Meningiomas are predominantly benign intracranial neoplasms, with extracranial distant metastasis occurring in fewer than 1% of all patients; pulmonary metastasis represents an exceedingly rare complication of meningioma progression and recurrence. We describe a 44-year-old male patient with sequentially recurrent intracranial meningioma exhibiting dynamic histopathological grade evolution combined with synchronous bilateral pulmonary metastatic lesions, followed for an unprecedented 18 clinical years. Across follow-up, the patient received four open craniotomies, two sessions of stereotactic Gamma Knife radiosurgery, a CT-guided percutaneous lung biopsy, and minimally invasive pulmonary radiofrequency ablation. Post-intervention serial neurological and radiological monitoring documented favorable functional recovery: final Glasgow Coma Scale (GCS) = 15 and Modified Rankin Scale (mRS) = 1 at latest follow-up, with complete resolution of initial left lower limb weakness and stable control of both intracranial residual sinus-associated tumor and all pulmonary metastatic nodules without newly emerging systemic metastasis. This long-duration real-world clinical cohort highlights the critical necessity of full-body systemic imaging screening and lifelong standardized periodic surveillance for meningiomas with superior sagittal sinus invasion and progressive pathological upgrading, to facilitate early identification of occult distant pulmonary metastasis and formulate individualized combined surgical-radiation-ablation treatment regimens for high-risk recurrent meningioma.

BACKGROUND The central nervous system (CNS) is a rare site for upper tract urothelial carcinoma (UTUC) metastasis and typically carries a poor prognosis. Little is known about effective treatments. This report describes a 64-year-old man with UTUC with brain and leptomeningeal metastases. He was treated with multiple lines of chemotherapy, immunotherapy, surgery, radiation, and intrathecal methotrexate as part of multimodal therapy delivered through multidisciplinary care. CASE REPORT A 64-year-old man with multiple sclerosis was diagnosed with UTUC. Initial management included a nephroureterectomy followed by platinum-based chemotherapy. Despite this treatment, his malignancy recurred with pulmonary metastases, treated with enfortumab vedotin and local ablation. After this treatment, he achieved systemic disease control. However, he later presented with neurologic symptoms, and imaging showed brain metastases. He underwent resection followed by stereotactic radiation therapy and immunotherapy. Even with this multimodal treatment, he developed leptomeningeal spread, evidenced by cytology-positive cerebrospinal fluid (CSF). Following progression on multiple systemic therapies, he received intrathecal methotrexate with temporary clearance of tumor cells from his CSF before disease progression. This treatment course, including chemotherapy, immunotherapy, and intrathecal methotrexate, prolonged the patient's life before he unfortunately died from his disease. CONCLUSIONS This case report outlines a treatment approach for a rare complication of UTUC. This regimen includes both standard-of-care therapy and inventive strategies extrapolated from data on other solid tumors. Additionally, it contributes to the limited data on the management of CNS metastasis in rare solid tumor malignancies, which could inform future clinical decision-making.

Brain metastasis (BM) represents a severe and common complication of advanced lung cancer, which is clinically categorized into brain parenchymal metastasis (BPM) and leptomeningeal metastasis (LM), with LM being the predominant subtype of meningeal involvement. In clinical practice, the concurrent occurrence of both parenchymal brain and leptomeningeal metastases in a single patient remains rare. Here, we report a case of an epidermal growth factor receptor (EGFR)-mutant NSCLC patient with simultaneous BPM and LM, along with a review of current research progress on the treatment of BM. The patient had previously undergone surgery and targeted therapy, and subsequently developed bone metastases, LM and BPM. After receiving ventriculoperitoneal shunting, intrathecal chemotherapy via an Ommaya reservoir, and resection of the brain metastatic lesion, the patient's condition was effectively controlled. This case suggests that some EGFR-mutant NSCLC patients may still experience CNS progression during EGFR-tyrosine kinase inhibitor (TKI) therapy. Moreover, local therapy (surgery) combined with intrathecal chemotherapy may improve quality of life and prolong survival, thus representing a feasible treatment option.

Brain metastases have traditionally been investigated primarily with regard to interactions between tumor cells, the surrounding brain microenvironment, and associated inflammatory responses. By contrast, the presence of a true intratumoral stromal compartment in brain metastases has received much less attention, partly because the normal brain parenchyma lacks classical interstitial fibroblasts. However, recent histological, transcriptomic, and spatial studies suggest that at least a subset of carcinoma brain metastases contains fibroblast-like or cancer-associated fibroblast-like cells associated with collagen-rich extracellular matrix deposition. This raises a fundamental biological question: where do these cells come from? In this review, we discuss seven non-mutually exclusive hypotheses for the origin of cancer-associated fibroblast (CAF)-like cells in brain metastases, including pseudostromal mimics, meningeal or perivascular fibroblast-related cells, vascular mural cells, glial cells, cancer stem cell plasticity, tumor-stroma clusters, and circulating mesenchymal precursors. We compare the current findings for each hypothesis and highlight their major limitations. Overall, the available data support a heterogeneous and context-dependent model rather than a single universal origin. A better understanding of these stromal cell states may help refine the biological classification of brain metastases and support the future development of more targeted stromal therapies.

Dural-based lymphomas are rare extranodal non-Hodgkin lymphomas that span from indolent primary dural entities, most commonly the extranodal marginal zone (mucosa-associated lymphoid tissue) lymphoma, to aggressive variants that are primary or represent secondary involvement from systemic lymphoma. They overlap radiologically with benign meningiomas, dural metastases, and immune-mediated pachymeningitis, creating a risk of anchoring bias, delayed diagnosis, and unnecessarily extensive resections when limited tissue sampling would be sufficient for diagnosis. We conducted a structured narrative review to synthesize the epidemiology, clinico-pathological classification, imaging phenotypes, and management principles of dural lymphomatous disease. This study will especially focus on primary dural lymphoma (PDL) with additional discussion of secondary dural involvement. Emphasis is placed on the clinical value of a multiparametric diagnostic approach that integrates computed tomography contrast-enhanced magnetic resonance imaging with functional techniques, and fluorodeoxyglucose positron emission tomography/computed tomography for systemic staging and for distinguishing truly localized primary dural lymphoma from secondary involvement. Potential diagnostic pitfalls related to somatostatin receptor-based tracer uptake will also be discussed. We introduced a pragmatic operational framework based on four clinico-biological clusters, translated into a step-by-step decision algorithm that prioritizes timely biopsy and comprehensive hematologic staging to guide surgical strategy. Given the absence of dedicated, multidisciplinary guidance for dural-based lymphomas, this algorithm is intended as a reproducible foundation for consensus recommendations and future multicenter validation.

Intracranial germinomas are exquisitely radiosensitive, and a tissue diagnosis obtained by minimal biopsy followed by radiotherapy (with or without chemotherapy) provides excellent long-term control; aggressive resection adds morbidity without oncological benefit. We report a 20-year-old man whose sellar and suprasellar mass was preoperatively interpreted as a pituitary adenoma and was treated by aggressive endoscopic endonasal transsphenoidal resection after an intraoperative frozen section suggested adenoma; final histology demonstrated germinoma. The postoperative course was complicated by a persistent skull-base cerebrospinal fluid (CSF) leak, methicillin-resistant Staphylococcus aureus meningitis/ventriculitis, and CSF dissemination documented by repeatedly positive CSF cytology and elevated CSF β-human chorionic gonadotropin. The initial skull-base reconstruction failed, and the resulting persistent CSF rhinorrhea required revision dural repair on postoperative day (POD) 29; proton craniospinal irradiation was delivered from POD 52. The patient achieved remission but, approximately 21 months after completing radiotherapy, developed a destructive germinoma lesion in the midline maxilla, with no recurrence at the primary site and no leptomeningeal disease at that time. In light of the anterior maxillary location and the relatively long interval after radiotherapy, we interpret the lesion as an isolated extracranial metastasis rather than a proven operative-tract event. The principal lesson is that accurate initial diagnosis and approach selection-measurement of tumor markers and minimal or transventricular biopsy in preference to resection-remain essential in young patients with sellar/suprasellar masses in whom germinoma is a diagnostic possibility.

Background Myeloid sarcoma, also called granulocytic sarcoma, extramedullary myeloid tumor, or chloroma, is a manifestation of a myeloid neoplasm. These tumors can develop in various anatomical sites, including the central nervous system, presenting as an extra-axial tumor affecting the meninges or the ependyma. Diagnosis is challenging due to its resemblance to other intracranial tumors such as meningiomas. Case Description We present the case of a 17-year-old male with intermittent left frontotemporal headache, diplopia during horizontal gaze, and proptosis of the left eye. During the imaging evaluation, an extra-axial tumor was observed, suggesting a meningothelial lesion of the left sphenoid wing. The patient had no previous hematological disease. Tumor resection was performed using an orbitozygomatic approach. After 2 months, the patient had recurrence of the lesion associated with spontaneous epistaxis and leucocytosis and thrombocytopenia. Bone marrow aspirate biopsy and histopathology results were consistent with myeloid sarcoma. Conclusion Intracranial myeloid sarcomas mimic meningiomas, metastases, lymphomas, and even Ewing's sarcoma, making it difficult to suspect myeloid sarcoma in a patient without prior hematologic disease. Surgery aids in diagnosis through biopsy or reduces the volume effect that could cause neurological deficit.

3D contrast-enhanced T1W black-blood imaging has become the standard for vessel wall imaging in vasculitis and shows high sensitivity for detecting brain and meningeal lesions. While primarily designed for intracranial assessment, 3D black-blood's high anatomical detail and high contrast-to-noise ratio also facilitates extracranial pathology detection on brain MRI. This pictorial review highlights the added diagnostic value of 3D contrast-enhanced black-blood MRI beyond the intracranial compartment. The first section reviews key technical principles of black-blood imaging, including sequence design, contrast mechanisms, and comparison with conventional contrast-enhanced T1W techniques. The second section outlines expected and unexpected extracranial findings detectable with this technique. The final section illustrates these concepts through representative cases. Particular attention is given to orbital pathology (optic neuropathies, thyroid eye disease, tumors), ear-nose-throat disorders (mastoiditis, sinusitis, salivary gland disease, perineural tumor spread), and musculoskeletal abnormalities of the head and neck (synovitis and subtle bone marrow changes relevant for inflammatory diseases and bone metastases). The review concludes by encouraging broader use of 3D contrast-enhanced black-blood MRI in clinical brain protocols, as the technique allows detection of relevant extracranial pathology in addition to its established intracranial applications.

The central nervous system (CNS) is surrounded by specialized immune interfaces, including the meninges and the olfactory bulb, which can serve both as permissive routes for metastatic colonization and as entry points for anti-tumor immune responses. Understanding how immune cell dynamics evolve within these structures during metastatic progression is essential for identifying mechanisms that either support or restrict tumor growth in the brain. This protocol details the establishment of a breast cancer brain metastases (BCBM) mouse model through intracranial injection of E0771 breast cancer cells into C57BL/6 mice. After tumor development, the meninges and olfactory bulb are carefully dissected, enzymatically digested, and processed into single-cell suspensions. These populations are then analyzed using multiparametric spectral flow cytometry to comprehensively characterize lymphoid, myeloid, and stromal cell subsets within CNS-associated immune niches. This workflow enables comparative analyses between tumor-bearing and non-tumor controls, identifying alterations within CNS immune interfaces that may underlie tumor immune evasion and represent potential therapeutic targets. Overall, the protocol provides a reproducible approach to study BCBM and interrogate immune regulation at CNS-peripheral immune system interfaces. It can be adapted for additional cancer cell lines, immunotherapies, or genetic mouse models to investigate immune resistance mechanisms and therapeutic response within the brain microenvironment.

Leptomeningeal metastasis (LM) is a life-threatening complication of lung cancer for which magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) cytology may miss disease and provide limited molecular guidance. Because the low cfDNA input typical of CSF constrains deep sequencing and mutation-focused approaches may underrepresent the copy-number-rich genomic architecture of CNS metastases, we developed a low-input shallow whole-genome sequencing approach to quantify genome-wide copy-number changes from trace CSF cfDNA. In 57 patients with lung cancer and CNS metastases (28 with LM and 29 with brain metastasis only), CSF showed stronger tumor-DNA signals and a higher burden of genome amplification than matched plasma (54 pairs), despite lower cfDNA concentrations. Among samples with detectable tumor DNA, genome amplification proportion (GAP), defined as the fraction of the genome showing amplification, identified LM with 86% sensitivity and no false positives observed in this cohort, and showed performance comparable to cytology as a complementary quantitative readout. Copy-number profiling further highlighted chromosomal regions and focal gene amplifications enriched within LM, supporting a CNV-enriched molecular state in the CSF compartment. Serial CSF sampling also captured treatment-associated molecular shifts, including progressive TYMS amplification during intrathecal pemetrexed in an exploratory case. Together, these findings support low-input CSF sequencing as a practical molecular approach to complement LM diagnosis and longitudinal monitoring in lung cancer and provide a rationale for prospective validation in independent multi-center cohorts.