Pain - classification, etiology, and pathogenesis
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
- It serves as a protective mechanism to prevent further injury.
Classification
- 1 According to duration
- 2 According to origin
- 3 According to location
Etiology (Causes)
- 1 Physical causes
Trauma, surgery, burns.
Mechanical compression (e.g., disc herniation).
- 2 Chemical causes
Inflammatory mediators (e.g., prostaglandins, bradykinin).
Acidic pH in ischemic tissues.
- 3 Thermal causes
Extreme heat or cold.
- 4 Ischemia
Reduced blood supply leads to metabolite accumulation (e.g., angina).
- 5 Neurological causes
Nerve injury, demyelination (e.g., trigeminal neuralgia).
Pathogenesis
- 1 Nociception
Definition: The neural process of encoding noxious stimuli.
Steps
- 1 Transduction
Conversion of noxious stimuli into electrical signals in nociceptors (free nerve endings).
Mediators: prostaglandins, bradykinin, serotonin, substance P.
- 2 Transmission
Signal conducted via:
- Aδ fibers: fast, sharp, well- localized pain.
- C fibers: slow, dull, poorly localized pain.
Enter dorsal horn of spinal cord → cross to contralateral side → ascend via spinothalamic tract to thalamus and cortex.
- 3 Perception
Conscious awareness of pain in cerebral cortex.
Modulated by emotions, cognition, and previous experiences.
- 4 Modulation
Pain signals can be amplified or dampened at spinal and supraspinal levels.
Descending inhibitory pathways involve:
- Endogenous opioids (endorphins, enkephalins).
- Monoamines (serotonin, norepinephrine).
Peripheral sensitization
Increased responsiveness of nociceptors due to inflammatory mediators → lower threshold → hyperalgesia.
Central sensitization
Increased excitability of spinal neurons → prolonged pain perception, allodynia (pain from non- painful stimuli).