Neural Therapy - Reno, NV

Neural Therapy: Procaine-Based Care for a Nervous System Locked Into Overdrive

A nervous system locked into overdrive is a core driver of PTSD, anxiety, and other trauma-related issues.

Neural therapy uses procaine, a short-acting local anesthetic, delivered at carefully selected sites, the sympathetic ganglia. The goal is to evaluate and influence the autonomic nervous system, and to address sympathetic overactivation and the hyperarousal associated with PTSD, anxiety, and trauma.

A "reset" opens a window for a rigid stress pattern to shift toward a more regulated, parasympathetic-dominant baseline, measured in your physiology. It is a family of individualized interventions, chosen from your history, symptoms, safety profile, goals, and response over time.

"A hyperaroused nervous system can appear outwardly calm, a freeze, a shutdown, or a well-practiced mask, while still running in threat mode underneath. That is exactly why we track heart-rate variability and objective measures rather than how someone appears in the room. We track what actually happens in you, not what a theory predicts should happen."

Clinical Note: Neural therapy at Peak Body and Mind is provided within an established clinician-patient relationship and an individualized consent discussion. It works alongside psychotherapy, medication, safety planning, and other indicated care, as one part of your overall plan, never a replacement for them. If you are in crisis, call or text 988, call 911, or go to the nearest emergency department.

The Mechanism

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A Brief Interruption, Then a Measured Response

Procaine briefly limits sodium movement across excitable cell membranes. Neural-therapy models focus on what happens next: an ongoing irritative signal into a ganglion is interrupted, muscle guarding eases, local circulation improves, and a rigid autonomic pattern loosens toward a more parasympathetic-dominant baseline. This is a measurable physiological shift.

The Approach

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Individualized, Not Standardized

The route, treatment area, sequence, and follow-up are chosen from your history, symptoms, safety profile, goals, and response. Nothing is pulled from a menu, and how you respond, including a limited or absent response, is itself clinically useful information that shapes what we do next.

What This Is Not

Icon of an intravenous (IV) bag with a diagonal prohibition symbol overlay, indicating no IV or infusion.

Greater Range, Not Numbing

The objective is not emotional numbing or prolonged loss of nerve function. It is greater range: the ability to feel without being immediately overwhelmed, and to return to baseline more readily.

The Mechanism, In Detail

The mechanism runs on multiple levels at once:

Autonomic

Reduced sympathetic overdrive and a shift toward parasympathetic dominance, the state in which the body rests, digests, and recovers rather than braces for threat. Human research using 24-hour heart-rate monitoring has documented exactly this shift after procaine-based therapy (Weinschenk 2025).

Neurochemical

Modulation of norepinephrine and nerve growth factor (NGF), both directly implicated as the link between memory consolidation and PTSD (Lipov 2012).

Immune

Reduced local inflammatory signaling.

Epigenetic

Sympathetic-ganglion blockade may help reverse PTSD-associated DNA methylation through the same NGF/BDNF cascade (Lipov 2017), and procaine itself has been identified in laboratory research as a DNA-demethylating compound (Villar-Garea 2003), relevant because chronic trauma is associated with epigenetic changes in stress-response genes.

Full mechanism detail and citations are on our Procaine page.

A note on the research behind this mechanism

Much of the modern clinical and mechanistic case for treating PTSD and trauma-related conditions through the stellate ganglion comes from the sustained work of Dr. Eugene Lipov, MD, of the University of Illinois, Chicago, who has published extensively on the NGF, cortisol, and epigenetic pathways above since pioneering PTSD-specific stellate ganglion block in 2008.

Not Anesthesia, Not A Nerve Block: What This Actually Is

We do not practice anesthesia, and this is not a nerve block. An anesthetic nerve block uses a local anesthetic to interrupt nerve conduction on purpose, numbing an area or shutting down a signal for a defined stretch of time. That is a different procedure with a different goal, and it is not what happens here.

We do not shut off the nerve. Neural therapy uses procaine to saturate and reset the ganglion, a biological, regenerative action on the tissue itself, not conduction blockade. The therapeutic target is the ganglion's own electrical and inflammatory state: normalizing the cell membrane's resting potential, calming local inflammatory signaling, and restoring healthier autonomic tone. The aim is repolarization and reset, not numbing, and not silencing the nerve's ability to do its job.

How safe this actually is

Procaine has been used in medicine for over a century and is cleared almost entirely by plasma cholinesterase, an enzyme present throughout the body's tissues, rather than requiring extensive liver processing. A double-blind, placebo-controlled study of 177 patients receiving 340 injections found no type-1 allergic reactions with procaine (Weinschenk 2017). Every injection is preceded by standard safety protocol, including aspiration technique to confirm safe needle placement before any medication is delivered, and administered by a trained, credentialed clinician. As with any injection or infusion, real risks exist and are reviewed with you individually at consent.

Two Core Elements

1

Procaine IV (Systemic)

IV infusions for a whole-system entry point, when broad autonomic, cognitive, sensory, or psychovegetative patterns matter more than one local target. We watch for a quieter physiological baseline and a faster return toward parasympathetic dominance afterward, tracked objectively rather than assumed from presentation. Procaine IV works on autonomic and HPA-axis regulation as one part of a broader plan.

2

Stellate Ganglion Reset (SGR)

Targeted saturation of the stellate region with procaine, for persistent upper-body threat physiology: hyperarousal, startle, nightmares, guarded breathing, and difficulty settling after stress. A multisite, randomized, sham-controlled trial of 113 active-duty service members found significantly greater PTSD symptom improvement following two sympathetic ganglion procedures than a sham procedure (Rae Olmsted 2020). A retrospective study of 114 patients documented a 52 percent average GAD-7 improvement sustained at three months following bilateral cervical sympathetic chain blocks (Mulvaney 2025), and a separate study documented significant improvement in traumatic-brain-injury symptom scores in patients with PTSD and a TBI history (Mulvaney 2024). Published trials typically use standardized cervical sympathetic chain block technique; we use targeted procaine saturation.

The Peak Method: How We Work Together

Define the
Pattern & Screen for Safety

Define the Pattern & Screen for Safety

We clarify symptom onset, triggers, autonomic and visceral features, sleep, trauma symptoms, history, and the real-life change you want. Then we screen allergies, medications, bleeding risk, infection, pregnancy when relevant, cardiopulmonary and neurologic history, and current stability.

What We Track, How Duration Works, And Safety

What we track

Baseline severity, startle and hyperarousal, sleep quality, GAD-7 or PCL-5 scores where relevant, heart-rate variability, WAVi EEG and Brain Gauge objective brain-function measures, and your own report of daily function, at intervals throughout your course of treatment.

How duration is determined

Session count and how long a given reset holds are set by your measured response, not predicted upfront. Response timing varies by patient and by element, immediate, delayed, or building gradually across a series, and we use that real data, not a projected number, to shape session frequency and what comes next.

Risks and when to seek help

All injections and infusions carry risk, including bruising, bleeding, infection, allergic reaction, and rare local-anesthetic systemic toxicity, plus region-specific considerations for the stellate procedure that are reviewed at consent.

F.A.Q.

Is neural therapy only for pain?

No. Local anesthetics are familiar from pain medicine, but neural therapy uses procaine within a broader autonomic and mental-health framework. Each use still requires an individualized rationale.

How long will a "reset" last?

Duration is individualized and tracked in you. For some patients a reset opens a window that psychotherapy and other treatment build on for an extended period; for others the effect is shorter and the procedure is repeated as part of a series. We measure your actual response and shape the plan around it.

Is SGR the same as the nerve blocks in the published research?

Closely related. Published studies typically use standardized cervical sympathetic chain block technique; we use targeted procaine saturation and document exactly what you receive. That research is real, directly relevant context for the approach and its mechanism.

Do I have to relive trauma or have an emotional release?

No. Neural therapy does not require reliving trauma, and an emotional release is not required or forced. Psychotherapy continues at a pace matched to your readiness and safety.

Can neural therapy replace psychotherapy or medication?

No. It is used as an adjunct, working alongside psychotherapy and medication rather than replacing them. Greater autonomic flexibility tends to help you use those treatments more effectively.

How many sessions will I need?

Frequency and sequence are individualized: set by the intervention, your response, safety, goals, and treatment burden, and reassessed at each step based on what your results actually show.

Josh Swigart Portrait

Josh Swigart, APRN, PMHNP-BC, KRI Fellow. Double Certified in Neural Therapy.

Trained directly under Gerald W. Grass, MD, founder of the Ketamine Research Institute and former Yale Anesthesiology faculty. Trained in procaine-based neural therapy directly under Dr. Suzanne Ferree, MD, a triple board-certified physician and nationally recognized neural therapy educator, along with Christina Finnerty, APRN, and Melissa Selby, APRN, both practicing neural-therapy clinicians within Dr. Ferree's training network.

Josh Swigart Portrait

Is neural therapy right for you?

The right option follows a clinical assessment: your dominant pattern, history, medical risk, preferences, and the least burdensome reasonable entry point. If a body-level pattern seems to be holding back your recovery, we can talk through whether neural therapy has a role in your plan.

This page is for general education and is not a diagnosis, prescription, or substitute for individualized medical evaluation and consent. Treatment availability and selection depend on clinical assessment. If you are in crisis, call or text 988, call 911, or go to the nearest emergency department.

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Research Behind This Approach

[1] Rae Olmsted EK, et al. (2020). Stellate ganglion block for PTSD, multisite RCT. JAMA Psychiatry, 77(2):130-138. PMID 31693083. 113 active-duty service members; significantly greater PTSD symptom improvement after two stellate ganglion procedures than sham. Gold-standard evidence for the SGR element.[2] Lipov E, Kelzenberg B, Rothfeld C, Abdi S (2012). NGF as the link between cortisol, memory consolidation, and PTSD. Medical Hypotheses, 79(6):750-753. PMID 22998954. Proposes stellate ganglion block's reduction of norepinephrine and NGF as the basis for symptom improvement.[3] Lipov EG, Candido K, Ritchie EC (2017). Stellate ganglion block and PTSD-associated DNA methylation. Journal of Molecular Neuroscience, 62(1):67-72. PMID 28364364. Proposes reversal of PTSD-associated methylation through the NGF/BDNF cascade.[4] Mulvaney SW, et al. (2025). Bilateral, two-level cervical sympathetic chain blocks and anxiety. Brain Sciences, 15(2). PMID 40002521. Retrospective study of 114 patients; 52 percent average GAD-7 improvement sustained at three months.[5] Mulvaney SW, et al. (2024). Cervical sympathetic chain block in PTSD with traumatic brain injury. Military Medicine. PMID 38771000. Retrospective study; significant symptom improvement in patients with PTSD and a TBI history.[6] Weinschenk S, et al. (2025). Procaine-based therapy and heart rate variability, controlled human study. Chronobiology International, 42(11):1577-1589. PMID 41020483. 24-hour Holter-ECG documenting shifts toward more parasympathetic-dominant HRV. Full detail on our Procaine page.[7] Weinschenk S, et al. (2017). Allergy risk of procaine versus other local anesthetics, double-blind placebo-controlled study. BioMed Research International, 2017:9804693. PMID 30035116. 177 patients; no type-1 allergic reactions with procaine. Full detail on our Procaine page.[8] Villar-Garea A, et al. (2003). Procaine as a DNA-demethylating agent in human cancer cells. Cancer Research, 63(16):4984-4989. PMID 12941824. Laboratory identification of procaine's epigenetic property. Full detail on our Procaine page.
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