## Pain Fibre Classification and Function **Key Point:** A-delta fibres are responsible for sharp, well-localized, fast pain (first pain), while C fibres mediate slow, burning, poorly localized pain (second pain). ### Fibre Types in Pain Transmission | Fibre Type | Diameter (μm) | Conduction Velocity (m/s) | Pain Quality | Latency | Receptor Type | | --- | --- | --- | --- | --- | --- | | **A-delta** | 2–5 | 5–30 | Sharp, pricking, well-localized | Fast (0.1 s) | Mechanical nociceptors | | **C** | 0.4–1.2 | 0.5–2 | Burning, aching, poorly localized | Slow (1–2 s) | Polymodal nociceptors | | A-beta | 5–15 | 30–70 | Touch, pressure (non-nociceptive) | — | Mechanoreceptors | | B | 1–3 | 3–15 | Preganglionic sympathetic (non-nociceptive) | — | Autonomic fibres | **High-Yield:** The dual pain response—initial sharp pain followed by delayed burning pain—reflects the sequential activation of A-delta and C fibres. This is clinically evident when you prick your finger: you feel a sharp sting immediately, then a duller ache. ### Anatomical Basis 1. **A-delta fibres** are lightly myelinated → faster conduction 2. **C fibres** are unmyelinated → slower conduction 3. Both synapse in the **dorsal horn** (substantia gelatinosa, laminae I–II) 4. Signals cross the midline and ascend in the **spinothalamic tract** **Clinical Pearl:** Patients with selective A-delta fibre damage (e.g., from certain toxins or neuropathies) lose sharp pain sensation but retain burning pain, confirming the functional dissociation. **Mnemonic:** **A-delta = Acute pain** (sharp, fast); **C = Chronic-type pain** (slow, burning).
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