Background: Migraine, a prevalent neurovascular disorder, affects millions globally and is associated with significant morbidity. Emerging evidence suggests a crucial role of the gut microbiota and adipose tissue in the modulation of migraine pathophysiology, particularly through mechanisms involving neuroinflammation and metabolic regulation. Material and Methods: A narrative review of the literature from 2000 to 2024 was conducted using the PubMed database. Studies addressing the relationships between microbiota, adipose tissue, and migraine—including dietary interventions and their impact—were analyzed. Results: The findings highlight a bidirectional gut–brain axis, with gut microbiota influencing neuroinflammation via metabolites such as short-chain fatty acids (SCFAs). Obesity exacerbates migraine severity through chronic inflammation and the dysregulation of adipocytokines like leptin and adiponectin. Dietary patterns, such as low glycemic index diets and Mediterranean diets, and the use of prebiotics, probiotics, and postbiotics show potential in migraine management. Conclusions: This review underscores the need for integrative approaches targeting the microbiota–gut–brain axis and adipose tissue in migraine therapy. Future studies should explore longitudinal effects and personalized interventions to optimize outcomes.

Background: The diagnosis of hemodynamically significant patent ductus arteriosus (hsPDA) occurs in 55% of very low birth weight (VLBW) preterm infants. There is no agreement on the best approach to ensure a quick hsPDA closure. Drug treatment of hsPDA fails in approximately 20% of cases with an increasing risk of prolonged ventilation, BPD, and NEC, as well as the need for surgical duct ligation. This study aims to highlight the efficacy of ibuprofen versus acetaminophen in the case of a second cycle of medical therapy after the failure of the first pharmacological approach for hsPDA closure. Methods: Every VLBW infant admitted to our NICU and treated for hsPDA was included in our retrospective research. Information about the clinical course, hsPDA diagnosis and treatment, and common complications associated with preterm birth was collected. A comparison was made between patients treated with acetaminophen or ibuprofen to assess effectiveness in hsPDA closing. Results: A total of 286 VLBW infants were included. First-course ibuprofen was effective in 87 of 115 infants (75.7%) treated, acetaminophen in 138 of 171 (80.7%). Second-course therapy with ibuprofen was effective in 62.5% of the patients, while acetaminophen was effective in 69.2%. No statistically significant difference was observed in the first-course and second-course success rates. Conclusions: This study confirms that acetaminophen is not inferior to ibuprofen in the closure of hsPDA in VLBW infants. Our data demonstrate that a second course of medical therapy after the failure of the first course could help close the majority of hsPDA cases without surgery.

Background: Epilepsy is a complex neurological disorder in which growing evidence supports a significant role for the microbiota–gut–brain axis (MGBA) in modulating neuroinflammation, neuronal excitability, and treatment responsiveness. Beyond their traditional role in inducing ketosis, dietary therapies may influence epilepsy by modulating gut microbial ecology, intestinal barrier integrity, immune signaling, and microbiota-derived metabolites. Methods: This narrative review critically examines current clinical and experimental evidence regarding the relationship between epilepsy, gut microbiota, and dietary interventions. Particular attention was given to ketogenic dietary therapies, the Modified Atkins Diet (MAD), low-glycemic-index treatment (LGIT), Mediterranean dietary patterns, restrictive diets, and microbiota-targeted supplementation, including probiotics, prebiotics, and postbiotics. Results: Available evidence suggests that patients with epilepsy exhibit alterations in gut microbial composition associated with impaired short-chain fatty acid production, intestinal inflammation, and altered neuroimmune regulation. Ketogenic and microbiota-supportive dietary approaches may modulate these pathways beyond ketosis alone, potentially contributing to seizure reduction through integrated metabolic, inflammatory, and microbial mechanisms. Emerging evidence also supports a role for probiotics, prebiotics, and postbiotics in modulating gut–brain communication and neuroinflammatory signaling, although current clinical data remain limited. Conclusions: Dietary therapies in epilepsy should no longer be viewed exclusively as metabolic interventions aimed at inducing ketosis, but rather as potential modulators of the microbiota–gut–brain axis and neuroimmune homeostasis. While further mechanistic and clinical studies are needed, microbiota-targeted nutritional approaches may represent valuable complementary strategies to be integrated alongside conventional antiseizure therapies within more personalized models of epilepsy management.