Pain pathways and labour pain
Pain pathways, labour pain and thermal sensation; the micturition reflex
Pain travels on two fibre types, crosses in the cord, ascends in the spinothalamic tract and can be damped at the dorsal horn. Labour pain, epidurals, post-dural puncture headache, heat loss in mother, fetus and newborn, and bladder control after delivery all rest on this physiology.
Nociceptors and thermoreceptors
- Nociceptors are unencapsulated (bare) nerve endings. They show little or no adaptation, so pain persists as long as the stimulus does (a toothache does not fade like the feel of clothes).
- In injured tissue COX-2 makes PGE2, which sensitises nociceptors (hyperalgesia); NSAIDs work by reducing sensitisation.
- Warmth receptors fire at about 30–45 °C and cold receptors below skin temperature. Above about 45 °C heat activates heat nociceptors (TRPV1), the channel also opened by capsaicin.
Two kinds of pain fibre
| Feature | Aδ fibres | C fibres |
|---|---|---|
| Myelin and speed | Thinly myelinated, 6–30 m/s | Unmyelinated, 0.5–2 m/s |
| Pain quality | Fast, first pain: sharp, pricking, well localised | Slow, second pain: dull, burning, poorly localised, distressing |
| Transmitter in dorsal horn | Glutamate | Glutamate plus substance P |
| Dorsal horn laminae | I and V | II (substantia gelatinosa), relaying to I and V |
| Tract and ending | Neospinothalamic: VPL thalamus to S1 cortex | Paleospinothalamic: reticular formation, intralaminar thalamus |
The ascending pathway
- First-order neuron: cell body in the dorsal root ganglion; synapses in the dorsal horn.
- Second-order neuron: in the dorsal horn; its axon crosses in the anterior white commissure within one or two segments and ascends in the lateral spinothalamic tract (pain and temperature). The anterior spinothalamic tract carries crude touch and pressure.
- Third-order neuron: thalamus to cortex. S1 gives location and intensity; the anterior cingulate cortex and insula give unpleasantness, which anxiety amplifies.
- A dense neuraxial block abolishes spinothalamic input, so a hot water bottle can burn a numb leg unnoticed.
Modulation: the gate and descending control
- Gate control theory: Aβ touch fibres excite inhibitory interneurons in the substantia gelatinosa, reducing C-fibre transmission; rubbing and TENS (early labour) work this way.
- Descending inhibition: beta-endorphin (rising in labour) acts in the periaqueductal grey, which drives the nucleus raphe magnus; descending serotonin and noradrenaline fibres inhibit the dorsal horn.
- Enkephalin interneurons inhibit substance P release. Epidural opioids act on mu receptors in lamina II, without motor or sympathetic block.
Referred pain and labour pain
- Referred pain arises from convergence of visceral and somatic afferents on the same dorsal horn neurons; the brain projects the pain to the skin of that segment. Heart: T1–T4, inner arm. Diaphragm: C3–C5, shoulder tip.
| Stage | Source | Nerves and segments | Where felt |
|---|---|---|---|
| First stage | Uterine contraction and cervical dilatation (visceral) | Afferents with sympathetic nerves via the hypogastric plexus to T10–L1 | Lower abdomen, above the pubis, lower back |
| Second stage | Stretch of vagina, perineum and pelvic floor (somatic) | Pudendal nerve, S2–S4 | Perineum, rectum; sharp and localised |
- Epidurals often show sacral sparing: the large L5–S2 roots take up drug slowly, so perineal pain may persist; sitting up for top-ups helps.
- Unrelieved pain causes a catecholamine surge: noradrenaline constricts uterine arteries (late decelerations) and adrenaline causes incoordinate contractions; effective analgesia lowers catecholamines.
Headache in obstetric practice
- Brain substance has no nociceptors; dura, sinuses and large vessels do. Above the tentorium pain travels in the trigeminal nerve (V1) (forehead, behind the eyes); below it in C2–C3 (occiput).
- Post-dural puncture headache: CSF leak lets the brain sag when upright, pulling on dura and veins. It is postural: worse sitting, relieved lying flat; MRI may show smooth dural enhancement. Prevent with a fine pencil-point needle; caffeine (adenosine antagonist) helps briefly; an epidural blood patch seals the leak.
- Raised CSF pressure (idiopathic intracranial hypertension) gives headache worse lying down, with papilloedema. Menstrual migraine follows oestrogen withdrawal and usually settles in mid-pregnancy.
Thermal physiology in pregnancy, fetus and newborn
- Pregnancy raises metabolic rate; skin vasodilatation (warm hands, palmar erythema) dissipates the heat.
- The fetus is about 0.5 °C warmer than the mother and loses about 85% of its heat through the placenta. Maternal fever therefore heats the fetus, raising its metabolism and causing fetal tachycardia (chorioamnionitis).
- A wet newborn loses heat mainly by evaporation, so dry at once. Cold stress drives brown fat non-shivering thermogenesis, using oxygen and glucose and causing hypoglycaemia and acidosis.
Micturition reflex
| Supply | Origin | Action |
|---|---|---|
| Parasympathetic (pelvic splanchnic) | S2–S4 | Detrusor contraction via M3 receptors |
| Sympathetic (hypogastric) | T11–L2 | Detrusor relaxation (β3); bladder neck contraction (α1A) |
| Somatic (pudendal) | S2–S4 | External urethral sphincter (nicotinic) |
- Stretch receptors in the filling bladder trigger the sacral spinal reflex; once contraction begins it raises afferent firing further, a positive feedback loop that empties the bladder.
- The pontine micturition centre coordinates detrusor contraction with sphincter relaxation; the medial frontal cortex inhibits voiding until convenient.
- Lesions: medial frontal (meningioma, anterior cerebral artery stroke) gives uninhibited but coordinated voiding; spinal cord above the sacrum gives a reflex bladder with detrusor–sphincter dyssynergia; sacral roots or cauda equina (central disc prolapse) give a large, insensate, areflexic bladder with overflow.
- Oxybutynin blocks M3 (urge incontinence); tamsulosin blocks α1A at the bladder neck.
Remember First stage pain is visceral and T10–L1; second stage pain is somatic and S2–S4 through the pudendal nerve.
Exam trap The micturition reflex centre is sacral (S2–S4) and its coordinating centre is in the pons, not the cortex; the cortex only inhibits.
Exam trap C fibres release substance P as well as glutamate; fast Aδ pain uses glutamate.
Test yourself on this topic
5 of the 35 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A primigravida in severe pain without analgesia has rising plasma adrenaline and noradrenaline, irregular contractions and a CTG showing late decelerations. After an effective epidural, her catecholamines fall and the CTG improves. How does unrelieved labour pain mainly threaten the fetus?
Answer: Catecholamines constrict the uterine arteries
Severe labour pain activates the sympathetic nervous system and adrenal medulla. Noradrenaline constricts the uterine arteries through alpha-adrenoceptors, reducing uteroplacental blood flow, while adrenaline's beta-2 effect on the myometrium can make contractions incoordinate. Pain-driven hyperventilation adds hypocapnia. Effective neuraxial analgesia lowers catecholamine levels and can improve placental perfusion.
Labour pain and the fetus
- Pain: sympathetic surge
- Noradrenaline: uterine vasoconstriction
- Adrenaline: incoordinate contractions
- Epidural lowers catecholamines
Remember Pain relief is also fetal protection.
Exam trap Epidural hypotension can also reduce placental flow, so BP must be maintained.
Why the other options are wrong
- Pain fibres directly slow the fetal heart Maternal pain fibres do not reach the fetus.
- Endorphins cross and depress the fetus Endorphins are not the cause of fetal compromise.
- Pain raises maternal haemoglobin Not the mechanism.
- Pain lowers maternal cardiac output Pain tends to raise cardiac output.
A woman with a poor urinary stream and high residual volume has urodynamic evidence of bladder neck obstruction with normal detrusor contractions. She improves on tamsulosin. On which receptors does this drug act?
Answer: Alpha-1 receptors at the bladder neck
The bladder neck and proximal urethra contain smooth muscle rich in alpha-1 (mainly alpha-1A) adrenoceptors. Sympathetic fibres from T11–L2 contract this muscle during bladder filling to help continence. Tamsulosin blocks these receptors, relaxing the bladder neck and lowering outflow resistance. Alpha agonists, such as decongestants, can do the opposite and precipitate retention.
Bladder outlet receptors
- Bladder neck: alpha-1A
- Sympathetic T11–L2
- Tamsulosin relaxes the outlet
- Alpha agonists can cause retention
Remember Alpha-1 tone keeps the bladder neck closed.
Exam trap Tamsulosin commonly causes postural hypotension, especially with the first dose.
Why the other options are wrong
- Muscarinic M3 receptors on the detrusor Blocking M3 would weaken voiding.
- Beta-3 receptors on the detrusor Beta-3 agonists relax the detrusor during storage.
- Nicotinic receptors on the sphincter The external sphincter is striated muscle with nicotinic receptors; tamsulosin does not act there.
- Dopamine receptors in the urethra Not the target.
At 20 weeks, an obese 28-year-old woman has daily headaches worse on lying down and in the morning, transient visual blurring and bilateral papilloedema. MRI shows no mass or venous thrombosis, and lumbar puncture opening pressure is 34 cm H2O with normal CSF. What causes her headache?
Answer: Raised CSF pressure stretching the dura
Idiopathic intracranial hypertension causes raised CSF pressure without a mass, hydrocephalus or abnormal CSF, probably from impaired CSF absorption and raised venous sinus pressure, and is associated with obesity and weight gain. The high pressure distends pain-sensitive dura and vessels, giving headache worse lying down, and is transmitted along the optic nerve sheaths, causing papilloedema and visual loss. It may worsen with weight gain in pregnancy.
Raised CSF pressure
- Obesity, young women
- Opening pressure > 25 cm H2O
- Papilloedema, visual blurring
- Headache worse lying down
Remember High-pressure headache is worse lying flat; low-pressure headache is worse standing.
Exam trap Vision, not headache, is what is at risk in idiopathic intracranial hypertension.
Why the other options are wrong
- Low CSF pressure from a leak Low pressure causes headache on standing, relieved by lying.
- Bleeding into the subarachnoid space CSF is normal.
- Infection of the meninges CSF is normal and there is no fever.
- Pituitary tumour compressing the chiasm MRI shows no mass.
A woman with a labour epidural has good relief of contraction pain from T10 to L1, but as the head descends she has persistent pain in the perineum and rectum. Top-ups given sitting up eventually relieve it. Why are the sacral segments often the last to be blocked by an epidural?
Answer: The sacral roots are thick
The L5, S1 and S2 nerve roots are the largest in diameter, so local anaesthetic takes longer to penetrate them, and the drug injected in the lumbar epidural space spreads more readily upwards than down to the sacral segments. This produces sacral sparing, leaving second-stage perineal pain carried by S2–S4 in the pudendal nerve. Larger volumes or top-ups in the sitting position encourage caudal spread.
Sacral sparing
- Large L5–S2 roots
- Slow drug penetration
- Spread favours upward
- Sit up and top up for sacral spread
Remember Thick sacral roots are slow to go numb.
Exam trap Perineal pain with a working epidural is often sacral sparing, not a failed catheter.
Why the other options are wrong
- The sacral roots lack myelin Sacral roots are myelinated.
- The epidural space ends at L2 The epidural space extends to the sacral hiatus.
- Sacral fibres are motor only Sacral roots carry sensory as well as motor fibres.
- Sacral pain is carried by the vagus Perineal pain is carried by the pudendal nerve (S2–S4).
At 30 weeks, a healthy woman notices warm hands, palmar redness and that she feels hot and sweats easily, even in mild weather. What is the main physiological purpose of the increased skin blood flow in pregnancy?
Answer: Dissipating extra metabolic heat
Pregnancy raises the metabolic rate through the fetus, placenta and increased maternal cardiac, respiratory and renal work, so more heat is produced. Hormone-driven vasodilatation increases skin blood flow, especially in the hands and feet, carrying heat to the surface for loss by radiation, convection and sweating. This keeps core temperature from rising, protecting the fetus, whose temperature runs about 0.5 °C above the mother's.
Heat loss in pregnancy
- Metabolic rate rises
- Skin vasodilatation
- Warm hands, palmar erythema
- Protects fetal temperature
Remember Pregnant women run warm and dump heat through the skin.
Exam trap Palmar erythema in pregnancy is usually physiological, not a sign of liver disease.
Why the other options are wrong
- Raising systemic vascular resistance Skin vasodilatation lowers SVR.
- Supplying the skin's own oxygen needs Skin flow far exceeds its own metabolic needs.
- Increasing venous return Skin pooling does not increase venous return.
- Storing blood for delivery Skin does not act as a reserve for delivery.
Where this sits in the CPSP syllabus
- Obstetrics & Gynaecology, Paper 2: Systems physiology for obstetrics, Pain pathways, labour pain and thermal sensation; micturition reflex
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