Fournier syndrome, also known as Fournier gangrene, is a rare and potentially fatal disease that affects the soft tissues of the genital and perineal region. It is usually caused by a serious bacterial infection, often from a nearby source such as the urinary tract, intestines or skin. This bacterial infection spreads rapidly through the subcutaneous tissue, resulting in inflammation, necrosis (tissue death), and possible sepsis (generalized infection). The objective of this article was to understand the surgical procedures performed on patients with this syndrome and to understand how the process of reconstruction and repair of these conditions occurs. After surgery to treat Fournier syndrome, patients can experience a number of post-operative benefits. This includes removing the infection, relieving symptoms such as pain and swelling, preventing serious complications such as sepsis, promoting proper tissue healing, and improving overall quality of life. Successful recovery from surgery is critical to ensuring these benefits and allowing patients to resume their daily activities. A síndrome de Fournier, também conhecida como gangrena de Fournier, é uma doença rara e potencialmente fatal que afeta os tecidos moles da região genital e perineal. Geralmente é causada por uma infecção bacteriana grave, muitas vezes proveniente de uma fonte próxima, como o trato urinário, intestinos ou pele. Esta infecção bacteriana se espalha rapidamente pelo tecido subcutâneo, resultando em inflamação, necrose (morte do tecido) e possível sepse (infecção generalizada). O objetivo deste artigo foi compreender os procedimentos cirúrgicos realizados em pacientes com essa síndrome e entender como ocorre o processo de reconstrução e reparação dessas condições. Após a cirurgia para tratar a síndrome de Fournier, os pacientes podem experimentar uma série de benefícios pós-operatórios. Isso inclui a remoção da infecção, alívio dos sintomas como dor e inchaço, prevenção de complicações graves como sepse, promoção da cicatrização adequada dos tecidos e melhoria geral da qualidade de vida. A recuperação bem-sucedida da cirurgia é fundamental para garantir esses benefícios e permitir que os pacientes retomem suas atividades diárias.

Background/Objectives: Fibromyalgia (FM) is a nociplastic pain syndrome characterized by chronic widespread pain, fatigue, sleep disturbance, cognitive dysfunction, and heightened sensitivity to somatic and environmental stimuli. Depressive symptoms and major depressive disorder (MDD) frequently co-occur with FM and are associated with greater disability, pain catastrophizing, sleep disruption, and poorer treatment response. Although pharmacological treatments can reduce symptoms in some patients, many individuals experience persistent functional and affective burden, highlighting the need for mechanism-based adjunctive strategies. Mindfulness-based interventions (MBIs), particularly mindfulness-based stress reduction (MBSR), have shown promise for improving functional impact, pain catastrophizing, perceived stress, depressive symptoms, sleep-related burden, and quality of life in FM. However, the effects of MBIs on pain intensity and biomarkers are less consistent. Methods: This narrative mechanistic review develops a hypothesis-generating multisystem neurobehavioral framework to explain how MBIs may influence pain–mood coupling in FM with depressive symptom burden. We define pain–mood recalibration as a reduction in the extent to which pain intensity, bodily vigilance, and interoceptive threat appraisal automatically drive depressive symptoms, rumination, avoidance, and functional disengagement. Results: Fibromyalgia-specific evidence most strongly supports cognitive–emotional mechanisms, including reduced catastrophizing, psychological inflexibility, rumination, perceived stress, and avoidance. Interoceptive, neural-network, autonomic, immune-inflammatory, and sleep-fatigue-behavioral pathways remain exploratory and require prospective mediation and moderation testing. Conclusions: Future trials should prioritize active controls, ecological momentary assessment, longitudinal biomarkers, neuroimaging, interoceptive tasks, and formal mediation/moderation models to determine which patients benefit, through which mechanisms, and under what biological and psychological conditions.

Background/Objectives: Gabapentin is a first-line treatment for neuropathic pain, classically understood to reduce neuronal excitability through binding to the alpha-2-delta-1 (α2δ-1) subunit of voltage-gated calcium channels. However, this neuron-centric model does not fully explain its variable clinical efficacy across pain syndromes. In parallel, chronic pain is increasingly conceptualized as involving neuron–glia–immune interactions, in which microglial activation, astrocytic signaling, and inflammatory mediators may contribute to central sensitization. Methods: A structured narrative review was conducted using PubMed, Web of Science, and Google Scholar for articles available through December 2025. The search focused on gabapentin/gabapentinoids, chronic and neuropathic pain, α2δ-1 mechanisms, neuron–glia interactions, neuroinflammation, central and peripheral sensitization, nociplastic pain, cytokine/chemokine signaling, and neuroimmune modulation. Basic science studies, animal models, translational studies, clinical trials, reviews, meta-analyses, and guidelines were narratively synthesized. Results: Preclinical evidence indicates that gabapentin reduces neuronal hyperexcitability and may secondarily attenuate neuron-to-glia signaling, glial activation, and cytokine- and chemokine-related pathways. However, these neuroimmune effects remain predominantly preclinical, model-dependent, and incompletely validated in humans. Clinical evidence supports gabapentin for selected neuropathic pain conditions, but human studies rarely evaluate glial activation, cytokine signaling, or neuroimmune biomarkers. Conclusions: Gabapentin remains best understood as a neuronal α2δ-1 modulator. Although preclinical and translational evidence suggests biologically plausible secondary effects on neuroimmune signaling, these mechanisms have not been validated as biomarkers or prescribing targets in humans. The conceptual framework presented in this review supports mechanism-informed clinical reasoning and individualized pain management but should not be interpreted as a biomarker-guided prescribing algorithm. Clinically, gabapentin should be prescribed selectively for patients with neuropathic or sensitized pain features, using predefined functional goals, appropriate renal dose adjustment, careful safety monitoring, and discontinuation when meaningful benefit is not achieved.