Gate Control Theory for Pain Modulation PDF
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Seneca Polytechnic
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Summary
This document explains the Gate Control Theory for pain modulation. It describes how different types of stimuli, such as mechanical, thermal, and chemical, affect pain signals. The theory involves various nerve fibers, and the role of inhibitory interneurons in modulating pain perception is explained.
Full Transcript
Gate Control Theory for pain modulation: Stimuli: Mechanical (needles, sharp objects), thermal (extreme heat or cold), and chemical (from ischemia, injury, swelling) stimuli. **A delta fibres** (myelinated and project sharp, tingling, localized pain sensations) and **C fibres (**unmyelinated and p...
Gate Control Theory for pain modulation: Stimuli: Mechanical (needles, sharp objects), thermal (extreme heat or cold), and chemical (from ischemia, injury, swelling) stimuli. **A delta fibres** (myelinated and project sharp, tingling, localized pain sensations) and **C fibres (**unmyelinated and project dull generalized throbbing pain sensations) carry pain signals for integration (ultimately at the primary somatosensory area of the cortex) via a **3 order neuron pathwa**y: **1st** neuron is peripheral and will synapse on a **second** neuron (projection neuron) in the spinal cord (central). This neuron projects to the **third** order neuron in the thalamus before relaying to the primary somatosensory area of the cortex. To modulate pain, **A beta fibres** (myelinated and carry the sensation for touch from mechanoreceptors). Myelinated fibres transmit their action potentials (APs) faster than unmyelinated fibres do. In the spinal cord, an **inhibitory interneuron** also forms a synapse with the second projection neuron. For pain to be transmitted, the C fibres send APs along their axons to the 2nd projection neuron and the pain is transmitted to the third neuron and then to the primary somatosensory area for perception. When the A beta fibres transmit their APs to the inhibitory neuron through shaking or squeezing the injured area, they arrive faster than the unmyelinated C fibre APs do. As a result the second projection neuron is inhibited (hyperpolarized) and the pain signal is reduced (reduced rather than stopped as there are many signals being sent along this pathway and some will be successfully blocked while others will not). This mechanism primarily applies to C fibres because they are notably slower in their transmission of signals (APs) 
