Pain Flashcards
What are the 4 stages linking pain stimulus to response?
- Pain sensing by Nociceptors
- Signals from nociceptors transmitted from dorsal horn to periphery via afferent nerves, first order synapse with second order neuron in dorsal horn.
- Signal transmitted through spinal cord to brain via ascending tracts. Decussation occurs, then ascent in spinothalamic tract through medulla.
- Synapse with 3rd order neuron in thalamus. 3rd order neuron transmits signal to cortex where somatosensory pain is consciously perceived, connected with prefrontal cortex where cognitive and motor responses occur.
What is the significance of the dorsal horn in pain signalling pathways?
Enables signals transmitted to the brain to be amplified or inhibited and for spinal level reflexes to initiate protective motor responses.
How can the way other types of stimulus make a painful stimulus seem less painful be explained?
Due to reduced transmission cell activity less pain is felt when there is more activity in the large diameter fibres such as touch, pressure and vibration, Relative to activity in the small diameter fibres for pain transmission.
What are 3 examples of excitatory neurotransmitters?
glutamate, substance P and CGRP
CGRP= Calcitonin Gene-related peptide
What are 5 examples of inhibitory neurotransmitters?
enkephalins, B-endorphin, GABA, glycine and cannabinoids.
How can descending inhibitory neuron pathway inhibit neurotransmission at the dorsal horn?
By releasing noradrenaline (NA) and 5-hydroxytryptamine (5-HT)
Explain the gate control theory of pain
The dorsal horn synapse is a gate through which afferent pain signals have to pass to be transmitted to the brain.
The degree to which the gate is open can be influences by factors such as descending inhibitory nerve impulses and other local sensory afferent inputs.
Where are the cell bodies of afferent neurons contained?
cell bodies are contained in the dorsal root ganglion.
What does unilateral spinal cord damage result in and how can you explain this?
results in loss of pain sensation on one side of the body and loss of fine touch on the other side.
It can be explained because the afferents for pain decussate to the contralateral spinal cord whereas the afferents for touch and vibration remain in the ipsilateral.
What are the two subtypes of nociceptor afferents?
- Slower unmyelinated C fibres for sustained dull pain (majority)
- Faster myelinated A fibres for rapid sharp pain sensation.
How are nociceptive nerve endings activated?
(and how is this faciltated?)
- Sufficient influx of Na+ ions to depolarize beyond threshold.
- Generation also facilitated by increased availability of Ca2+ ions.
What effect does cellular damage have on Na+ conductance?
increases availability of H+ ions, ATP, and reactive partially reduced derivatives of Oxygen which all increase Na+ conductance.
How do Potassium ions generate pain in tissues?
Potassium ions reduce the transmembrane gradient hence favourising depolarisation at nociceptors.
What are 2 ways in which products of inflammation increases activation of nociceptive nerve endings?
- Prostaglandins, prostacyclin and leukotrienes are agonists at g-protein coupled receptors linked to adenylate cyclase which indirectly up-regulate Na+ influx hence depolarisation at nociceptive nerve endings.
- Histamine, serotonin, bradykinin and noradrenaline are agonists at G-protein coupled receptors linked to enzyme phospholipase C which initiates a cascade of phosphorylation reactions leading to the production of inositol triphosphate which indirectly increases intracellular Ca2+ concentration.
What is the function of adenylate cyclase?
An enzyme that generates 2nd messenger CAMP (cyclic AMP) from ATP.
