The post-operative realm for hepatic transplant patients presents many challenges, but of them all, we take a deeper dive into an increased risk of associated cerebrovascular events. Cerebrovascular diseases, such as cerebral arteriovenous malformation (AVM), are a leading cause of death following a liver transplant. We present a unique case of a liver transplant patient who presented with no brainstem reflexes three months into the post-transplant period. Imaging studies revealed a ruptured AVM within the foramen magnum and cervicomedullary junction, as well as substantial cerebral hemorrhage. While establishing the exact cause of the AVM is not as trivial as it may appear, side effects associated with post-transplantation management regimens and possible congenital factors do shed some light on notable considerations. Given the potential damage associated with ruptured AVMs, poor patient outcomes are unfortunately not as rare as one would hope. This case highlights a rare but highly possible occurrence for cerebrovascular complications, specifically AVM rupture linked to liver transplantation and the systemic changes associated with a procedure as invasive as liver transplantation.

BACKGROUND Pulsed low-dose-rate radiotherapy (pLDR) is an accepted reirradiation technique for recurrent glioma, but its upfront use, concurrent with temozolomide (TMZ) following resection of high-grade glioma is currently under investigation. Evaluating the response to upfront radiation can be challenging and there is limited data on expected rates of pseudoprogression with pLDR. Standard magnetic resonance imaging (MRI) has limitations in differentiating pseudoprogression from tumor progression, sometimes necessitating surgery for pathologic confirmation. Advanced MRI can be used to create fractional tumor burden (FTB) maps that spatially distinguish active tumor from treatment-related effect (pseudoprogression), perhaps providing a more reliable imaging biomarker in the absence of additional surgery. METHODS We performed a retrospective chart review to report the responses of four patients with glioblastoma to upfront pLDR and TMZ following resection. Each patient received advanced surveillance MRI and redo surgery. Tumor pathology included IDH-wild type (n = 4) and O6-methylguanine-DNA methyltransferase (MGMT) methylated (n = 1) tumors. RESULTS The median age of patients was 57.5 years (range 55-60 years) and all were male. One patient experienced mortality and another was transitioned to hospice. In all four cases, there were concerns of tumor progression in postcontrast MRI. Pathologic diagnosis revealed either treatment effect (n = 2) or tumor (n = 2). FTB maps were predominantly indicative of lesion volumes being comprised of treatment effect (n = 3) and tumor (n = 1). From the three FTB maps in the former category, the median fraction of the enhancing tumor volume comprised of vascular tumor was 6.4% (range 1.8-6.8%). CONCLUSION This case series provides insight into response to upfront pLDR and TMZ following resection of glioblastoma and demonstrates the capacity for FTB mapping to spatially distinguish tumor progression from treatment effect in this patient population.

BACKGROUND The response of cystic brain metastases (BMets) to radiotherapy is poorly understood, with conflicting results regarding local control (LC), overall survival (OS), and treatment-related toxicity. This study aims to examine the role of Gamma Knife (GK) in managing cystic BMets. METHODS Volumetric analysis was conducted to measure tumor and edema volume at the time of GK and follow-up MRI studies. We evaluated the association of 4 variables with survival using Cox regression analysis and used the Kaplan-Meier method to estimate median survival times (MST). RESULTS Between 2016 and 2021, 54 patients with 83 cystic BMets were treated with GK at our institution. Lung cancer was the most common pathology (51.9%), followed by breast (13.0%). The mean target volume was 2.7 cc (range, 0.1-39.0 cc) and the mean edema volume was 13.9 cc (range, 0-165.5 cc). The median prescription dose of single fraction and fractionated GK was 20 Gy (range, 14-27.5 Gy). With a median follow-up of 8.9 months, MST was 11.1 months, OS was 33.3%, and the one-year LC rate was 75.9%. GK was associated with decreased tumor and edema volumes over time, although 68.5% of patients required steroids post-GK. Patients whose tumors grew beyond baseline following GK received significantly more pre-GK whole-brain radiation therapy (WBRT) than those whose tumors declined following GK. Higher age at diagnosis of BMets and pre-GK systemic therapy were associated with worse survival, with an MST of 7.8 months in patients who received it compared to 23.3 months in those who did not. CONCLUSIONS Pre-GK WBRT may select for BMets with increased radioresistance. This study highlights the ability of GK to control cystic BMets with the cost of high post-treatment steroid use.