussion

There has been considerable discussion about the mechanisms underlying the MR signal intensity characteristics of the rim of abscesses.^{19⇓⇓–22} On nonenhanced T1-weighted images, the capsule may be isointense or slightly hyperintense, on T2-weighted images, hypointense compared with the necrotic core and the surrounding edema. The signal intensity properties of the abscess periphery on these conventional MR images were believed to be due to collagen, products of hemorrhages, or presence of free paramagnetic radicals in macrophages participating in phagocytosis, heterogeneously distributed on the abscess periphery.^{19⇓⇓–22} Successful surgical or therapeutic treatment of abscess leads to decrease of activity of macrophages and disappearance of the hypointense rim on T2-weighted images.

SWI is a high-resolution 3D gradient-echo sequence used to create new sources of contrast.^14,15 It may provide additional clinically important information that might be complementary to conventional MR imaging sequences. In some of our brain abscess cases, SWI phase images showing the hypointensity rim delineate the periphery of the lesion, suggesting an increased venous vasculature (paramagnetic deoxy-hemoglobin), blood products from hemorrhages, or presence of paramagnetic free radicals in these patients. While the 3 explanations stated herein are all in agreement with the negative phase values found in phase images, we think that the existence of free radicals is probably a more plausible hypothesis than the other 2 for the following reasons.

First, an increased venous vasculature in the abscess capsule would probably be accompanied by an increase in blood volume. In the experimental setting, brain abscesses have been shown to have relatively high amounts of mature collagen and decreased neovascularity.^22,23 During early capsule formation (day 10–13), increase of the layer of the fibroblasts with a rim of neovascularization at the periphery of the necrotic zone forms the abscess capsule. These newly formed capillaries lack tight junctions and leak proteinaceous fluid, suggesting that the postcontrast enhancement of the abscess capsules on T1-weighted images is probably due to increased permeability of the capillary wall rather than an increase in blood volume. Surrounding this is the beginning of a reactive astrocyte response, along with persistent white matter edema. In the late capsule stage (day 14 and later), the volume of the necrotic center and the number of inflammatory cells decrease. The capsule becomes thicker and consists of fibroblasts, reticulin, and collagen. More recently, some authors have reported the additional information given by MR perfusion imaging with rCBV maps to distinguish abscess from other ring enhancement lesions.^24,25 Findings from these articles suggest that the abscess rim seems to have lower rCBV values than high-grade tumor rim. The abscess collagen capsule, theoretically, is associated with low capillary attenuation and consecutively low rCBV values.^24,25 Although further studies are required to establish the perfusion role in brain abscess, up to the present time, no evidence on increased venous vasculature in the abscess capsule has been reported.

Second, hemorrhage often results in prominent hypointensity on the SWI phase images, which are heavily T2*-weighted in nature. In fact, in the original design of SWI, the lengthened TE and the phase mask multiplication are used intentionally for the purpose of enhancing hemorrhage that may not be visually conspicuous on conventional gradient-echo images.^14,15 In our patients, the abscess capsules on SWI phase images were isointense to mildly hypointense compared with the abscess cavity and the brain parenchyma, as opposed to being substantially hypointense, which would be expected in hemorrhage on gradient-echo T2*WI. Consequently, blood products from hemorrhage may not be largely present in the capsules, at least for our patients. These findings of the lack of hemorrhage in the abscess capsule are consistent with a prior report employing histologic evaluation.¹⁹ This leaves the paramagnetic free radicals¹⁹ as the most likely cause for the phase behavior of abscess capsule on SWI.

If the free radicals from phagocytosis were indeed responsible for the phase behavior of the abscess capsule on SWI, it would be interesting to further explore the possibility of a quantitative estimation of the free-radical concentration via SWI phase imaging. Because preliminary attempts on the use of SWI to quantify iron deposition in the human brain in vivo have been reported with initial success,^26⇓–28 the potential capability of SWI to measure free radical concentration for staging of cerebral abscess, or for monitoring of therapeutic effectiveness, should not be overlooked. At this stage, however, it is admittedly too early to extrapolate the potential of SWI based on the limited data presented in our study. Therefore, a suggestion of routine inclusion of SWI in clinical evaluation of abscesses would be made only after comprehensive prospective investigations covering a large range of bacterial infections at different stages.

One disadvantage of 3D SWI at 1.5T is the lengthy scan time. In addition, because blood vessels would change signals after contrast injection, whereas hemorrhage would not, hemorrhages can be easily distinguished from veins if SWI is performed both before and after administration of contrast agent,^14,15 increasing the total examination time even further. The issue of scan time in 3D SWI very likely may be overcome with the advent of a parallel acquisition technique and highly sensitive receiver coils. Compared with 1.5T, 3T SWI allows for optimal susceptibility effects at an increased speed, coverage, and signal intensity–to-noise ratio of MR images.^{13⇓⇓–15,29,30}

Our study has several limitations. First of all, we did not have the histopathological proof of the abscess wall in our cases, as this was a retrospective study for which not all data were available. In fact, once diagnosed as having an abscess, these patients underwent surgical aspiration of the pus for culture of the bacteria to choose the appropriate antibiotics for effective treatment. Surgical removal of the abscess capsule was not clinically indicated in any of these cases. As a result, the presence of free radicals in the capsule due to phagocytosis remains merely a hypothesis for which a firm proof would need to be explored in a prospective investigation. Nevertheless, we believe that the analysis, as shown in this article, could serve the purpose of idea stimulation for investigators who are interested in proceeding with further exploration in this direction. Second, a relatively small sample size of abscesses was noted in this study, for which the individual difference precludes comprehensive characterization of the abscess capsule. In particular, although the negative phase behavior observed for the abscess capsule was present in many of our patients on SWI phase images, the degrees of hypointensity varied to some extent, probably related to different stages of abscess formation or different properties of the infecting bacteria. Whether the SWI phase behavior could be used to help identify the infecting type or stage cannot be drawn from our results due to the current inclusion of only 1 or 2 cases in each bacterial species. Further studies with a larger number of brain abscesses should be performed to validate the phase quantification of the rim with SWI protocols.