11.3 Chemical Messengers

Time To Read

3–5 minutes

Date Last Modified

Age 45


Dysautonomia

1

Multi-Organ Autonomic Dysfunction

2

‘Revved’ Flares

3

Autonomic Symptoms Track Inflammation

4

Trigeminal Neuralgia

5

Cochlear Hair-Cell Injury

6

Two Cranial Nerves Affected 

7

Dysautonomia

The thing Stina’s doctors kept getting wrong was timing. Her racing heart and dry mouth didn’t track with anxiety or caffeine — they tracked with her flares. When her inflammatory markers climbed, so did her autonomic chaos; when the fire banked, her body settled. That coupling pointed away from “nerves” in the colloquial sense and toward the actual chemistry of the autonomic synapses — chemistry that inflammation is known to disturb.

Autonomic signaling runs on two main neurotransmitters and a small family of receptors. Every preganglionic neuron — sympathetic and parasympathetic alike — releases acetylcholine (ACh) onto nicotinic receptors at the ganglion. From there the divisions diverge: parasympathetic postganglionic neurons release ACh again, this time onto muscarinic receptors on the target organ, while most sympathetic postganglionic neurons release norepinephrine (NE) onto adrenergic receptors. So three receptor families do the work — nicotinic, muscarinic, and adrenergic — and the identity of the messenger and receptor determines whether an organ speeds up or slows down.

Here is the FMF connection: inflammatory cytokines can alter neurotransmitter release, shift receptor sensitivity, and bias the whole system toward sympathetic “revving.” Stina’s autonomic symptoms rose and fell with her inflammation because the inflammation was, quite literally, tampering with the chemistry of her autonomic synapses.

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