Stellate ganglion block, or SGB, involves injecting a local anesthetic near the stellate ganglion, a cluster of sympathetic nerve cells located in the neck. The goal is to modulate autonomic nervous system activity, and the technique has a long history in pain management and certain circulatory disorders. More recently, it has been investigated as an option for patients with stubborn insomnia who have not responded to conventional treatments. The appeal is understandable: the procedure is minimally invasive, can be performed on an outpatient basis, and some studies suggest it may improve sleep quality and overall well-being in selected patients. But as this case demonstrates, the neck is a crowded anatomical neighborhood, and needles placed near the sympathetic chain sit close to structures that the body cannot easily spare.

The patient in question had endured six months of severe insomnia before arriving at the clinic. She was sleeping roughly four hours a night, taking about ninety minutes to fall asleep, and waking four to five times nightly. Standardized questionnaires confirmed moderate-to-severe chronic insomnia: her Pittsburgh Sleep Quality Index score was 16 and her Insomnia Severity Index score was 21. She had already tried sleep hygiene education, the sedative estazolam, and melatonin with limited benefit. Her medical history included well-controlled hypertension but no cervical spine disease, trauma, or neurological disorders. Neurological examination and cervical MRI before the procedure were normal, and she showed no clinical features suggesting sleep apnea or other sleep-related movement disorders. With conservative options exhausted, her care team proceeded with a right-sided stellate ganglion block.

The procedure itself followed the modern playbook. An experienced anesthesiologist used a high-frequency linear ultrasound transducer to visualize the anatomy at the level of the sixth cervical vertebra, identifying the carotid artery, internal jugular vein, thyroid gland, and the longus colli muscle before advancing a 22-gauge needle from the side in real time. Color Doppler imaging confirmed that no vessels lay along the planned trajectory. After negative aspiration for blood and cerebrospinal fluid, the physician slowly injected 3 milliliters of 0.2 percent ropivacaine combined with 1 milliliter of compound betamethasone, a corticosteroid added to prolong the block’s effect and dampen local inflammation. Throughout needle advancement and injection, the patient reported no radiating pain, tingling, or weakness — and the injection was completed as planned.

Then, roughly one minute after the needle was withdrawn, everything changed. The patient suddenly reported severe, electric shock-like pain radiating from her right shoulder down the lateral aspect of her upper arm, followed by weakness in shoulder abduction and elbow flexion. Because the symptoms appeared only after the injection had finished, there had been no opportunity to halt the procedure in response to warning signs. Two hours later, examination revealed Medical Research Council grade 3 out of 5 strength in the right deltoid and biceps muscles, reduced pinprick sensation over the lateral upper arm in the C5 dermatome, and a diminished biceps tendon reflex. Emergency cervical MRI ruled out disc herniation, hematoma, or any other compressive lesion that could explain the sudden deficit.

Three days after the procedure, with symptoms persisting well beyond the expected duration of the local anesthetic, electromyography was performed. The results showed abundant spontaneous electrical activity — fibrillation potentials and positive sharp waves — along with markedly reduced recruitment in the deltoid and biceps, muscles predominantly supplied by the C5 nerve root. Critically, sensory nerve action potentials were preserved, a pattern that points toward a preganglionic nerve root lesion rather than an injury to a distal peripheral nerve. The authors were careful to note, however, that the clinical picture of deltoid and biceps weakness also overlaps with partial involvement of the upper trunk of the brachial plexus, and because the patient declined dedicated brachial plexus MRI and no repeat electromyography was available, definitive anatomical localization remained out of reach. The findings were therefore interpreted as favoring C5-predominant involvement rather than proving an isolated root injury.

The mechanism of injury remains uncertain, and the authors are candid about that limitation. Real-time ultrasound never provided unequivocal evidence of an intraneural or intrafascicular injection, and the stored images, being static snapshots, could not confirm that the needle had penetrated a specific neural structure. Inadvertent needle-to-nerve contact, unintended perineural or limited intraneural spread, and injection-related neural irritation all remained plausible explanations. Previous MRI research has shown that even small-volume injectate can distribute across vertebral levels from roughly C5 to T1, lending anatomical plausibility to the idea that the solution reached nerve root territory, though the authors stress this evidence supports only possibility, not proof of what happened in this patient. The role of the betamethasone additive is likewise unclear; its use was extrapolated from other regional anesthesia settings, and direct evidence for corticosteroid adjuncts in SGB for insomnia remains thin.

The recovery trajectory offers a measure of reassurance. Treatment with neurotrophic support — mecobalamin and vitamin B1 — combined with physical therapy, including ultrashort-wave therapy and medium-frequency electrical stimulation, began promptly. Pain on a 10-point visual analogue scale fell from 8 at onset to 3 at two weeks and 1 at three months. Muscle strength in the deltoid and biceps improved from grade 3 to grade 4+ out of 5 by the three-month follow-up, sensory abnormalities had largely resolved, and, somewhat remarkably, the patient’s insomnia symptoms had also improved. Still, the absence of repeat electromyography and validated functional outcome measures means the full extent of electrophysiological recovery could not be objectively characterized.

What makes this case resonate beyond a single patient is the broader context. C5 and C6 nerve root injuries have been described after cervical spine surgery and nerve root injections, but C5-predominant neurological injury following SGB performed for a sleep disorder has rarely, if ever, been documented. As SGB attracts growing interest for psychiatric and sleep-related indications — including post-traumatic stress disorder and menopausal insomnia — the population of patients exposed to the procedure is expanding well beyond the pain clinics where it was first refined. The authors argue that neurological complications may become apparent only after the block is complete, even when patients report no warning symptoms during needle placement, which means vigilance cannot end when the needle comes out. They recommend continuous needle-tip visualization, careful puncture route selection, avoidance of excessive depth, conservative injection volumes, and consideration of alternative approaches such as the anterolateral cervical technique, which may reduce nerve root exposure in selected cases.

For patients considering SGB for insomnia, the message is not that the procedure should be abandoned, but that informed consent should include an honest discussion of neurological risk, however uncommon. New radiating pain, focal weakness, sensory loss, or reflex asymmetry after any such block should trigger immediate neurological examination, appropriate imaging, and electrophysiological testing. As a single case report, the findings cannot be generalized — anatomical variation, comorbidities, and injection characteristics all influence individual risk. But the case stands as a vivid reminder that even ultrasound-guided procedures performed by experienced hands under ideal imaging conditions can produce serious complications, and that the expanding off-label use of regional anesthesia techniques demands the same rigorous safety standards, standardized training, and post-procedural monitoring applied in their original clinical homes.

Subject of Research: Suspected C5 nerve root injury temporally associated with stellate ganglion block for refractory insomnia

Article Title: Suspected C5 Nerve Root Injury Temporally Associated With Stellate Ganglion Block for Refractory Insomnia: A Case Report

Article References: Ji, X., Niu, Z., & Wang, Y. (2026). Suspected C5 Nerve Root Injury Temporally Associated With Stellate Ganglion Block for Refractory Insomnia: A Case Report. Clinical Case Reports, 14(10), Article e73603. https://doi.org/10.1002/ccr3.73603

Image Credits: AI Generated

DOI: 10.1002/ccr3.73603

Keywords: stellate ganglion block, C5 nerve root injury, refractory insomnia, ultrasound-guided injection, electromyography, regional anesthesia, neurological complications, ropivacaine, brachial plexus, patient safety, case report, autonomic nervous system

At the center of the review is the observation that surgical trauma activates two major neuroendocrine systems. The hypothalamic–pituitary–adrenal axis floods the circulation with glucocorticoids, which suppress the synthesis of pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha through their effects on transcription factors like nuclear factor kappa B, while also impairing antigen presentation and lymphocyte proliferation. In parallel, the sympathetic nervous system releases catecholamines that bind beta-adrenergic receptors expressed on tumor cells, endothelial cells and immune populations. These signals promote epithelial-mesenchymal transition, angiogenesis and metastatic dissemination, and they reshape immunity by suppressing natural killer cell cytotoxicity, expanding myeloid-derived suppressor cells and regulatory T cells, and even upregulating the CD47/SIRPalpha “don’t eat me” pathway that shields tumor cells from macrophage phagocytosis. With an estimated ninety percent of cancer-related deaths attributable to metastatic disease after tumor resection, the authors contend that this axis deserves far more clinical attention than it currently receives.

The inflammatory arm of the axis is equally intricate. Surgery triggers a cytokine surge dominated by IL-6 and TNF-alpha, which activate the JAK/STAT3 and NF-kappaB pathways respectively, driving tumor cell proliferation, survival and immune evasion. These cytokines can also endow tumor cells with cancer stem cell-like properties, enhancing resistance to chemotherapy and radiotherapy, and they bias tumor-associated macrophages toward a pro-tumor M2 phenotype that fosters angiogenesis and metastasis. The review also highlights neutrophil extracellular traps, or NETs, web-like structures of DNA, histones and neutrophil proteins released in response to inflammatory stimuli such as IL-8, TNF-alpha and damage-associated molecular patterns. NETs can capture circulating tumor cells, promote their adhesion and colonization at distant sites, and suppress NK and cytotoxic T cell activity. In metastatic hepatocellular carcinoma models, NET internalization activates TLR4/9-COX2 signaling in a feed-forward loop that amplifies both NET formation and metastatic potential, while DNase I combined with anti-inflammatory agents reduced metastasis in mouse models.

The review then details how surgery expands immunosuppressive cell populations. Myeloid-derived suppressor cells accumulate from the bone marrow under the influence of tumor-derived factors, including exosomal PD-L1 that stimulates MDSC proliferation via IL-6/STAT3 signaling. Once activated, MDSCs deplete L-arginine through arginase 1 and inducible nitric oxide synthase, reducing CD3-zeta expression and interferon-gamma and IL-2 secretion, while granulocytic MDSCs nitrate the T-cell receptor through reactive oxygen species. MDSCs also inhibit NK cell cytotoxicity in a cell contact-dependent manner reliant on the NKp30 receptor. In patients undergoing cancer surgery, this expansion has been linked to impaired Th1 immune function, higher postoperative infection risk and increased tumor recurrence. Regulatory T cells follow a parallel trajectory: peripheral Treg levels rise significantly one week after radical mastectomy, accompanied by enhanced inhibitory activity and upregulated checkpoint molecules such as CTLA-4 and PD-1, and propranolol can abolish this catecholamine-driven increase.

Against this mechanistic backdrop, the review systematically appraises anesthetic agents, and the picture that emerges is deliberately nuanced. Propofol emerges as the most frequently discussed “immune-friendly” option. It inhibits cyclooxygenase activity in monocytes and macrophages, lowering prostaglandin E2 production and thereby relieving constraints on NK cell interferon-gamma output. Preclinical work shows it does not reduce NK activity or increase metastatic seeding compared with ketamine, thiopental or halothane, and it suppresses hypoxia-inducible factor-1alpha and RhoA-linked invasion pathways. Clinical studies report more favorable postoperative NK-cell cytotoxicity and reduced VEGF-C release with propofol-based regimens, though a large multicenter randomized trial found no breast cancer recurrence benefit from paravertebral block plus propofol compared with sevoflurane plus opioids. Direct evidence that propofol independently improves long-term oncologic outcomes therefore remains inconclusive.

Other agents complicate any simple classification. Dexmedetomidine, a selective alpha2-adrenergic agonist, blunts sympathetic and neuroendocrine stress responses and reduced circulating stress hormones and IL-6 in tumor-bearing mice, yet rodent studies have reported both increased and decreased metastatic burden depending on dose and model, and clinical outcome data are similarly mixed. Etomidate suppressed PD-L1 expression and improved antitumor immunity in hepatocellular carcinoma models but enhanced migration in colorectal cancer models, underscoring lineage dependence. Opioids engage mu-opioid receptors on immune cells; morphine suppresses NK cytotoxicity in humans and may activate pro-angiogenic signaling, whereas tramadol appears comparatively immune-sparing. Observational studies linking opioid exposure to recurrence point in conflicting directions across cancer types, and associations between opioid use and poorer immunotherapy response are vulnerable to confounding by pain burden and disease severity. Volatile anesthetics have been associated with blunted interferon-driven NK augmentation, T and B cell apoptosis and higher pro-tumor cytokines and matrix metalloproteinases in breast surgery, yet a large population-based study of stage III breast cancer reported lower mortality with inhalational maintenance, illustrating how context can invert apparent signals.

Regional and neuraxial techniques, including epidural and paravertebral blockade, are framed not as standalone anti-recurrence interventions but as components of a stress-attenuating bundle. Combined general and epidural anesthesia has been associated with increased intratumoral CD8-positive T-cell infiltration, reduced FOXP3-positive cell accumulation and lower postoperative inflammatory markers in lung and gastric cancer studies, and thoracic epidural analgesia reduced IL-6, norepinephrine, cortisol and ACTH during esophagectomy. Local anesthetics add direct biological signals: ropivacaine suppressed invasion through NaV1.5 channel effects, bupivacaine inhibited mitochondrial respiration and RhoA/ROCK-mediated migration in gastric cancer cells, and perioperative lidocaine reduced lung metastases in a murine breast tumor model. Randomized evidence, however, has not shown a stable recurrence benefit from anesthetic technique alone, and the authors emphasize that analgesia and recovery remain the most reliable benefits of regional approaches.

Pharmacologic adjuncts targeting the axis itself are attracting growing interest. Because prostaglandin E2 signaling through EP2 and EP4 receptors drives myeloid immunosuppression, perioperative NSAIDs or COX-2 inhibitors may partially relieve constraints on effector T and NK cells, and in vivo work shows COX inhibition can restrain tumor growth and alter PD-L1 expression and myeloid composition within tumors, although a single preoperative ketorolac dose did not improve disease-free survival in high-risk breast cancer. Beta-blockade combined with COX-2 inhibition improved markers of malignant potential, reduced epithelial-to-mesenchymal transition and remodeled immune infiltrates in a phase II breast cancer trial, and the PROSPER trial in pancreatic surgery confirmed safety with preliminary favorable signals. Immunonutrition, particularly omega-3 fatty acids that serve as precursors for pro-resolving lipid mediators, may further support inflammatory control and tissue repair within enhanced recovery pathways.

The review closes with an executable framework for individualized anesthetic planning built around three phases. Preoperatively, clinicians are encouraged to stratify risk using inflammatory and nutritional trajectories such as CRP-to-albumin ratios, neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios, and, in selected cases, circulating tumor DNA with standardized sampling windows. Intraoperatively, priorities include high-quality opioid-sparing multimodal analgesia, appropriate regional techniques, stable hemodynamics, normothermia and balanced fluid management, while avoiding unnecessary anesthetic depth. Postoperatively, trend-based monitoring should prompt early pain reassessment, early enteral nutrition and mobilization to shorten the duration of stress and inflammatory exposure. Embedded within ERAS pathways, the authors argue, anesthetic management becomes an integrated component of perioperative oncologic care: no single drug or technique constitutes an anti-recurrence strategy, but reducing stress peaks, limiting avoidable immunosuppressive exposure and accelerating recovery may collectively narrow the biological window through which cancer can exploit its own surgery.

Subject of Research: The perioperative stress–inflammation–immunosuppression axis and its influence on tumor progression and anesthetic management in cancer surgery

Article Title: Perioperative stress–inflammation–immunosuppression axis and tumor progression: mechanistic integration and anesthetic management strategies

Article References: Ye, L., Shen, H., Lin, J., Pei, S., Lin, F., Li, X., Chang, E., & Pan, L. (2026). Perioperative stress–inflammation–immunosuppression axis and tumor progression: mechanistic integration and anesthetic management strategies. Holistic Integrative Oncology, 5(1), Article 63. https://doi.org/10.1007/s44178-026-00280-x

Image Credits: AI Generated

DOI: 10.1007/s44178-026-00280-x

Keywords: perioperative stress, surgical inflammation, immunosuppression, tumor progression, anesthetic management, natural killer cells, myeloid-derived suppressor cells, regulatory T cells, neutrophil extracellular traps, regional anesthesia, opioid-sparing analgesia, ERAS pathways