Pippa Haney

Title: Could stellate ganglion blocks act as a potential adjunctive intervention for functional neurological disorder?

Abstract

Functional Neurological Disorder (FND) is increasingly conceptualised as a disorder of impaired threat discrimination and autonomic dysregulation. Patients often demonstrate persistent sympathetic overactivation, reduced interoceptive clarity, and difficulty integrating top-down cognitive strategies during periods of heightened arousal. Stellate ganglion block (SGB), an established intervention for treatment-resistant PTSD, has been shown to rapidly modulate sympathetic output and reduce physiological markers of threat activation. Despite theoretical overlap between PTSD-related hyperarousal and the autonomic profiles commonly observed in FND, SGB has not been systematically investigated as a targeted intervention for this population.

Argument / Hypothesis:

This paper proposes that SGB may serve as an adjunctive tool for patients with FND by temporarily dampening the sympathetic “noise” that drives functional symptoms. By reducing baseline hyperarousal and promoting parasympathetic recalibration, SGB may create an optimal neurophysiological window in which patients can more effectively engage with cognitive-behavioural therapy (CBT), physiotherapy-based retraining, and self-regulation techniques. In clinical practice, many patients report that although they understand CBT strategies intellectually, they struggle to apply them during episodes of autonomic overwhelm. SGB could offer a stabilising effect that enhances the uptake, integration, and practical use of these therapeutic tools.

Mechanistic Rationale and Theoretical Framework

Findings from stellate ganglion block (SGB) trials in Post-Traumatic Stress Disorder (PTSD) provide an important foundation for understanding its potential relevance to Functional Neurological Disorder (FND). Multiple controlled studies have demonstrated that SGB can lead to rapid and clinically significant reductions in hyperarousal, irritability, exaggerated startle, sleep disturbance, and emotional reactivity. The speed of improvement—often within minutes to hours—has been attributed to the procedure’s ability to acutely inhibit sympathetic outflow along the cervical chain, preventing the downstream activation of limbic threat circuits, particularly the amygdala. Functional neuroimaging in PTSD populations supports this mechanism, showing post-SGB reductions in amygdala reactivity and enhanced top-down modulation from prefrontal regulatory regions.

Neuroanatomically, the stellate ganglion is a key node within the sympathetic nervous system, interfacing with the amygdala, insula, anterior cingulate cortex, hypothalamus, and brainstem autonomic centres. Prolonged stress exposure, trauma, and repeated states of hypervigilance can lead to sensitisation of these pathways. Although not a literal site of memory storage, the sympathetic chain can become conditionally “tuned” to rapid defensive activation, contributing to what some trauma theorists describe as peripheral or autonomic threat encoding. This results in an overactive baseline that maintains chronic arousal long after the initial danger has passed. By temporarily interrupting these conditioned signalling patterns, SGB may disrupt the physiological cascade that ordinarily amplifies limbic alarm.

SGB as a Temporary Nervous System Reset

This interruption can be understood as a form of “nervous system reset.” Many patients describe an immediate sense of internal quiet, clarity, or emotional steadiness following SGB—an experience that aligns with known reductions in sympathetic tone and restored balance between limbic and prefrontal systems. While this reset does not resolve underlying vulnerabilities, it may reduce the physiological “noise” that overwhelms cognitive control and makes application of therapeutic strategies difficult. In this quieter autonomic state, individuals may be more able to access CBT-based techniques, grounding strategies, interoceptive retraining, and physiotherapy interventions. Thus, SGB should be conceptualised not as a standalone treatment, but as a potential adjunct that enhances the nervous system’s capacity to benefit from rehabilitation.

Parallels With Pregnancy-Related Amygdala Modulation

Compellingly, the physiological profile observed after SGB mirrors several well-documented neurobiological changes that occur during pregnancy. Across gestation, the amygdala demonstrates reduced reactivity to threat cues, driven by increased levels of progesterone, oestrogen, oxytocin, and neurosteroids such as allopregnanolone. These substances enhance GABAergic inhibition within the amygdala, dampen cortisol reactivity, and promote a shift toward parasympathetic dominance. Clinically, many pregnant individuals report decreased anxiety, improved emotional stability, and remission or reduction of certain chronic conditions—including, anecdotally, Functional Neurological Disorder symptoms.

This pregnancy-induced attenuation of limbic threat sensitivity offers a natural parallel to the autonomic changes produced by SGB. Both appear to temporarily buffer the amygdala, reduce sympathetic dominance, and create a neurobiological environment more conducive to emotional regulation and adaptive behavioural change. In this sense, SGB may act as an artificial analogue of the hormonal “calming” observed during pregnancy, providing a transient window of neurophysiological stability that supports therapeutic engagement.

Conclusion

Given the overlap between PTSD hyperarousal pathways, pregnancy-related autonomic modulation, and the dysregulated threat processing seen in FND, the rationale for exploring SGB as an adjunctive intervention is strong. Further clinical research is required to determine efficacy, optimal timing, and patient selection, but the mechanism of a targeted, time-limited nervous system reset represents a promising avenue for enhancing recovery in FND.