SGB is a deceptively simple procedure with an ambitious target. It involves injecting a small volume of local anesthetic around the cervicothoracic sympathetic chain, a bundle of nerve cells in the neck that forms part of the body’s fight-or-flight machinery. The idea is that chronic insomnia coexisting with anxiety is sustained partly by sympathetic overdrive: racing heart, mental vigilance, sleep-related worry. By transiently damping this output, the block may rebalance autonomic tone and lower the physiological arousal that undermines both sleep and the confidence to taper medication. The procedure has previously been investigated for posttraumatic stress symptoms, anxiety, and sleep disturbance, but most studies have measured symptom scales rather than the outcome that matters most for long-term safety: whether patients actually take fewer hypnotic drugs.

The research team screened 420 medical records from January 2022 through December 2025 and assembled two carefully matched groups of 80 adults each, all of whom had chronic insomnia lasting at least three months, documented anxiety symptoms, and ongoing use of at least one hypnotic or sedative medication. The treated group completed a standardized four-session SGB pathway, delivered once daily on four consecutive days with left and right sides alternated. Each procedure was performed under real-time ultrasound guidance at the C7 vertebral level, with a 22-gauge needle advanced to the prevertebral fascial plane in front of the longus colli muscle before 5 milliliters of 2% lidocaine was injected. Successful blockade was confirmed by the appearance of Horner signs, the expected constellation of eyelid drooping and pupillary constriction indicating that the sympathetic chain had indeed been anesthetized. Controls were drawn from contemporaneous routine care using calendar-time risk-set sampling, with each control encounter falling in the same month and within two weeks of the corresponding treated patient’s index date.

The primary outcome was deliberately pragmatic: at one month, a patient had to hit at least one of three medication-reduction milestones, namely a 50% or greater drop in an operational medication-burden score, a transition from combination therapy to a single agent, or complete discontinuation maintained for at least two weeks. The results were striking. Thirty-two of 80 patients in the SGB-based pathway, or 40%, met the composite outcome, versus 12 of 80 routine-care patients, or 15%. That crude difference of 25 percentage points survived adjustment. A parsimonious robust Poisson model, restricted to age, sex, baseline medication burden, and baseline medication count because only 44 outcome events were available, yielded an adjusted risk ratio of 2.43. Marginal standardization, which predicts each participant’s outcome under both exposure states while preserving the observed covariate distribution, put the adjusted risks at 38.0% versus 16.7%, an absolute difference of about 21 percentage points.

Digging into the components revealed where the signal truly lived. The strongest and most consistent association was with substantial dose reduction: 33.8% of SGB-pathway patients achieved at least a 50% cut in medication burden compared with 11.2% of controls, an adjusted risk ratio of 2.77. Class-specific analyses told a compatible story. Among baseline benzodiazepine users, doses expressed as approximate diazepam equivalents fell by half or more in 28.2% of treated patients versus 8.9% of controls. Z-drug reductions, quantified in World Health Organization defined daily dose units, were directionally similar but less statistically precise. By contrast, transition to monotherapy and complete discontinuation were numerically more frequent in the SGB group but came with wide confidence intervals that spanned the null. In plain terms, the pathway appears to help patients take much less medication, but the evidence that it helps them stop entirely remains inconclusive.

The benefits appeared to persist. At three months, a maintained response was recorded in 31.3% of treated patients with follow-up versus 13.6% of controls, and the association held when missing follow-up was conservatively counted as failure and when inverse-probability-of-censoring weighting was applied. The treated group also showed greater standardized improvement in sleep, anxiety, and depression symptoms, though the heterogeneous symptom scales make these supportive findings harder to interpret. Safety data were reassuring within the limits of retrospective documentation: across 320 procedures, 15 patients, or 18.8%, experienced a recorded procedure-related event, all mild or moderate. Transient dizziness, hoarseness, puncture-site pain, and two vasovagal reactions resolved with rest, observation, oxygen, or fluids, and no serious event was recorded.

What sets this study apart methodologically is the battery of sensitivity analyses. The authors deployed propensity-score matching, overlap weighting, and trimmed stabilized inverse probability weighting, each targeting a different population average, and every approach converged on an adjusted risk ratio between roughly 2.3 and 2.7 with absolute risk differences between 18 and 23 percentage points per 100 patients. One thousand bootstrap resamples converged, and adding potential confounders such as depression severity, antidepressant use, thyroid disease, or body mass index one at a time did not reverse the treatment coefficient. Firth penalized logistic regression confirmed stability in the face of sparse events, a well-known pitfall of standard logistic regression when outcomes are rare.

Yet the authors are refreshingly candid about what the design cannot prove. Because treatment allocation was nonrandomized, the results speak to an SGB-containing care pathway, not to an independent causal effect of the injection itself. Baseline imbalances were real: treated patients had more severe depression, far more antidepressant use, and slightly lower starting medication burdens. Clinician-directed taper plans were documented somewhat more often in the SGB pathway, raising the possibility that physicians simply encouraged tapering more intensively after the procedure. And the authors raise a subtle point that plagues many procedural interventions: receiving an invasive treatment may itself boost expectancy, perceived treatment intensity, and willingness to reduce medication, independently of any physiological effect of sympathetic blockade. No sham-controlled comparison was possible, and treatment expectations were not measured.

The study also grapples honestly with its measurement choices. Benzodiazepine doses were converted to approximate diazepam equivalents using published guidance, while Z-drugs were handled in defined daily dose units, and the broader cross-class burden score was explicitly labeled exploratory rather than a validated pharmacological scale. Missingness, though modest, was linked to baseline medication burden, and the statistical corrections for it rest on unverifiable assumptions. Propensity-score distributions overlapped imperfectly, and residual imbalance persisted even after matching and weighting, reminders that observational data can narrow but never eliminate the fog of confounding.

For now, the take-home message is cautiously intriguing rather than practice-changing. In a clinical landscape where guidelines recommend cognitive behavioral therapy for insomnia and gradual, patient-centered tapering but where access to CBT-I is often limited and anxiety makes deprescribing fragile, a four-session ultrasound-guided procedure associated with roughly 20 additional medication reductions per 100 treated patients warrants serious attention. The researchers call for prospective multicenter trials with randomized or strong quasi-experimental allocation, standardized de-prescribing protocols, class-specific dose measures, autonomic biomarkers, and, crucially, sham-controlled designs that can separate the physiology of sympathetic blockade from the psychology of undergoing a procedure. Until then, the stellate ganglion remains a tantalizing but unproven ally in one of sleep medicine’s hardest problems: helping patients finally put down the pill bottle.

Subject of Research: Association of stellate ganglion block-based care with hypnotic medication reduction in chronic insomnia with anxiety symptoms

Article Title: Association of a stellate ganglion block-based care pathway with hypnotic medication reduction in chronic insomnia with anxiety symptoms: a real-world retrospective cohort study

Article References: Wang, D., Wang, X., Wang, W., & Wang, Y. (2026). Association of a stellate ganglion block-based care pathway with hypnotic medication reduction in chronic insomnia with anxiety symptoms: a real-world retrospective cohort study. Frontiers in Sleep, 5, Article 1923070. https://doi.org/10.3389/frsle.2026.1923070

Image Credits: AI Generated

DOI: 10.3389/frsle.2026.1923070

Keywords: stellate ganglion block, chronic insomnia, anxiety symptoms, hypnotic deprescribing, benzodiazepines, Z-drugs, retrospective cohort study, propensity score, sleep medicine, real-world evidence, autonomic nervous system, Association