Microsoft word - pathophysiology summary v3.0.doc

Pathophysiology of Pain: Summary

The greatest advances in our understanding of the pathophysiology of pain stem from
the appreciation that pain mechanisms are much more complex than the simple linear
pathways that we learned about initially. The central corridor for pain transmission is
susceptible to down and up modulation from sources that are both above and below the
brainstem. The bottom line is that patients are heterogeneous in how they process pain
and even any one given patient can change how they process pain over time.
Considering the four dimensions of pain presented in this module helps us stay
cognizant of the complexity and diversity of pain that each patient presents to us.
The First Dimension – The Central Corridor of Nociception

ƒ A mechanical, chemical, or temperature stimulus or light energy stimulates the peripheral nociceptor and triggers the transduction of the stimulus into an action potential that is then propagated (transmitted) along the first order nociceptive neuron. ƒ The stimulus is transmitted to the second order nociceptive neuron in the substantia gelanosa of the dorsal horn. ƒ The second order nociceptive neurons transmit the stimulus to the thalamus where the impulses are sorted and transmitted by third order nociceptive neurons to the appropriate cortical areas where they are consciously identified, somatotropically localized, and perceived as pain.
Inhibition of pain:
ƒ Possible medications to inhibit pain along the course of the “first dimension”: o Local anaesthetics (e.g., lidocaine, bupivacaine) work by blocking sodium channels along nociceptive neurons, which thereby block nerve conduction and the transmission of nociceptive signals.

The Second Dimension – Focus on the antinociceptive system
Inhibition of pain through the ascending pathway:

• The “power of touch” (i.e., rubbing the painful area) keeps the C-fibres “quiet” and closes the gate: Gate control theory o Therefore, massage and touch are considered to have analgesic benefits o Transcutaneous electrical nerve stimulation (TENS) and implantable dorsal column stimulators also work through the gate mechanism Inhibition of pain through the inhibitory descending pathway (antinociceptive
Neurotransmitters in the substantia gelatinosa and medications that enhance the
antinociceptive system:
• Endogenous endorphins and enkephalins o Role for opioid medications in down modulating pain • Noradrenaline (via alpha-2 adrenoreceptors) o Possible role for tricyclics in down modulating pain o Possible role of clonidine in down modulating pain o Possible role of SSRI’s in down modulating pain * Tramadol is active on opioid, alpha-2 adrenergic, and 5-HT2 serotonergic sites and
therefore has good potential to augment the antinociceptive system.
The Third Dimension – Focus on the pronociceptive system
Facilitatory descending pathways and glial activation (pronociceptive system):

• The facilitatory descending neurons transmit impulses that increase synaptic transmission between primary and secondary neurons. o The facilitatory descending neurons’ neurotransmitters bind to neuronal membrane receptors that mediate changes in the pre- and post- neuronal excitability (central sensitization) o These changes can become permanent o The excitatory neurotransmitters include glutamate and aspartate. They play an important role in central sensitization via N-methyl-D-aspartate (NMDA) receptors and others • Spinal cord glia may become activated by a host of factors to release pro- inflammatory cytokines that may induce hyperalgesia. A striking cause of glial activation is the administration of opioids, explaining why, in some patients, opioids may induce hyperalgesia. Inhibition of pain:
• Possible medications to inhibit pain that has been amplified by the pronociceptive
o NMDA receptor antagonists (e.g., ketamine, d-methadone) inhibit the o Gabapentin and pregabalin block the alpha-2 subunit of calcium channels, which leads to anti-hyperalgesic effects o Medications to block glial activation are being explored
Peripheral sensitization: The inflammatory soup:
ƒ When body tissue is damaged, chemicals, such as Substance P and prostagandins, are released to respond to the injury at the nociceptor. These chemicals are collectively called the “inflammatory soup”. o Also, other nerve endings not normally involved in nociception are recruited and become active in nociception. The resulting pain is often called inflammatory pain. Inhibition of pain:
ƒ Possible medications to inhibit pain caused by the “inflammatory soup”:
o Capsaicin: Decreases Substance P o Non-steroidal production through inhibition of cyclooxygenase (COX) enzymes (peripheral and central sites of action)
The Fourth Dimension – Focus on Total Pain
Cortex and limbic system:

• The complex interplay of all four dimensions of pain is not well understood. However, we know pain impacts the physical, psychological, sociocultural, and spiritual dimensions of an individual. This is the concept of “Total Pain” and requires a holistic approach to address the suffering. Inhibition of pain:
• Approaches to address Total Pain in the “fourth dimension”: • Endogenous endorphins and enkephalins have roles in a person’s sense of exogenous opioids also probably have a similar effect • Mood and affect impact the perception of pain and anxiety will increase pain thresholds, thus • Role of activities such as meditation, guided imagery, relaxation


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