Search Results (3)

Migraine is a prevalent and disabling neurological disorder with multifactorial origins and complex clinical manifestations. While pharmacologic therapies remain the cornerstone of management, a growing body of evidence highlights the role of extracranial peripheral nerve compression as a significant contributor to migraine pathophysiology in selected patients. This recognition has expanded the therapeutic role of plastic surgery, offering anatomically targeted interventions that complement or surpass traditional medical approaches for refractory cases. From a plastic surgeon’s perspective, optimal migraine care begins with accurate identification of clinical patterns, trigger-site mapping, and the judicious use of diagnostic tools such as nerve blocks and botulinum toxin. Surgical decompression techniques, including endoscopic and open approaches, address compression of the supraorbital, supratrochlear, zygomaticotemporal, greater and lesser occipital, auriculotemporal, and intranasal contact-point trigger sites. Adjunctive strategies such as autologous fat grafting further enhance outcomes by providing neuroprotective cushioning and modulating local inflammation through adipose-derived stem cell activity. Recent advances, including neuromodulation technologies, next-generation biologics, and innovations in surgical visualization, underscore the ongoing shift toward precision-based, mechanism-driven therapy. As understanding of migraine heterogeneity deepens, the integration of surgical expertise with modern neuroscience offers a comprehensive and personalized therapeutic framework. Plastic surgeons, equipped with detailed knowledge of peripheral nerve anatomy and minimally invasive techniques, play an increasingly pivotal role in the multidisciplinary management of refractory migraine. Full article

Tyramine (TRM) is a biogenic catecholamine neurotransmitter, which can trigger migraines and hypertension. TRM accumulated in foods is reduced and detected using additive cyclodextrins (CDs) while their association characteristics remain unclear. Here, single-crystal X-ray diffraction and density functional theory (DFT) calculation have been performed, demonstrating the elusive pseudopolymorphs in β-CD inclusion complexes with TRM base/HCl, β-CD·0.5TRM·7.6H₂O (1) and β-CD·TRM HCl·4H₂O (2) and the rare α-CD·0.5(TRM HCl)·10H₂O (3) exclusion complex. Both 1 and 2 share the common inclusion mode with similar TRM structures in the round and elliptical β-CD cavities, belong to the monoclinic space group P2₁, and have similar herringbone packing structures. Furthermore, 3 differs from 2, as the smaller twofold symmetry-related, round α-CD prefers an exclusion complex with the twofold disordered TRM–H⁺ sites. In the orthorhombic P2₁2₁2 lattice, α-CDs are packed in a channel-type structure, where the column-like cavity is occupied by disordered water sites. DFT results indicate that β-CD remains elliptical to suitably accommodate TRM, yielding an energetically favorable inclusion complex, which is significantly contributed by the β-CD deformation, and the inclusion complex of α-CD with the TRM aminoethyl side chain is also energetically favorable compared to the exclusion mode. This study suggests the CD implications for food safety and drug/bioactive formulation and delivery. Full article

Cortical spreading depolarization (CSD) is the neuronal correlate of migraine aura and the reliable consequence of acute brain injury. The role of CSD in triggering headaches that follow migraine aura and brain injury remains to be uncertain. We examined whether a single CSD occurring in awake animals modified the expression of proinflammatory cytokines (Il1b, TNF, and Il6) and endogenous mediators of nociception/neuroinflammation-pannexin 1 (Panx1) channel and calcitonin gene-related peptide (CGRP), transforming growth factor beta (TGFb) in the cortex. Unilateral microinjury of the somatosensory cortex triggering a single CSD was produced in awake Wistar rats. Three hours later, tissue samples from the lesioned cortex, intact ipsilesional cortex invaded by CSD, and homologous areas of the contralateral sham-treated cortex were harvested and analyzed using qPCR. Three hours post-injury, intact CSD-exposed cortexes increased TNF, Il1b, Panx1, and CGRP mRNA levels. The strongest upregulation of proinflammatory cytokines was observed at the injury site, while CGRP and Panx1 were upregulated more strongly in the intact cortexes invaded by CSD. A single CSD is sufficient to produce low-grade parenchymal neuroinflammation with simultaneous overexpression of Panx1 and CGRP. The CSD-induced molecular changes may contribute to pathogenic mechanisms of migraine pain and post-injury headache. Full article