week 3 Flashcards
Peripheral sensitisation
- damage to tissue or nerve occurs causing proinflammatory mediators to creat swelling
- constant release of these substances leads to increased sensitization (more active nociceptors)
what happens with constant activation of nociceptors over a long time
result in enhanced excitability of the
peripheral nerve and enhanced release of CGRP and SP, thus maintaining a
state of peripheral sensitization
what is smudging?
this is central sensitisation
- Order neuron: we have nociceptive neurons these neurons would be in the peirpheral nerve
- each neurone has a receptive field which sends a stimuli into nerve impulses and sends it to the dorsal horn of the spinal cord
- where it synapses on another neuron
- creating a receptive field of neurons which is where you will feel pain on your body, example your hand
- Now picture a 2nd oder neuron right next door with everything from steps 1-4, which is how we feel loaclised pain
- But afferents always branch to other neurons (order neuron), and when it becomes sensitised it will expand the receptive field of the order neuron and now will feel pain over a larger area
Nociceptors release what?
GRP
o Substance P
o Glutamate
* These are involved in inflammation (neuroinflammation)
* These in turn activate nociceptors
* The body is trying to protect itself
why do we need peripheral sensitisation
Biologically advantageous protective mechanism
* Body will naturally heal damaged tissue
* To optimise the healing environment, the organism reduces stress on the tissue
* Pain stops us from moving a body part- protective
Disinhibition
Disinhibition occurs when dorsal horn neurons are more susceptible to activation by excitatory inputs including non-nociceptive A-fibers, and is a key mechanism in triggering and maintaining central sensitization
Central sensitisation
what happens, why, signs of central sensitisation
What Happens?
The spinal cord and brain become hyper-responsive to pain signals, amplifying pain sensations beyond normal levels.
🔹 Why Does This Happen?
Increased neurotransmitter release (like glutamate and substance P) makes spinal cord neurons fire more frequently.
Reduced inhibition—normally, the brain has systems to dampen pain, but in chronic pain conditions, these fail.
The nervous system memorizes pain signals, leading to a persistent pain response even when no actual injury remains.
🔹 Signs of Central Sensitization:
Allodynia – Pain from things that shouldn’t hurt, like a gentle breeze or clothing rubbing on the skin.
Hyperalgesia – Increased pain from mildly painful stimuli (e.g., a small pinprick feeling excruciating).
Spreading pain – Pain that starts in one area but spreads to others over time.
Dorsal Horn sensitisation
Activation of NMDA Receptors on 2nd order neurons (hyperalgesia)
o A∂ afferents activate 2nd order neurons (allodynia)
o Decreased inhibition (disinhibition)
Neuropathic pain
Pain caused by a lesion or disease of the peripheral somatosensory nervous system,
i.e., the nervous system itself is under threat
symptoms and signs of neuropathic pain
Negative symptoms and signs (uncomfortable but not painful)
* Tactile hypoesthesia
* Pin prick hypoalgesia
* Loss of vibration sensation
Positive symptoms and signs
* Paresthesia
* Dysesthesia
* Paroxysmal pain
* Hyperlagesia
* Allodynia
patient will describe, pins + needles, burning, itching, numbness etc
Ectopic impulse
An ectopic discharge is when a nerve fires pain signals on its own, even when nothing is actually causing pain.
🔹 What Happens?
Normally, pain signals start at the end of a nerve (peripheral terminal) when it detects injury.
In ectopic discharge, pain signals start in the middle of the nerve pathway instead—like a glitch in the system.
This causes pain without any real injury or stimulus.
common in phantom limb
Dorsal horn axonal sprouting is what?
Normally, Aδ fibers (which carry sharp pain signals) connect to laminae III & IV in the spinal cord.
But when there’s nerve injury or inflammation, these fibers start growing (sprouting) into lamina II, where C-fibers (which carry dull, long-lasting pain) usually connect.
This change rewires pain pathways, making the nervous system more sensitive.
