Autonomic outflow

Sudomotor fibres to eccrine sweat glands, which act on M3 muscarinic receptors. This is why antimuscarinic drugs stop sweating (hot, dry skin in anticholinergic toxicity), why botulinum toxin treats hyperhidrosis, and why hypoglycaemic sweating persists in a patient on β-blockers even though tremor and palpitations are masked. The adrenal medulla is also cholinergic, but that is a preganglionic synapse on nicotinic receptors.

Sudomotor fibres to the face leave the pathway at the superior cervical ganglion with the external carotid artery, so facial anhidrosis means the lesion is central or preganglionic (brainstem, cervical cord, T1 root, lung apex, cervical chain). A postganglionic lesion along the internal carotid (dissection, cavernous sinus) spares facial sweating and is often painful. Pharmacologically, apraclonidine reverses the anisocoria in any Horner but does not localise; hydroxyamphetamine dilates a central or preganglionic Horner pupil but not a postganglionic one.

At the splenic flexure, roughly the distal third of the transverse colon — the midgut–hindgut boundary. Beyond that, the pelvic splanchnic nerves (S2–S4) ascend through the inferior and superior hypogastric plexuses to the descending colon, sigmoid and rectum. Sympathetic and referred-pain levels follow the same embryological split: foregut T5–T9, midgut T10–T11, hindgut L1–L2.

Acetylcholine on neuronal nicotinic (N_N) receptors, in both sympathetic and parasympathetic ganglia and on adrenal chromaffin cells. This is why ganglion-blocking drugs abolished both divisions at once, and why muscarinic antagonists such as atropine leave ganglionic transmission intact and act only at postganglionic parasympathetic targets (and sweat glands). Neuromuscular junction nicotinic receptors (N_M) are a different subtype, so non-depolarising muscle relaxants largely spare the ganglia.

Preganglionic pupillomotor fibres from the Edinger–Westphal nucleus run superficially in CN III with their own pial blood supply. External compression by a posterior communicating artery aneurysm or uncal herniation hits them first, giving a dilated pupil early. Microvascular infarction from diabetes or hypertension affects the core of the nerve and leaves the superficial fibres perfused, so the pupil stays reactive.

Erection ('point') is parasympathetic, S2–S4, mediated by nitric oxide from the cavernous nerves; emission and ejaculation ('shoot') are sympathetic, L1–L2, via α1 receptors on the vas deferens, seminal vesicles and bladder neck. Injury to the superior hypogastric plexus therefore causes retrograde ejaculation with preserved erection, whereas injury to the pelvic plexus or cavernous nerves causes erectile dysfunction with preserved emission.