Diffusion-weighted MR imaging of the brain relies on different diffusion rates of water, or Brownian motion. Although it is primarily used for the diagnosis of acute infarction in the brain due to its ability to detect cytotoxic edema caused by water diffusion that changes due to cellular damage, it is also widely used in the evaluation of tumor pathology in the field of neuro-oncology (2). Specifically, DWI-derived ADC values have been shown to correlate with tumor cellularity, glioma grade, and treatment response(3).
Although the findings of restriction on DWI of the solid portion of brain metastases may be associated with their histology and tumor cellularity, these relationships continue to be systematically investigated. In studies, it was determined that the restriction in diffusion-weighted images predicted the histology of metastases and ADC values reflected the cellularity of the tumor(5). Studies have supported this finding by detecting lower ADC values in metastases of poorly differentiated cancers such as melanoma and small cell cancer(6). In addition, it has been thought in the literature that ADC values in the peritumoral region may be related to the infiltration pattern of metastases or the underlying vascular permeability(7).
Most metastases have a hyperintense signal on T2-weighted series. Studies have found T2 hypointensity in approximately 15% of metastases(8). T2 hypointensity was observed in 20.9% of metastases in our study.
In the literature, the hypointensity observed in brain metastases was thought to be due to the natural T2 effect due to calcium, mucin and iron(4) Egelhof et al. found that T2 hypointensity was statistically significantly higher in metastatic gastrointestinal adenocarcinomas, and they attributed this to intralesional mucin deposition(9). On the other hand, Carrier et al. did not find a significant relationship between the presence of mucin and T2 hypointense appearance in their study(10).
Contrary to the vasogenic edema that occurs due to infiltration in gliomas, both the cause and the survival of the accompanying vasogenic edema in metastasis cases remain unclear. Studies have suggested that vasogenic edema accompanying metastases is due to mass effect or inflammatory cytokines(11). In some studies, the theory that metastasis is due to direct infiltration has been studied, but living tumor cells could not be detected in the adjacent brain parenchyma(12). In the study of Berghoff et al.(13), autopsy brain specimens of patients with brain metastasis were examined for integrins and adhesion molecules to evaluate infiltration patterns, and diffuse vascular infiltration was detected only in 50% of the specimens.
In our retrospective study, we evaluated the relationship between T2 hypointensity, diffusion restriction, presence and amount of vasogenic edema in 292 metastatic brain lesions.
Unlike studies that evaluated perilesional edema independently of lesion size, we evaluated the size of edema by proportioning it to the size of the metastatic lesion in our study. We could not find any other study evaluating edema in this way in the English literature.
According to the results of our study, we found that the incidence of vasogenic edema and EMR rates were higher in patients in T2 hypointense metastases and metastases accompanied by diffusion restriction in MRI. We thought that this result of our study may be related to the hypercellularity of the metastatic lesions and pathogenesis may be common.