Sensory Physiology & Pain

The somatosensory system converts physical stimuli (touch, temperature, pain, position) into neural signals, codes their modality, intensity, location and duration, and relays them to the cortex through two great ascending highways. Pain physiology, in particular, is a NEET PG favourite because it ties receptor biology, tract anatomy, the gate-control theory and analgesic pharmacology into one integrated story.

Sensory receptor classification

A receptor is the peripheral transducer that converts a stimulus into a graded receptor (generator) potential, which, on reaching threshold, triggers action potentials in the afferent fibre. Receptors are classified two ways — by the modality (form of energy) they detect and by their rate of adaptation.

By modality (the classic five classes)

Receptor class	Stimulus detected	Examples
Mechanoreceptors	Mechanical deformation/pressure	Meissner, Pacinian, Merkel, Ruffini, hair-cell, muscle spindle
Thermoreceptors	Temperature change	Cold (Krause), warm endings; TRP channels
Nociceptors	Tissue-damaging stimuli	Free nerve endings
Chemoreceptors	Chemical concentration	Carotid/aortic bodies, taste, smell
Photoreceptors	Light	Rods, cones

High-yield: The Pacinian corpuscle is the prototype receptor for studying transduction. Its onion-like lamellated capsule is responsible for its rapid adaptation; if you strip the capsule and apply pressure directly to the naked nerve ending, adaptation slows dramatically. This proves the capsule (not the nerve) causes rapid adaptation.

By rate of adaptation

Adaptation = decline in receptor firing despite a maintained stimulus.

Type	Adaptation	Detects	Examples
Tonic (slowly adapting)	Slow / minimal	Sustained stimulus, position	Muscle spindle, Merkel disc, Ruffini, nociceptors, baroreceptor (partially), carotid body
Phasic (rapidly adapting)	Fast	Change/rate of stimulus, velocity	Meissner, hair follicle
Very rapidly adapting	Very fast	Vibration, acceleration	Pacinian corpuscle

High-yield: Nociceptors do NOT adapt — in fact they sensitise (hyperalgesia). This is teleologically protective: pain should persist as long as tissue damage continues. Smell and touch (Meissner/Pacinian) adapt strongly; muscle spindle and pain adapt poorly.

Cutaneous mechanoreceptor map (very commonly asked):

Receptor	Adaptation	Field	Function
Meissner corpuscle	Rapid	Small	Light/flutter touch, low-frequency vibration (~30–50 Hz)
Merkel disc	Slow	Small	Steady pressure, texture, form (2-point discrimination)
Pacinian corpuscle	Very rapid	Large	Deep pressure, high-frequency vibration (~250–300 Hz)
Ruffini ending	Slow	Large	Skin stretch, sustained pressure

Mnemonic — "SA = Surface/Steady, deep = Pacinian": small fields (Meissner, Merkel) sit superficially for fine discrimination; large fields (Pacinian, Ruffini) sit deep.

Nerve fibre types & sensory transduction

The conduction velocity and diameter of the afferent fibre determine which sensation it carries.

Fibre	Diameter / Myelin	Velocity	Function
Aα (Ia, Ib)	Large, myelinated	~70–120 m/s	Proprioception (spindle, GTO)
Aβ (II)	Large, myelinated	~30–70 m/s	Touch, pressure, vibration
Aδ (III)	Small, thinly myelinated	~5–30 m/s	Fast/first pain, cold
C (IV)	Smallest, unmyelinated	~0.5–2 m/s	Slow/second pain, warmth, itch

High-yield: Pain is carried by Aδ (fast, sharp, well-localised, "first pain") and C fibres (slow, dull, burning, poorly localised, "second pain"). The double-pain phenomenon (a sharp prick followed seconds later by a throbbing ache) reflects the velocity difference between Aδ and C fibres.

Transduction TRP channels (frequently tested):

• TRPV1 — capsaicin receptor; activated by heat >43°C and protons (acid). Central to burning pain and inflammatory hyperalgesia.
• TRPM8 — menthol/cool receptor (~8–28°C).
• TRPA1 — noxious cold, mustard oil, allyl isothiocyanate.

Sensory coding

The CNS extracts four attributes of every stimulus:

1. Modality → coded by the labelled line (specific receptor + dedicated pathway).
2. Intensity → coded by frequency of firing (rate code) and number of receptors recruited (population code).
3. Location → coded by receptive field size and lateral inhibition (sharpens contrast/edges, improves 2-point discrimination).
4. Duration → coded by adaptation (tonic vs phasic).

High-yield: Weber–Fechner law — perceived intensity is proportional to the logarithm of stimulus strength. Stevens' power law is a more general refinement. Law of specific nerve energies (Müller) — stimulating a sensory pathway by any means evokes that pathway's specific modality (e.g., pressure on the eye produces light/phosphenes, not pressure).

Dermatomes & spinal organisation

A dermatome is the strip of skin innervated by a single dorsal (spinal) nerve root. Adjacent dermatomes overlap, so a single root lesion rarely produces complete anaesthesia.

High-yield dermatome landmarks:

• C6 – thumb; C7 – middle finger; C8 – little finger
• T4 – nipple; T10 – umbilicus; L1 – inguinal/groin
• L4 – medial malleus/knee; L5 – dorsum of foot, big toe; S1 – lateral foot/little toe
• S2–S4 – perianal "saddle"

High-yield: T4 = teat (nipple), T10 = belly butT-TEN (umbilicus), L1 = IL1nguinal. Saddle anaesthesia (S2–S4) suggests cauda equina syndrome.

Ascending pathways — the two highways

DCML (fine touch, vibration, proprioception)   Anterolateral / Spinothalamic (pain, temperature, crude touch)

Dorsal Column–Medial Lemniscus (DCML)

Fine (epicritic) touch, vibration, conscious proprioception, two-point discrimination.

1° neuron (DRG) → ascends ipsilaterally in fasciculus gracilis (lower limb) / cuneatus (upper limb) → synapses in nucleus gracilis/cuneatus (medulla) → 2° neuron decussates as internal arcuate fibres → medial lemniscus → VPL of thalamus → 3° neuron → postcentral gyrus (S1).

Decussation is in the medulla (high). Lesion below decussation → ipsilateral loss; above → contralateral loss.

Anterolateral / Spinothalamic system

Pain, temperature, crude touch (protopathic).

1° neuron (DRG) → enters dorsal horn, synapses (often via Lissauer's tract, substance P / glutamate) → 2° neuron decussates within 1–2 segments in the anterior white commissure → ascends contralaterally as the lateral (pain/temp) & anterior (crude touch) spinothalamic tract → VPL of thalamus → 3° neuron → S1.

High-yield: The crucial clinical contrast — DCML decussates in the medulla; spinothalamic decussates in the spinal cord (1–2 segments above entry). Hence a hemisection (Brown-Séquard) gives ipsilateral loss of fine touch/proprioception/motor below the lesion but contralateral loss of pain/temperature (starting ~1–2 segments below).

The spinoreticular tract is the second pain pathway: it is bilateral, polysynaptic, terminates in the reticular formation → intralaminar thalamic nuclei → diffuse cortex. It mediates the affective–arousal, poorly localised, dull aching component of pain and is the substrate of "slow" C-fibre pain. The spinomesencephalic (spinotectal) tract activates the periaqueductal grey (PAG) for descending analgesia.

Pain physiology

Pain = an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Nociception is the neural detection of noxious stimuli; pain is the conscious percept.

Sensitisers (inflammatory soup): bradykinin (most potent algogen), prostaglandins (PGE2 sensitises nociceptors — basis of NSAID action), substance P, H⁺, K⁺, histamine, serotonin, ATP, leukotrienes, nerve growth factor.

• Hyperalgesia — exaggerated pain to a normally painful stimulus.
• Allodynia — pain from a normally non-painful stimulus (e.g., light touch).
• Primary hyperalgesia (at injury site) vs secondary hyperalgesia (surrounding skin, central sensitisation, "wind-up" via NMDA receptors).

Melzack–Wall Gate Control Theory (1965)

The central NEET PG concept linking touch and pain.

Premise: the substantia gelatinosa (lamina II of dorsal horn) acts as a "gate" controlling transmission from afferents to the projection (T) cell that feeds the spinothalamic tract.

Mechanism (flow):

1. Large Aβ fibres (touch/vibration) → excite the inhibitory interneuron in substantia gelatinosa → this closes the gate → less pain transmitted to the T cell.
2. Small Aδ/C fibres (pain) → inhibit the inhibitory interneuron → open the gate → more pain.
3. Descending fibres from the brain also modulate the gate.

Net rule: Activity in large fibres closes; activity in small fibres opens the gate.

High-yield: Gate control explains why rubbing/massaging a painful area, TENS (transcutaneous electrical nerve stimulation) and dorsal column stimulation relieve pain — they recruit large Aβ fibres that close the gate. This is the single most asked pain-physiology concept.

Referred pain — convergence

Visceral pain is felt at a distant somatic (cutaneous) site supplied by the same spinal segment.

High-yield: Mechanism = convergence-projection theory — visceral and somatic afferents converge on the same second-order spinothalamic neuron; the brain, having more experience with somatic input, mislocalises visceral pain to the skin dermatome.

Classic referrals: diaphragm/heart → C3–C5 → shoulder/left arm (MI); gallbladder → right inferior scapula; appendix → periumbilical (T10) then RIF; ureter → groin/testis; diaphragmatic irritation → tip of shoulder (Kehr's sign).

Endogenous analgesic (descending) system

A built-in opioid pathway that dampens pain at the dorsal horn.

Flow: PAG (periaqueductal grey, midbrain) → nucleus raphe magnus (serotonergic) + locus coeruleus (noradrenergic) → descend in the dorsolateral funiculus → dorsal horn → release serotonin/noradrenaline + enkephalin → presynaptic & postsynaptic inhibition of pain transmission.

High-yield: Stimulation of the PAG produces profound stimulation-produced analgesia, reversed by naloxone — proving it is opioid-mediated.

Endogenous opioids and receptors:

Peptide	Precursor	Main receptor
β-endorphin	POMC	μ (mu)
Met/Leu-enkephalin	Proenkephalin	δ (delta)
Dynorphin	Prodynorphin	κ (kappa)

• μ (MOR) — analgesia (supraspinal/spinal), euphoria, respiratory depression, miosis, constipation, dependence (morphine's main target).
• κ (KOR) — spinal analgesia, dysphoria, miosis, less respiratory depression.
• δ (DOR) — analgesia, mood modulation.

High-yield: Opioid receptors are Gi-protein coupled → ↓ adenylyl cyclase/cAMP, open K⁺ channels (hyperpolarise, postsynaptic) and close voltage-gated Ca²⁺ channels (↓ neurotransmitter release, presynaptic). Net effect = reduced excitability and reduced substance P release.

Analgesic pharmacology integration

• NSAIDs / paracetamol — inhibit COX → ↓ prostaglandin → ↓ peripheral sensitisation. Paracetamol acts largely centrally; ceiling effect; good for nociceptive/somatic pain.
• Opioids (morphine, fentanyl, tramadol) — agonise μ receptors centrally and at the dorsal horn; tramadol additionally inhibits serotonin/noradrenaline reuptake (boosting descending analgesia).
• Local anaesthetics — block voltage-gated Na⁺ channels; small unmyelinated C and Aδ fibres are blocked first (order of loss: pain/temperature → touch → pressure → motor).
• Adjuvants for neuropathic pain — TCAs (amitriptyline) and SNRIs (duloxetine) enhance descending noradrenergic/serotonergic inhibition; gabapentin/pregabalin act on the α2δ subunit of voltage-gated Ca²⁺ channels; carbamazepine for trigeminal neuralgia.
• WHO analgesic ladder: non-opioid → weak opioid → strong opioid, with adjuvants at each step.

Diagnosis & clinical assessment

Sensory testing localises lesions:

• Vibration (128 Hz tuning fork) + proprioception + 2-point discrimination → test DCML / dorsal columns.
• Pinprick + temperature → test spinothalamic.
• Romberg's sign positive → dorsal column (proprioceptive) lesion (e.g., tabes dorsalis, B12 deficiency / subacute combined degeneration).
• Dissociated sensory loss (loss of pain/temperature with preserved touch/proprioception) → central cord lesion, classically syringomyelia (damages crossing fibres in anterior white commissure → "cape" distribution).
• Pain quantified by Visual Analogue Scale (VAS) / Numerical Rating Scale; neuropathic pain screened by DN4 / LANSS.

Complications & key clinical syndromes

Syndrome	Lesion	Sensory hallmark
Brown-Séquard	Cord hemisection	Ipsilateral DCML + motor loss; contralateral pain/temperature loss
Syringomyelia	Central canal expansion	Bilateral "cape" loss of pain/temperature, touch spared (dissociated)
Tabes dorsalis / SCD	Dorsal columns	Loss of vibration/proprioception, +Romberg, sensory ataxia
Anterior spinal artery	Ventral 2/3 cord	Bilateral pain/temp + motor loss below; DCML spared
Thalamic (Déjerine-Roussy)	VPL thalamus	Contralateral loss + spontaneous central pain
Causalgia / CRPS	Peripheral nerve	Burning pain, allodynia, autonomic changes

Key differentials of sensory loss

• Glove-and-stocking distribution → peripheral neuropathy (diabetes, B12).
• Dermatomal band → single nerve root / herpes zoster.
• Hemisensory (one side, including face) → contralateral thalamus or cortex.
• Dissociated, suspended → intramedullary (syringomyelia).
• Crossed (face one side, body other) → lateral medullary (Wallenberg) syndrome.

Recently asked / exam angle

• Receptor that adapts most rapidly → Pacinian corpuscle; capsule causes the rapid adaptation.
• Which receptor does not adapt → nociceptor (pain).
• Fast vs slow pain fibres → Aδ (fast/first), C (slow/second).
• Site of decussation: DCML = medulla; spinothalamic = spinal cord (anterior white commissure, 1–2 segments up).
• Gate control "gate" location → substantia gelatinosa (lamina II); large fibres close the gate (basis of TENS).
• Referred pain mechanism → convergence-projection.
• PAG-stimulation analgesia reversed by naloxone → opioid system.
• Capsaicin/heat >43°C receptor → TRPV1; menthol/cold → TRPM8.
• Most potent endogenous algogen → bradykinin; NSAIDs work by ↓ prostaglandin (PGE2).
• VPL thalamus = body sensation relay; VPM = face.
• Opioid receptor signalling → Gi, ↑K⁺ efflux, ↓Ca²⁺ influx.
• Romberg-positive sensory ataxia → dorsal column lesion.

Rapid revision

1. Pacinian = fastest-adapting, vibration/deep pressure; capsule = cause of adaptation.
2. Nociceptors don't adapt; they sensitise (hyperalgesia).
3. Meissner = light touch (small RF); Merkel = sustained pressure/texture; Ruffini = stretch; Pacinian = vibration.
4. Aδ = fast sharp first pain; C = slow dull burning second pain.
5. DCML = fine touch/vibration/proprioception, decussates in medulla → VPL.
6. Spinothalamic = pain/temp/crude touch, decussates in cord → VPL.
7. Brown-Séquard: ipsilateral DCML/motor, contralateral pain/temp loss.
8. Gate control (Melzack–Wall): large Aβ fibres close the gate at substantia gelatinosa → basis of TENS/rubbing.
9. Referred pain = convergence-projection on shared spinothalamic neuron (MI → left arm; diaphragm → shoulder).
10. Descending analgesia: PAG → raphe magnus/locus coeruleus → dorsal horn; PAG-stimulation analgesia is naloxone-reversible.
11. Opioid receptors μ/κ/δ are Gi-coupled (↑K⁺, ↓Ca²⁺); μ = analgesia + respiratory depression.
12. TRPV1 = capsaicin/heat >43°C; bradykinin = strongest algogen; syringomyelia = dissociated cape-like pain/temp loss.