Background: Radiation necrosis (RN) is a delayed and potentially debilitating complication of radiotherapy for central nervous system (CNS) tumors. It presents significant diagnostic and therapeutic challenges due to the variable clinical manifestations and overlap with tumor recurrence. Although advances in radiotherapy have improved tumor control, RN remains incompletely understood and inadequately addressed. This narrative review synthesizes current evidence on RN pathophysiology, risk factors, diagnostic strategies, and management approaches. Methods: A literature search was conducted for English-language literature published between January 1990 and December 2024. Studies were included if they addressed RN incidence, diagnosis, treatment, or novel preventive strategies in CNS tumor populations. Relevant findings were synthesized to produce a narrative review summarizing pathophysiology, diagnostic challenges, and treatment strategies. Results: RN results from radiation-induced neurovascular injury, inflammation, and vessel permeability, with incidence ranging from 3 to 26% depending on tumor type, location, and treatment parameters. Risk is influenced by dose, fractionation, cumulative exposure, re-irradiation, and adjuvant therapies. Advanced modalities such as SRS, HFSRT, brachytherapy, proton therapy, and IORT reduce but do not eliminate RN risk. Diagnosis remains challenging despite advanced MRI and PET techniques, with histopathology as the gold standard. Management includes corticosteroids, bevacizumab, surgery, LITT, and experimental therapies. Connectomics-based planning shows promise in minimizing RN by sparing critical brain networks. Conclusions: RN is a clinically significant and multifactorial complication of CNS radiotherapy. Precision treatment modalities and advanced imaging have improved prevention and detection, but diagnostic uncertainty and recurrence risk persist. Integration of connectomics into treatment planning may offer future promise of a reduction in RN-related morbidity by preserving structural and functional network integrity.

Background/Objectives: Cephalic-phase insulin responses (CPIRs) are characterized as the pre-absorptive release of insulin triggered by sensory stimuli associated with eating or drinking. CPIRs are beneficial because they reduce postprandial elevations in blood glucose. Methods: We investigated whether the flavor of two different types of laboratory chow elicits a CPIR in mice (C57BL/6). Results: First, we tried unsuccessfully to replicate a prior report that a single bite from a familiar chow pellet elicits a CPIR. Second, we determined that a minimum of 15 s of chewing on a familiar chow was necessary to elicit a CPIR. Third, we asked whether the chow-induced CPIR required prior exposure to the same chow. We tested the responses to a standard and a purified chow, which had similar macronutrient compositions. Mice raised on standard chow generated a CPIR to standard chow but not the novel purified chow. After 4 (but not 2) weeks of exposure to the purified chow, however, the mice generated a CPIR to it. Likewise, mice raised on purified chow generated a CPIR to purified chow but not to the novel standard chow. After 2–4 weeks of exposure to standard chow, however, the mice conditioned a CPIR to it. It follows that mice had to condition CPIRs to each type of chow. Fourth, we established that olfactory impairment eliminated the conditioned CPIR to standard chow (when it was familiar), but not to purified chow (when it was familiar). Conclusions: The flavor of familiar chow reliably triggered a CPIR in mice, but this response had to be conditioned through dietary exposure. Olfaction was a critical component of the conditioned stimulus for standard but not purified chow.