Purpose Prior reports on the location and sizes of brain metastases almost entirely focus on patients with primary breast and pulmonary cancer. This is the first study comparing multiple other types of cancer that metastasize to the brain. Methods This monocentric retrospective study includes 369 untreated patients with 3313 intraaxial brain metastases. Following semi-manual segmentation of metastases on post-contrast T1WI, cumulative spatial probability distribution maps of brain metastases were created for the whole group and for all primary tumors. Furthermore, mixed effects logistic regression model analysis was performed to determine if the primary tumor, patient age, and patient sex influence lesion location. Results The cerebellum as location of brain metastases was proportionally overrepresented. Breast and pulmonary cancer caused higher number of brain metastases to what would normally be expected. Multivariate analyses revealed a significant accumulation of brain metastases from skin cancer in a frontal and from breast and gastrointestinal cancer in a cerebellar location. Conclusion Distribution of brain metastases is very heterogeneous for the distinct primaries, possibly reflecting the diversity of mechanisms involved in brain metastases formation. In daily clinical practice distribution patters may be beneficial to predict the primary cancer site, if unknown.

Background and Purpose: To date, imaging studies quantifying the amount of vasogenic edema reduction (VE) in patients with brain metastases (BM) treated with glucocorticoids (GC) have included a very limited number of patients and showed ambiguous results. Here, we aim to determine the radiological effect of GC on VE in BM patients in a large cohort with multiple primary tumor entities in a cross-sectional approach. Materials and Methods: This monocentric retrospective study includes 299 patients first-ever diagnosed with 2,759 intra-axial BM on the respective MRI. 126/299 patients received GC prior to MRI due to mass effect of edema on cranial CT scan and clinical symptoms (GC-pos) and 173 patients did not (GC-neg). GC dose was documented in 85/126 patients. All BM and their respective VE were semi-automatically segmented on post-contrast T1-weighted images. Results: VE volumes were higher in GC-pos compared to GC-neg ( p = 0.009) and did not correlate with GC dose. Multivariate linear regression analysis with interaction terms on the assumption that BM volume and BM number influence the probability of GC administration shows that large and higher numbers of BM under GC treatment generate less VE than without ( p < 0.001 and p = 0.038, respectively). The primary tumor type and total BM volume did not influence VE volume. Conclusion: Use of GC is especially effective for treatment of VE formation in patients with larger and multiple BM regardless of primary tumor type and dosage. However, based on the present data a direct causative relationship between GC and VE cannot be proven.

No prior systematic study on the extent of vasogenic edema (VE) in patients with brain metastases (BM) exists. Here, we aim to determine 1) the general volumetric relationship between BM and VE, 2) a threshold diameter above which a BM shows VE, and 3) the influence of the primary tumor and location of the BM in order to improve diagnostic processes and understanding of edema formation. This single center, retrospective study includes 173 untreated patients with histologically proven BM. Semi-manual segmentation of 1416 BM on contrast-enhanced T1-weighted images and of 865 VE on fluid-attenuated inversion recovery/T2-weighted images was conducted. Statistical analyses were performed using a paired-samples t-test, linear regression/generalized mixed-effects model, and receiver-operating characteristic (ROC) curve controlling for the possible effect of non-uniformly distributed metastases among patients. For BM with non-confluent edema (n = 545), there was a statistically significant positive correlation between the volumes of the BM and the VE (P < 0.001). The optimal threshold for edema formation was a diameter of 9.4 mm for all BM. The primary tumors as interaction term in multivariate analysis had a significant influence on VE formation whereas location had not. Hence VE development is dependent on the volume of the underlying BM and the site of the primary neoplasm, but not from the location of the BM.