Chronic pain is increasingly regarded as a condition of glia–neuronal dysregulation driven by persistent neuroinflammatory signaling. Following injury to nerves or tissues, glial cells, including astrocytes or satellite glial cells, undergo changes in their phenotype, thereby amplifying painful stimuli mediated by cytokines, chemokines, or ATP signaling. In response to injuries, activated microglia release several mediators such as BDNF, IL-1β, or TNF-α, thereby disrupting chloride homeostasis and inducing disinhibition in the dorsal horn, and sustaining maladaptive neuroimmune activity. Dysfunction of astrocytes, characterized by impaired glutamate clearance via excitatory amino acid transporter 2 and elevated C-X-C motif chemokine ligand 1 (CXCL1) and ATP release, drives neuronal sensitization, loss of neuroprotective metabolic support, and persistence of pain. In peripheral ganglia, connexin–43–mediated satellite glial cell coupling leads to hyperexcitability, resulting in neuropathic and orofacial pain and contributing to peripheral neuroinflammation. Presently, there is no unified framework for glial cell types, and the molecular mechanisms underlying microglial, astrocyte, and satellite glial cell contributions to the transition to chronic pain from acute pain are not completely elucidated. This review synthesizes current evidence on cellular and molecular mechanisms linking glial reactivity to pain chronification through sustained neuroinflammatory remodeling and impaired neuroprotection. It evaluates therapeutic strategies, including purinergic receptor P2X4 and toll-like receptor 4 antagonists, to metabolic reprogramming, exosome therapy, and neuromodulation, aimed at restoring homeostatic glial function and re-establishing neuroprotective glia–neuron interactions. A deeper understanding of the temporal and spatial dynamics of glial activation may enable personalized, non-opioid interventions that not only achieve durable analgesia but also prevent progressive neuroinflammatory damage and support long-term functional recovery.

Takotsubo syndrome (TTS) is an acute condition involving left ventricular dysfunction that may present clinically as acute coronary syndrome without obstructive coronary disease or congestive heart failure. Initially considered benign, TTS is now recognized as a complex neurocardiac disorder with hospital morbidity rates comparable to those of myocardial infarction, as well as similar long-term risks. Recent evidence establishes TTS as a multifactorial process involving catecholamine overload, coronary microvascular dysfunction, myocardial energetic abnormalities, and dysregulation of the brain and heart axes. Developments in echocardiography, cardiac magnetic resonance imaging, and improvements in diagnostic criteria have enhanced the recognition of syndromic phenotypes. Management of TTS continues to remain primarily supportive; however, recent studies have revealed improved functional outcomes with structured cardiac rehabilitation and cognitive behavioral therapies as the first long-term disease-altering approaches. Future studies should combine neurocardiology, imaging, and therapy-focused research. This review integrates the understanding of the epidemiology, pathophysiology, clinical features, diagnostic work-up, and management of TTS, with particular emphasis on developments emerging from the past decade.

Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) characterized by distinctive chronic cutaneous manifestations. Although immune-mediated and microvascular mechanisms are well established, the role of metabolic dysfunction, particularly hyperglycemia, is underexplored in dermatological conditions. This review synthesizes mechanistic, clinical, and translational evidence to explore the relationship between dysglycemia and cutaneous disease severity in DM. Hyperglycemia is associated with oxidative stress, advanced glycation end-product formation, endothelial injury, and proinflammatory cytokine signaling. These processes may plausibly amplify DM-associated vasculopathy, impair wound healing, and worsen cutaneous inflammation. Limited DM-specific studies demonstrate increased insulin resistance and a higher prevalence of diabetes compared with healthy controls. Meanwhile, case reports suggest that poor glycemic control can exacerbate cutaneous disease. Evidence from other inflammatory dermatoses supports a biologically plausible role for dysglycemia in increasing flare frequency, infection risk, and delayed tissue repair. Dietary patterns characterized by high glycemic index and coexisting metabolic syndrome may further intensify systemic and cutaneous inflammation. Collectively, these findings suggest hyperglycemia as a biologically plausible contributor to cutaneous disease severity in DM that warrants further investigation. These observations highlight the need for future studies to evaluate whether metabolic screening, dietary patterns, and interdisciplinary care influence cutaneous disease activity and wound healing in DM. Prospective clinical investigation is needed to determine whether targeted glycemic optimization is associated with changes in cutaneous and systemic outcomes in DM.

This narrative review seeks to delve into the different on and off-label medications commonly used with intrathecal drug delivery systems (IDDS) and their clinical applications specifically in pain management settings. This review utilizes a variety of studies including reviews, retrospective chart analyses, and more to analyze the current effectiveness of various pharmacological agents on reducing chronic pain through IDDS. The initial results of intrathecal delivery of these medications have provided benefit in pain reduction and overall patient satisfaction; however, this review will seek to analyze the current data and understanding and suggest areas of strength and improvement within the field and our current understanding.

Chronic pain is a multisystem disorder involving neuroimmune activation, metabolic dysregulation, mitochondrial dysfunction, and alterations in autonomic and sensory signaling, leading to peripheral and central sensitization, reduced responsiveness to standard analgesics, and persistent symptoms. Growing evidence suggests that several widely used systemic drugs, initially developed for metabolic, cardiovascular, immunological, or neurological conditions, interact with biological mechanisms involved in pain pathophysiology. This narrative review examines the mechanistic and emerging clinical evidence describing how systemically administered pharmacological agents interact with pathways implicated in chronic pain, focusing on glucagon-like peptide-1 receptor agonists, sodium–glucose cotransporter-2 inhibitors, metformin, statins, minocycline, ibudilast, low-dose naltrexone, beta-blockers, and cannabinoids. The mechanisms reviewed include glial activation, cytokine signaling, oxidative stress, mitochondrial dysfunction, ion channel sensitization, and autonomic imbalance. The use of these systemic agents may provide additional treatment options for patients with chronic neuropathic, centralized, or mixed pain states who have limited response to conventional therapies, although current clinical evidence remains preliminary.

Postoperative nausea and vomiting (PONV) remain a leading preventable perioperative complication despite advances in anesthetic and surgical care, significantly affecting recovery within Enhanced Recovery After Surgery (ERAS) pathways. ERAS protocols provide a structured, multidisciplinary framework for perioperative optimization; however, variability in the implementation of PONV prevention strategies persists. This narrative review synthesizes current evidence on perioperative strategies for PONV prevention within ERAS pathways, focusing on patient risk stratification, multimodal pharmacologic prophylaxis, anesthetic techniques, and adjunctive non-pharmacologic interventions. We evaluate validated risk prediction tools, including the Apfel score, and highlight the importance of individualized prophylactic strategies based on patient, surgical, and anesthetic risk factors. Multimodal antiemetic regimens, opioid-sparing anesthesia, total intravenous anesthesia (TIVA), and regional techniques are discussed as key components of perioperative management. In addition, non-pharmacologic interventions such as optimized fluid therapy, early mobilization, and supportive perioperative care are reviewed as integral elements of ERAS-based recovery pathways. Complementing existing consensus guidelines, this review provides a practical, workflow-based framework spanning preoperative risk assessment, intraoperative decision-making, and postoperative monitoring for direct application within ERAS protocols.