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Cerebral edema is the abnormal accumulation of fluid in any of the tissue compartments of the cerebral parenchyma. It remains a significant challenge in neurotrauma care because it contributes to secondary brain injury, affecting prognosis. This review analyzes the recent literature, including foundational studies, to describe the mechanisms of distinct types of cerebral edema following traumatic brain injury (TBI). Emerging concepts, such as the role of the glymphatic system and heme-derived inflammasomes, offer new insights into new types of edemas, differentiated by pathogenesis and potential treatments. Recent advancements in understanding these molecular mechanisms can improve therapeutic strategies, facilitating a better approach in the era of precision and personalized medicine.

Brain metastases are a major clinical concern in metastatic breast cancer, particularly in HER2-positive and triple-negative disease. Over time, approximately 25% to 50% of patients with these subtypes develop brain metastases, which can lead to neurological disability, cognitive impairment, reduced independence, and substantial deterioration in quality of life.

Despite this risk, routine brain imaging is not consistently recommended for patients without neurological symptoms.

An article published in The Breast argues that it may be time to reconsider this symptom-directed approach. Sarah Sammons, Nayan Lamba, and Nancy U. Lin outline a growing case for brain MRI screening in selected patients with metastatic breast cancer, while also acknowledging that survival benefit, optimal timing, cost-effectiveness, and potential harms remain uncertain.

Cerebral edema is the abnormal accumulation of fluid in any of the tissue compartments of the cerebral parenchyma. It remains a significant challenge in neurotrauma care because it contributes to secondary brain injury, affecting prognosis. This review analyzes the recent literature, including foundational studies, to describe the mechanisms of distinct types of cerebral edema following traumatic brain injury (TBI). Emerging concepts, such as the role of the glymphatic system and heme-derived inflammasomes, offer new insights into new types of edemas, differentiated by pathogenesis and potential treatments. Recent advancements in understanding these molecular mechanisms can improve therapeutic strategies, facilitating a better approach in the era of precision and personalized medicine. Although there has been notable progress, a proposal to customize treatments for diverse types of edemas is necessary to improve outcomes following traumatic brain injury. In this review, we describe the current subtypes of post-traumatic brain edemas and link them to a specific management approach.

As patients live longer with advanced cancer, brain metastases are now becoming a frequent and even chronic condition managed with a variety of systemic agents and local treatments.¹ Radiotherapy plays a key role in treatment of intracranial lesions. Whole brain radiation therapy (WBRT) has the benefit of treating both imaging-apparent and microscopic disease. This approach can offer general intracranial disease control, but can damage healthy brain tissue, resulting in neurocognitive impairment associated with irradiation of the hippocampus.² The innovation of hippocampal-avoidance WBRT (HA-WBRT) maintains global intracranial disease control while reducing neurocognitive decline relative to traditional WBRT, even in the setting of the neuroprotectant memantine (0.74; 95% CI, 0.58−0.95; P = .02), making HA-WBRT a standard-of-care approach to appropriate patients.^3-5 Nevertheless, HA-WBRT requires several weeks of daily treatments and often time off systemic therapy. Conversely, stereotactic radiation (SRT) is given over 1 to 3 treatments to the visible lesions, allowing for higher radiation dose, better focal disease control, and sparing of healthy brain tissue, which further reduces neurocognitive toxic effects. SRT is appropriate for patients with a finite number of visible lesions but may allow microscopic disease elsewhere in the brain to progress, necessitating subsequent treatments or even salvage WBRT. In addition, the higher dose of SRT can cause radiation necrosis and inflammation, requiring steroids or other medical and surgical interventions.⁴ The optimal balance of intracranial disease control with patient-reported outcomes (PROs) is of increasing importance as patients live longer with the subacute and chronic toxic effects of radiotherapy.

To find that balance, multiple randomized clinical trials have confirmed that SRT offers improved efficacy and PROs compared with WBRT in patients with 1 to 4 brain metastases.^{2, 6-9} However, with advances in systemic therapy and surveillance, patients now frequently present with multiple brain metastases, high performance status, and expected survival of months to years. Without any high-level evidence comparing the efficacy and toxic effects of HA-WBRT with SRT in patients with 5 or more brain metastases, radiation oncologists have been left to make recommendations between each modality on a case-by-case basis. Shared decision-making attempts to account for lesion number, velocity, distribution, size, histologic findings, symptomatology, available systemic therapeutics with central nervous system penetrance, treatment goals, and tolerance for cognitive decline.