Psychophysiology of pain Flashcards
(39 cards)
Define pain
An unpleasant sensory or emotional experience with actual or potential damage. It is a personal experience that is influenced by biological, psychological & social components. It exists when and where a person says
Why do we feel pain?
- To alert us of danger
- Protective mechanism
- Warn us of real/potential harm
- creates behavior changes to avoid or protect ourselves from harm
What are the 3 types of pain?
Somatic Superficial: Caused by tissue damage, occurs in the skin, short & localised, sharp sensation
Somatic Deep: Occurs in muscles, joints & tendons, a slow pain, itching, burning & aching sensation, long-lasting
Visceral: Occurs in internal organs, slow pain that feels like itching, burning & gnawing, It can be referred pain, can cause sweating/nausea
Define acute pain & chronic pain
Acute: short-term pain, is momentarily moderate to severe, resolved in a few days to weeks, less than 3-6 months duration, Acute pain serves as a protective mechanism, helping the body avoid further injury by encouraging rest or modification of behavior, Acute pain usually responds to basic treatments (e.g., rest, ice, or medication),
Chronic: long-term/intermittent, persistent, gives emotional effects e.g. depression, creates complex lifestyle & social implications, greater than 3-6 months duration, chronic pain often requires a multifaceted approach involving medication, physical therapy, psychological interventions, and lifestyle adjustments.
What causes the absence of pain
Known as analgesia, can be psychological, pharmacological or physiological
The body produces its own pain-relieving chemicals, such as endorphins and enkephalins, that bind to opioid receptors in the brain and spinal cord, blocking pain signals.
(CIP): This is a rare condition in which a person is born without the ability to feel pain due to mutations in genes responsible for pain signaling pathways, particularly in the nociceptors (pain receptors).
Pharmcological: Drugs like opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or topical analgesics can block or reduce pain transmission and perception. As well as local & general anesthesia
Define nociception
The detection of noxious stimuli by the NS through specialized receptors known as nociceptors, which signal the brain in the presence of pain, found over the skin surface
Describe and explain the 4 types of nociceptors
- Thermal: These detect extreme temperature changes which could cause harm. Heat receptors respond to temps above 43+ degrees, and cold receptors respond to temps below 5 degrees
- Mechanical: respond to stimuli that could cause physical damage, e.g. cutting or pressure, activated by the presence of mechanical forces
- Polymodal: Versatile, responds to many types of stimuli, detect many noxious events. often involved in pain from injuries
- Chemical: Sensitive to chemical substances e.g., kinins/histamine released during inflammation/tissue damage
Describe how free nerve endings detect pain
Are unencapsulated nerves (no connective tissue layered capsule)
Found in skin. joints & organs, responds to wide range of stimuli, sensitive to noxious stimuli
When noxious stimuli is detected free nerve endings send electrical signals through peripheral nerves to the SC and from there to brain.
Free nerve endings can become more sensitive by a process called sensitization, which causes a pain reaction to non-noxious stimuli, via presence of inflammatory mediators increasing sensitivity
Define peripheral sensitization
Where inflammation/ tissue damage causes nociceptors to become more sensitive leading to exaggerated pain responses.
This is caused by inflammatory mediators, changes in ion activity & neuroinflammation
Describe the stages in peripheral sensitization
- Pain is experienced at lower thresholds as 1st neuron becomes more sensitive
- Inflammatory mediators such as bradykinins, prostaglandins, histamine and P substance are released during tissue damage/inflammation.
- These mediators sensitize nociceptors e.g., Bradykinin & P substance increase excitability of pain receptors and promote local inflammation.
- When they become sensitized they become reactive to mild stimuli causing AP’s to fire that are interpreted as pain in the brain, heightened response known as hyperalgesia
- This leads to a greater frequency of AP’s carried along A & C fibers, therefore more pain signals are delivered to the SC & brain
- Macrophages & mast cells also release inflammatory chemicals e.g., cytokines which increase receptor sensitivity.
Describe the ion channel changes during peripheral sensitization
TRPV1 (Transient Receptor Potential Vanilloid 1) channels, which are sensitive to heat and capsaicin (the compound in chili peppers), are activated by prostaglandins and bradykinin, making nociceptors more responsive to thermal pain.
Sodium (Na+) channels such as NaV1.7 may also become more active or expressed in higher quantities, contributing to increased excitability of nociceptors and the heightened perception of pain.
Describe the positive feedback loop in peripheral sensitisation
Positive feedback loops can occur. For example, the activation of nociceptors can cause the release of more inflammatory mediators, such as substance P, from the nerve terminals. These mediators can then sensitize the nociceptors further, exacerbating the pain.
Summarise Peripheral sensitization
1.Injury or inflammation causes the release of inflammatory mediators (prostaglandins, bradykinin, substance P, histamine).
2. These mediators sensitize nociceptors, lowering their pain threshold and making them more excitable.
3. Nociceptors fire action potentials more easily, leading to increased pain transmission to the spinal cord.
4. Ion channels like TRPV1 and NaV1.7 become more active, contributing to heightened nociceptor responsiveness.
5. Increased nerve firing leads to more intense pain and the possibility of chronic pain due to neuroinflammation.
6. Positive feedback loops between inflammatory mediators and nociceptors may sustain or escalate pain.
Describe the function of A (beta) & A (gamma) fibers
are myelinated and small in diameter with a fast conduction speed of 12-30m/s,
transmits sharp acute localized pain & some temperature sensations. A fibers are found in thermal or mechanical nocioreceptors located in skin/other tissues, transmits signals through peripheral nerves to the dorsal root ganglion, these fibers then enter the dorsal horn. (uses the spinothalamic pathway).
In the dorsal horn the A fibers synapse with 2nd neurons and project signal into SC. 2nd neurons cross over to the opposite side of the spinal cord and ascend to the thalamus.
3rd order neurons in the thalamus project signal to somatosensory complex which processes & localises the pain.
Describe the function of C fibers
These fibers are unmyelinated and small in diameter, due to lack of myelination conduction speed is lower at 0.5-2m/s. C fibers transmit dull & throbbing pain, temperature information, itching. They transmit slow pain and is less localised compared to A fibers,
C fibers enter through dorsal root and synapse with 2nd neurons in the dorsal horn of spinal cord. After synapsing in the spinal cord 2nd neurons cross over and ascend to thalamus. 3rd-order neurons send signals to various regions of the brain, including the somatosensory cortex, where the pain is perceived in a more diffuse, aching form.
Additionally, information from C fibers contributes to the limbic system, which is involved in the emotional and affective aspects of pain
How does pain reach the spine?
Nociceptors detect pain at the site of injury or damage.
The pain signals are transmitted by Aδ and C fibers to the spinal cord through the dorsal roots.
In the spinal cord, the signals synapse with second-order neurons in the dorsal horn, which then cross to the opposite side (decussate) and ascend to the thalamus via the spinothalamic tract.
From the thalamus, the pain signals are relayed to the somatosensory cortex (for localization) and the limbic system (for emotional responses).
Define central sensitization
Where the CNS becomes increasingly sensitive to sensory stimuli e.g., pain, the brain and spinal cord become more responsive, amplifying pain perception in the absence of harmful stimuli. Occurs in chronic pain.
Hyperalgesia (increased pain response) & allodynia (pain response from non-harmful stimuli) occurs
Increased excitability of neurons in the spinal cord & brain, due to changes in neurotransmitter concentrations, NMDA receptors and synaptic connections
Pain processing is impaired leading to abnormal pain perception
Describe the central sensitization pathway
Noxious stimuli activate nocioreceptors in peripheral tissues, A & C fibers carry pain signals to the spinal cord, where they synapse with second order neurons in the dorsal horn of the spinal cord.
Wind-up occurs where the intensity of the nocioceptive input causes increased excitability in second order neurons, this occurs due to accumulation of glutamate & P substance. These substances activate NMDA receptors.
NMDA receptor activation results in an influx of ca2+ leading to long-term potentiation, where signals are strengthened & amplified, generating a greater pain signal
dorsal horns become more responsive to pain stimuli leading to hypoalgesia & allodynia. The increased excitability of the second order neurons inhibit control mechanisms & create a lower threshold for pain
Pain signals ascend via spinothalamic pathway to the thalamus. Signals are altered to become exaggerated as they pass along the spinal cord. The brain therefore receives amplified pain signals and becomes more receptive to pain
The thalamus relays pain signals and sends the amplified signals to the somatosensory cortex & the limbic system. This creates neuroplastic changes that activate pain-processing regions and can result in heightened emotional responses to painful stimuli
Central sensitisation is a positive feedback mechanism where pain signals are repeated & amplified, CNS becomes more sensitive even to non-noxious stimuli. Chronic pain e.g., migraines may result of this as the CNS becomes stuck in a loop of hypersensitivity to pain.
Key concepts of the central sensitization pathway
AMPA receptors prime the activation of NMDA receptors, which further potentiates the pain signal and contributes to wind-up and the development of central sensitization.
NMDA receptors become activated by accumulation of glutamate and P substance which release calcium ions that create LTP which amplifies & strengthens pain signals. it promotes neuroplastic changes in the brain
The control pathway is inhibited by increased excitability of second order neurons
Inflammatory chemicals e.g., cytokines & glial cells can influence the CS pathway by increasing the sensitivity of pain processing neurons
Glutamate & P substance contribute to the wind-up process and are importance in regulating & maintaining CS pathway
What are the role of AMPA receptors on the CSP
AMPA receptors are found on the second-order neurons in the dorsal horn. When glutamate is released, it binds to AMPA receptors, this activates them creating an influx of Na+ into the postsynaptic neuron, leading to depolarisation.
Repeated sustained actions of AMPA receptors lead to wind-up process, which excites second order neurons with repeated stimulation. This makes the neurons more sensitive to & amplifies pain signals
AMPA & NMDA receptors interact in the CSP. As AMPA receptors aid in depolarisation of postsynaptic neuron this makes NMDA more likely to be activated by glutamate leading to the influx of calcium ions to further strengthen synaptic transmission.
Over time, the repeated activation of AMPA receptors contributes to the plasticity of the synapse, essentially making the spinal neurons more responsive to incoming pain signals. This enhances the amplification of pain & creates a lower pain threshold.
In central sensitization, AMPA receptor-mediated changes result in the spinal cord neurons becoming hyper-responsive to normal stimuli, contributing to the persistent pain experience. (allodynia and hyperalgesia)
Compare and contrast central & peripheral sensitization
Similarities: Both lead to heightened pain sensitivity (hyperalgesia and allodynia).
Both can be part of the process that leads to chronic pain.
Both involve changes in the way the nervous system processes pain signals, though at different levels (peripheral vs. central).
Differences:
Location: Central sensitization happens in the CNS (spinal cord and brain), whereas peripheral sensitization occurs at the site of injury or inflammation in the PNS.
Duration: Peripheral sensitization is usually temporary and resolves with the healing of the injury or inflammation, whereas central sensitization can become chronic and persist even after the initial injury has healed.
Impact: Central sensitization often leads to generalized pain sensitivity, while peripheral sensitization results in localized pain sensitivity.
Define referred pain
Is when pain from site of injury/damage is felt in another area of the body, This occurs as sensory fibers from different areas converge at the same SC segment, therefore the brain has difficulty distinguishing where the pain is coming from as the fibers share the same spinal nerve pathway
Describe and explain the pain gate theory
The theory that suggests the pain is not a direct result of injury/damage, It suggests that pain is modulated via a gate at which the SC regulates the flow of pain to the brain
1. The gate located in the dorsal horn can be open/closed to allow pain signals to flow/blocked
2. The gate is influenced by A & C fibers which are activated by pain and can inhibit/promote flow of pain
3. Theory suggests that the brains view of pain is related to the activity of the A & C fibers. A fibers can inhibit the pain by closing the gate and C fibers can promote the flow of pain to the brain by opening the gate
4. The gate is influenced by sensory input & cognitive factors e.g. emotions. Beliefs, past experiences etc,
Name some factors that may open & close the ‘gate’ in the pain gate theory
Open: Stress, tension, depression, worry & boredom
Close: Relaxation, optimism, content, happy & distraction
