Stellate Ganglion Block and the Question of Treatment Readiness
Featuring Dr. Remi Drozd
Founder • Lucid Therapeutics
Written by Gavin Hart
Interventional Psychiatry News
Ketamine has reshaped expectations for treating severe depression. For some patients, improvement can begin within days rather than the weeks often associated with conventional antidepressants. However, the same rapid action that makes ketamine so compelling also highlights one of its central limitations: outcomes remain highly variable. Some patients experience a marked and lasting reduction in symptoms, others improve only partially, and some see little meaningful benefit despite completing an appropriate course of treatment.
Efforts to explain that variability have largely focused on the brain, including dose, route of administration, medication interactions, neuroplasticity, and differences in the neural circuits involved in mood and cognition. Those questions still matter. However, Dr. Remi Drozd, founder and medical director of Lucid Therapeutics in Santa Barbara, California, believes clinicians may also need to look beyond the central nervous system, particularly when treating patients with extensive trauma histories and persistent physiological hyperarousal.
After years of providing ketamine treatment, Drozd began noticing a recurring pattern among some patients who responded only partially. Many seemed unable to settle physically during treatment. Even in a controlled therapeutic environment, they remained guarded, activated, or persistently oriented toward potential threat.
“We ultimately realized, through asking enough questions, that the bulk of them experienced a significant amount of trauma or were still in a state of constant arousal,” Drozd told Interventional Psychiatry News.
His working hypothesis was that these patients were not necessarily failing to respond because ketamine had no therapeutic effect. Instead, persistent activation of the sympathetic nervous system might have limited their ability to engage with certain aspects of the treatment experience.
That observation led him to stellate ganglion block, or SGB, a procedure historically used in anesthesiology and pain medicine. More recently, SGB has drawn interest in psychiatry because of its potential to reduce symptoms associated with post-traumatic stress disorder, particularly hyperarousal and other manifestations of excessive sympathetic activation.
Drozd does not present SGB as a direct treatment for depression, nor does he view it as an alternative to ketamine. Instead, he selectively considers the procedure as a way of preparing certain patients for continued treatment. The question is not whether SGB can replace an established psychiatric intervention, but whether reducing autonomic overactivation might help some trauma-affected patients engage more meaningfully with a treatment they have already begun.
“How do we prepare a client’s nervous system to receive this medicine?” he said.
A Procedure Moving Into Psychiatry
The stellate ganglion is part of the cervical sympathetic chain, a network of nerves involved in regulating the body’s fight-or-flight response. During an SGB procedure, a clinician injects a local anesthetic near sympathetic structures in the neck, temporarily interrupting their activity. At Lucid Therapeutics, SGB is performed using ultrasound guidance.
SGB has long been used for sympathetically mediated pain and other conditions associated with abnormal sympathetic signaling. Interest in its psychiatric use has focused primarily on PTSD.
One of the most significant clinical trials of SGB in psychiatry was a multisite, randomized, sham-controlled study involving 113 active-duty service members with PTSD symptoms. Participants received either two right-sided stellate ganglion blocks administered two weeks apart or two sham procedures. At eight weeks, the SGB group showed a greater reduction in clinician-rated PTSD symptom severity than the sham group.
The adjusted mean reduction on the Clinician-Administered PTSD Scale for DSM-5 was 12.6 points in the SGB group, compared with 6.1 points in the sham group. The authors concluded that SGB deserved further study as an adjunctive intervention for PTSD. They also noted that the participants’ relatively mild-to-moderate baseline symptoms and the short follow-up period limited how broadly the findings could be applied.
The broader literature is less definitive. A systematic review examining SGB across psychiatric disorders found that most published research had focused on PTSD and that much of the evidence came from small case reports, case series, and open-label studies. The randomized trials included in the review produced inconsistent findings. The reviewers characterized the evidence as preliminary and called for larger studies involving more diverse populations, longer follow-up periods, and better-defined treatment protocols.
Support for SGB in depression and other psychiatric disorders remains especially limited. Published research does not establish SGB as a treatment for ketamine nonresponse, nor does it demonstrate that SGB reliably strengthens ketamine’s antidepressant effects.
That distinction is essential to understanding Drozd’s clinical model. His approach applies an emerging physiological hypothesis to a specific clinical problem: carefully selected patients with substantial trauma-related hyperarousal who have experienced only a limited or partial response to ketamine treatment.
The Hyperarousal Hypothesis
PTSD is not only a disorder of traumatic memories. It can also involve persistent changes in arousal, sleep, attention, startle response, irritability, and threat perception. For some patients, the body continues to respond as though danger is present even after the immediate threat has passed.
Drozd believes this physiological state may influence how some patients experience ketamine. A patient’s ability to relax, tolerate uncertainty, and temporarily loosen ordinary patterns of cognitive control may affect how the treatment unfolds, particularly when ketamine is delivered within a psychotherapeutic framework.
It is important to distinguish ketamine treatment generally from ketamine-assisted psychotherapy. Ketamine may be administered primarily for its pharmacological antidepressant effects without making the patient’s subjective experience the central focus of treatment. In ketamine-assisted psychotherapy, by contrast, the patient’s engagement with emotional, psychological, and experiential material is a more intentional part of the therapeutic process.
In psychedelic medicine and ketamine-assisted psychotherapy, clinicians sometimes describe a patient’s ability to “surrender” or “drop into” an experience. These are subjective expressions rather than established biological endpoints. Still, they describe a recognizable clinical pattern. Some patients remain tense, vigilant, and physiologically guarded during the experience, while others appear better able to engage with changes in perception, emotion, memory, and self-reference.
This distinction matters because describing patients as “resisting” the experience could imply that they are consciously or intentionally preventing the treatment from working. Drozd’s concern is different. He believes some trauma-affected patients may remain physiologically organized around protection even when they consciously want to participate in treatment.
Drozd uses a scuba-diving analogy to illustrate the difference.
“Some of these people are just getting wet,” he said. “They’re not having the psychological or experiential component of it.”
His concern is not simply whether a patient dissociates or enters an unusual subjective state. It is whether chronic sympathetic activation keeps the patient physiologically organized around threat. In that state, a person may continue monitoring the environment, maintaining control, or preparing for a perceived threat despite being in a safe clinical setting.
Drozd’s hypothesis is that temporarily reducing sympathetic output may create a window in which a patient feels less guarded and is better able to engage with ketamine-assisted treatment.
The proposed mechanism remains speculative. Researchers do not yet fully understand how temporarily interrupting cervical sympathetic signaling might affect PTSD symptoms, and systematic reviews identify the mechanism as an unresolved question. Proposed explanations include reduced sympathetic outflow, changes in autonomic balance, and downstream effects on brain systems involved in arousal, fear, and stress regulation.
These explanations may be biologically plausible, but none has been established as the definitive mechanism behind psychiatric improvement following SGB.
A Clinical Observation, Not an Established Response Rate
Drozd’s formulation is best understood as a clinical hypothesis developed through repeated observation rather than as a proven model of ketamine response.
His interest in SGB grew from a practical clinical problem. Some patients with extensive trauma histories completed ketamine sessions, tolerated the medication, and sometimes experienced temporary or partial improvement, yet appeared to remain physiologically guarded throughout treatment.
Instead of assuming that ketamine had entirely failed, Drozd began considering whether chronic autonomic activation might be limiting how these patients experienced or engaged with treatment.
“In our clinical experience, approximately 30% of patients who had previously shown only a partial response appeared to respond more robustly after receiving a stellate ganglion block,” Drozd said.
This observation was not derived from systematically collected outcomes, a controlled trial, or a formal assessment of everyone receiving SGB. It should therefore not be interpreted as a response rate or as evidence that SGB will improve ketamine outcomes for a predictable proportion of patients.
The changes Drozd observed were not universal and were not always dramatic. Some patients described feeling calmer. Others found psychotherapy easier. Some reported that later ketamine sessions felt qualitatively different, as though they could settle more fully into the experience rather than remaining physiologically guarded.
Those observations led Drozd to evaluate more than depression severity and trauma history. He also began considering whether a patient’s autonomic state appeared regulated enough to tolerate and engage with a rapid-acting intervention.
2A Question of Treatment Readiness
This approach points toward a broader question in interventional psychiatry. The field has become increasingly skilled at delivering treatments that act rapidly on mood symptoms, neural circuits, and synaptic function. It has been less successful at predicting who will respond, why they will respond, and what conditions may support or limit that response.
In practice, clinicians often proceed through treatments one at a time, learning whether an intervention works only after a patient has completed a substantial portion of therapy.
Drozd’s model suggests that treatment readiness may deserve greater attention in that process. A patient may meet diagnostic criteria for depression, PTSD, or another condition and still arrive for treatment in a physiological state that affects how the intervention is experienced.
This does not mean hyperarousal necessarily causes ketamine nonresponse. It also does not mean that reducing hyperarousal will reliably convert a nonresponder into a responder. It suggests only that a patient’s autonomic state may be a clinically relevant variable worthy of further study.
This is not a strategy Drozd considers for every patient. Rather, he reserves it for individuals with clear evidence of persistent sympathetic hyperarousal despite otherwise appropriate treatment.
For Drozd, this idea has changed how treatment begins. Rather than waiting until an intervention has clearly failed, his team looks earlier for signs of persistent sympathetic activation, trauma-related hyperarousal, compulsive coping behaviors, disrupted sleep, and difficulty reaching a state of physical calm.
In some cases, SGB may be discussed before ketamine treatment begins. In others, it may be considered after several sessions when a carefully selected patient remains physiologically guarded or has experienced only a limited or partial response.
SGB is considered only after an individualized assessment of trauma-related hyperarousal, medical suitability, potential contraindications, and the risks and limitations of the procedure. It is not presented as appropriate for every patient with depression, trauma exposure, PTSD, or an incomplete response to ketamine.
The procedure also requires appropriate training, technical expertise, and clinical safeguards.
The broader takeaway is not that every ketamine clinic should begin offering stellate ganglion block. The evidence does not support that conclusion. The more important possibility is that treatment response may depend on more than selecting the appropriate medication, dose, device, or route of administration.
It may also depend, in part, on the physiological state of the patient’s nervous system at the time treatment is delivered.
While Drozd’s clinical observations have centered on ketamine-assisted therapy, the broader question is whether preparing the autonomic nervous system may influence engagement with any treatment that depends on neuroplasticity, psychotherapy, or emotional processing.
If future research supports this hypothesis, assessing autonomic state could become as important as selecting the medication itself, allowing clinicians to better match patients with interventions that optimize treatment response.
That possibility remains unproven, but it represents a clinically relevant and testable hypothesis.
Drozd’s observations do not establish SGB as a treatment for depression or ketamine nonresponse. Instead, they raise a focused scientific question: whether autonomic hyperarousal may be an important variable affecting how certain trauma-affected patients engage with treatment.
The answer will require prospective research, standardized selection criteria, carefully defined treatment protocols, and systematic measurement of both psychiatric and autonomic outcomes. Until then, Drozd’s model remains what he intends it to be: a cautious clinical hypothesis shaped by patient observation, grounded in an emerging body of research, and offered as a question for the field rather than as a settled conclusion.
