6.4 Neurophysiology, Pain and the Autonomic Nervous System
Key Takeaways
- Local anaesthetics bind the intracellular face of the voltage-gated sodium channel, so the un-ionised base must first cross the nerve membrane.
- Small unmyelinated C fibres are blocked before large myelinated fibres, which is why pain is lost before pressure sensation.
- Orofacial nociception relays in the subnucleus caudalis of the spinal trigeminal nucleus before ascending to the thalamus.
- Gate control theory explains why rubbing the cheek after an injection reduces pain, through A-beta activation of inhibitory interneurones.
- The four parasympathetic ganglia of the head are the ciliary, pterygopalatine, submandibular and otic, the last supplying the parotid via the auriculotemporal nerve.
The Neurone and the Action Potential
The resting membrane potential of about -70 mV is maintained by the Na⁺/K⁺-ATPase pump and by selective potassium permeability. Depolarisation to threshold opens voltage-gated sodium channels, sodium enters, and the membrane potential rapidly reverses. Repolarisation follows from sodium channel inactivation and delayed potassium efflux.
This is the sequence that local anaesthetics interrupt. They bind the intracellular surface of the voltage-gated sodium channel, preferentially in its open or inactivated state, so the un-ionised base must cross the axolemma before the protonated cation can act. Myelinated fibres conduct by saltatory conduction between nodes of Ranvier and therefore require blockade of only two to three consecutive nodes.
Sensory Fibre Types
| Fibre | Myelination | Diameter | Conduction | Modality |
|---|---|---|---|---|
| A-alpha | Heavy | 13–20 µm | 80–120 m/s | Proprioception, motor |
| A-beta | Heavy | 6–12 µm | 35–75 m/s | Touch, pressure, vibration |
| A-delta | Thin | 1–5 µm | 5–30 m/s | Fast, sharp, well-localised pain; cold |
| C | None | 0.4–1.2 µm | 0.5–2 m/s | Slow, dull, poorly localised pain; heat |
Small unmyelinated C fibres are blocked by local anaesthetic before large myelinated fibres, which is why patients typically lose pain sensation before touch and pressure and can still feel the pressure of an elevator while feeling no pain.
Pain Pathways and Modulation
Nociceptive input from the orofacial region enters through the trigeminal nerve to the trigeminal brainstem sensory nuclear complex. The spinal nucleus of the trigeminal nerve, specifically its subnucleus caudalis, is the principal relay for pain and temperature; second-order neurones then decussate and ascend in the trigeminothalamic tract to the ventral posteromedial nucleus of the thalamus and on to the somatosensory cortex.
Two modulation mechanisms explain everyday clinical observations:
- Gate control theory. Large A-beta afferents activate inhibitory interneurones in the dorsal horn that reduce transmission from C fibres. Rubbing the cheek after an injection genuinely reduces pain.
- Descending inhibition. Periaqueductal grey and rostral ventromedial medulla projections release endogenous opioids, serotonin and noradrenaline onto the dorsal horn. Anxiety and poor sleep suppress this system, which is part of why anxious patients experience more pain from identical stimuli.
Referred pain occurs because trigeminal afferents from different structures converge on shared second-order neurones. This is why pulpal pain is poorly localised across the midline of a quadrant, why maxillary sinusitis presents as upper posterior toothache, and why cardiac ischaemia can refer to the left mandible.
The Autonomic Nervous System in the Head and Neck
| Ganglion | Preganglionic source | Postganglionic target |
|---|---|---|
| Ciliary | CN III (Edinger-Westphal nucleus) | Sphincter pupillae, ciliary muscle |
| Pterygopalatine | CN VII via greater petrosal nerve | Lacrimal gland, nasal and palatal glands |
| Submandibular | CN VII via chorda tympani and lingual nerve | Submandibular and sublingual glands |
| Otic | CN IX via lesser petrosal nerve | Parotid gland, via auriculotemporal nerve |
Sympathetic supply to the whole head arises from T1–T2, synapses in the superior cervical ganglion, and travels on the carotid arteries. Interruption of this chain produces Horner's syndrome — ptosis, miosis and anhidrosis — which may be the first sign of an apical lung tumour or of a carotid dissection presenting with facial pain.
Exam link. Aberrant regeneration of parasympathetic fibres from the otic ganglion into sweat glands after parotid surgery produces Frey's syndrome: gustatory sweating and flushing over the parotid region. The anatomy explains the symptom, and the minor starch-iodine test confirms it.
Pain Mechanisms Behind Common Dental Presentations
The classification of pain into nociceptive, inflammatory and neuropathic categories does clinical work in the exam. Nociceptive and inflammatory pain arises from tissue injury and mediator release; it is reproducible by stimulus, responds to removal of the cause and to anti-inflammatory analgesia, and is the mechanism of pulpitis and apical periodontitis. Neuropathic pain arises from a lesion or disease of the somatosensory system; it is often described as burning, shooting or electric, may be accompanied by altered sensation, does not respond to conventional analgesics, and is the mechanism of trigeminal neuralgia and of persistent idiopathic facial pain. The clinical consequence is that a patient whose pain does not fit the nociceptive pattern should not receive irreversible dental treatment in the hope of relief — repeated endodontic treatment and extraction for undiagnosed neuropathic pain is a recognised iatrogenic harm and a favourite examination scenario.
Sensitisation, Referred Pain and Local Anaesthetic Failure
Peripheral sensitisation is the reduction in nociceptor threshold produced by inflammatory mediators, and explains why an inflamed pulp responds painfully to a stimulus that a healthy pulp ignores. Central sensitisation is amplified processing in the dorsal horn and trigeminal nucleus, and explains allodynia, secondary hyperalgesia and the spread of pain beyond the injured tooth. Convergence of afferents from different structures onto the same second-order neurones in the trigeminal nuclear complex explains referred pain — why a lower molar pulpitis is felt in the ear or the ipsilateral upper quadrant, and why patients so often misidentify the offending tooth.
Sensitisation also explains a practical problem: local anaesthetic failure in an acutely inflamed tooth. Inflamed tissue is acidic, so less of the anaesthetic exists in the un-ionised form that crosses the nerve membrane; inflamed nociceptors also up-regulate tetrodotoxin-resistant sodium channels that are less sensitive to blockade, and the nerve is already firing spontaneously. The correct response is supplementary technique — intraosseous, intraligamentary or intrapulpal anaesthesia, or a more proximal block — not simply more solution at the same site.