helps reduce sympathetic to parasympathetic ratio
And treating cPTSD obvs
Probing prefrontal-sgACC connectivity using TMS-induced heart–brain coupling | Nature Mental Health slighly related
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Have you tried this?
adic
@adic_9
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6h
Replying to @seanstidston
Iirc stellate ganglion block and LDA made the biggest difference + pacing like crazy
Thought for 6s
- @adic_9
replies to a question about Physics Girl (Dianna Cowern) improving enough to fly after being bedridden with ME/CFS from long COVID, citing stellate ganglion block, LDA, and strict pacing as the main factors.
- Stellate ganglion block is a procedure injecting anesthetic near neck nerves to disrupt sympathetic overactivity, used experimentally for autonomic dysfunction and fatigue in long COVID cases.
- LDA refers to low-dose aripiprazole (Abilify), an off-label antipsychotic that some ME/CFS patients report reduces fatigue and brain fog via dopamine effects, though results vary and lack large-scale clinical trials.
The main downside: SGB is a precision procedure
A stellate ganglion block is near the carotid artery, vertebral artery, recurrent laryngeal nerve, esophagus/trachea area, and sympathetic chain. Serious complications are rare, but a systematic review of reported SGB complications found both medication/systemic and local/procedure-related complications, including very rare catastrophic events.
That does not mean “don’t do it.” It means: you want the doctor using image guidance, monitoring, resuscitation capability, and not treating your neck like a dartboard at a county fair.
Sedation can slightly reduce your ability to give real-time feedback. Not always a dealbreaker, but with a neck block, I’d prefer awake enough to communicate.
SGB also changes heart-rate variability markers in ways consistent with sympathetic inhibition. One 2026 study found ultrasound-guided SGB changed HRV in a pattern suggesting selective sympathetic inhibition of the heart without affecting vagal tone, while another older study found left-sided SGB increased parasympathetic-related HRV measures in head/neck pain patients.
in SF you can get it via 450 Sutter St #1504 but it’s v. expensive $2000 first side, $1500 second side
there are other sites where you can get $750 per side
There’s a chance SGB could increase sleep quality/reduce awakenings (bc too much sympathetic arousal)… Thus worth trying
The thing that makes this genuinely uncertain — and kind of fascinating — is a laterality wrinkle. The right stellate ganglion dominates sinus-node innervation, and it’s usually the right side that gets blocked for anxiety/PTSD-type indications. In healthy volunteers, right SGB dropped both the sympathetic (LF) and the parasympathetic (HF) HRV components — right stellate block attenuated not only sympathetic but also parasympathetic activity. So it flattened total autonomic modulation rather than tilting cleanly toward vagus. Left-sided blocks look better on paper — one study in head/neck pain patients found a significant increase in high-frequency power and a decrease in the LF/HF ratio after left stellate block, suggesting increased parasympathetic activity — but even there the literature contradicts itself (another readout of that same dataset shows lnHF falling), and the field openly calls the cardiovascular effect controversial. Net: “SGB → higher HRV” is not a safe prediction from the physiology. You could nudge it down. PubMedPubMed Central
So, hypotheses, roughly ranked:
H1 — real autonomic “reset,” durable (plausible, ~0.4). The PTSD story is the strongest thing going for this: symptom relief outlasts the anesthetic by weeks, implying some central recalibration of the arousal circuitry rather than just a numb ganglion. And there’s mechanistic breadcrumbs for sleep specifically — a double-blind GAD+insomnia RCT reported greater reductions in anxiety and depression scores with SGB than with CBT plus estazolam, alongside measured drops in norepinephrine. The awakenings angle has its own origin story: Lipov’s 2008 pilot showed SGB reduced hot flushes and night awakenings in breast cancer survivors — i.e., fewer sympathetically-driven nocturnal surges, fewer wake-ups. If your awakenings ride on autonomic spikes, that’s the mechanism you’re betting on. nihFrontiers
H2 — real but mostly nonspecific / expectancy-loaded (plausible-to-likely, ~0.35). Most of the sleep evidence is open-label or active-comparator, heavily Chinese, and some of it reports response rates like 98.4% efficacy — which, for insomnia, is a flashing red light for weak blinding and publication bias, not a triumph. A needle-in-the-neck with a visible droopy eyelid is about the most placebo-potent thing you can do to a nervous system. A 2026 meta-analysis on SGB-for-sleep basically says “promising, now please do real multicenter RCTs.” Translation: the clean sham-controlled PSG+HRV trial in ordinary chronic insomniacs doesn’t really exist yet. nih
H3 — your awakenings aren’t stellate-gated in the first place (plausible, ~0.3, and this is the one that actually decides your outcome). Awakenings have many generators: apnea/UARS (extremely common, produces sympathetic-flavored microarousals — but the fix is airway, not a ganglion), PLMD, circadian misalignment, cortisol/HPA timing, alcohol. Only the “hyperarousal insomnia” phenotype is the clean fit for SGB’s rationale. If that’s you, great fit. If you’ve got undiagnosed mild apnea, SGB does nothing for the cause.
H4 — Janusian / it’s downstream (can’t rule out, ~0.1). The overarousal might be a readout of bad sleep and anxiety, not the generator — in which case peripherally muting one ganglion treats the gauge, not the engine.
(Plus real mass reserved for something none of these captures.)
Here’s the part I’d actually act on — the distinguishing evidence. Before anyone puts a needle near your vertebral artery, test the premise cheaply and reversibly:
- Pharmacological probe. A short trial of something that dampens sympathetic outflow chemically — prazosin (α1-blocker, the classic for nocturnal sympathetically-mediated arousals, dosed at night) or clonidine/guanfacine (α2 agonists, cut central sympathetic drive). If one of these measurably shrinks your awakenings, you’ve confirmed the model and you might just keep using the cheap reversible thing. If they do nothing, the whole sympathetic hypothesis is shaky and SGB is a poor bet. This is worth more than any confidence number I can give you.
- Rule out the apnea confounder with a night of home oximetry / a home sleep test. Cheap, and it’s the single most common thing masquerading as “arousal.”
- Free version of the mechanism: resonance-frequency breathing (~5.5–6 breaths/min) for 10–15 min pre-sleep directly raises HRV and baroreflex gain and lowers sympathetic tone. It’s basically an at-home, nightly, zero-risk dry run of “shift toward parasympathetic.” If it helps, that’s your answer too.