MODULATION OF PAIN

MODULATION OF PAIN

Introduction:

• Noxious stimuli of comparable intensity producing varying degrees of pain in same individual under different circumstances.
• Forms basis for pain modulation.
• Eg: An injury acquired by an athlete in sports field is less painful than a comparable injury suffered in road accident.
• Ie., pain can be modulated.

Mechanism:

• Caused by central pain inhibitory system –
• Dorsal horn gating (Gate control hypothesis).
• Endogenous pain relief system.

1. Dorsal horn gating:

Steps:

• Step 1: Substantia gelatinosa (SG) in dorsal horn of spinal cord contains enkephalinergic inhibitory interneurons.
• Step 2: Inhibits nociceptive spinothalamic neurons, presynaptically & postsynaptically.
• Step 3: Stimulated by tactile (touch-pressure) large myelinated Aβ fibers of dorsal root, via collaterals.
• Step 4: Inhibits pain conduction by spinothalamic tract.
• Thus, SG inhibitor interneurons serve as a gate in pain pathway.
• Gate remains open only if Aβ & C fibers are stimulated simultaneously.
• Close if Aβ fibers aren’t stimulated simultaneously.

Gate control theory:

• Provides basis for reducing pain by other tactile stimuli.

Eg:

• Application of counterirritant balm or liniments massage.
• Transcutaneous electric stimulation (TEN).
• Skin stimulation (By applying hot water bag over an area of visceral stimulation).
• Acupuncture.

2. Endogenous pain relief system:

• SG inhibitory enkephalinergic interneurons are stimulated by serotonergic neurons.
• Serotonergic neurons descend from raphe (raphe magnus) nuclei  in medulla.
• Periaqueductal gray matter in midbrain inhibits pain by stimulating these raphe medullary nuclei, via descending enkephalinergic & dynorphinergic neurons.

3. Serotonergic & adrenergic neurons:

• These are in brain stem activating opioid interneurons –> Suppressing spinothalamic tract activity.
• Thus, inhibits ascending pain pathway at midbrain level.

Difference between 2 mechanisms:

• Pain modulation by opioid activation of serotonergic & adrenergic neurons – Inhibits ascending pain pathway at midbrain level.
• Pain modulation by gate mechanism, descending neurons from midbrain & medullary raphe nuclei  – Inhibits pain in spinal cord.

Other pain modulation methods:

• By Nicotinic cholinergic receptors –> By acetylcholine release.
• Eg: Epibatidine – Cholinergic agonist & potent nonopioid analgesic agent.

By cannabinoids anandamide & palmitoylethanolamide(PEA):

• Produced endogenously.
• Binds to CB1 & CB2 receptors.
• Anandamide has analgesic eftect & PEA augments anandamide’s analgesic effects.

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