Chronic Pain as an Outcome of Surgery
Mohammed Reda AbdelFattah Mohammed Ashour;
Abstract
The highest incidence of chronic post-surgical pain follows a variety of surgical procedures, including limb amputation, thoracotomy, mastectomy, hernia repair, open cholecystectomy, cesarean section, hip replacement and median sternotomy (for coronary artery bypass graft surgery).
A four-point definition has been proposed of Persistent Post-Surgical Pain (PPSP). Postoperative pain qualifies as chronic if: the pain has emerged as a consequence of surgery; its duration is at least two to three months; no other explanation exists for the pain and the pain is not a continuation of a preexisting chronic pain condition for which the surgery was performed.
Several theoretical frameworks have been proposed to explain the physiological basis of pain. The Gate Control Theory is the cornerstone while discussing the anatomy of the pain pathway. Other theories demonstrated that in chronic pain conditions, brain structure and function undergo plasticity proving that cognitive effects can alter sensory discrimination.
Primary afferent nociceptors send a peripheral axon to innervate the skin and a central axon to synapse on second-order neurons in the dorsal horn of the spinal cord or the trigeminal nucleus. They transmit to the somatosensory cortex via the thalamus. Other projection neurons engage the cingulate and insular cortices via connections in the brainstem and amygdale. This ascending information also accesses neurons of the rostral ventral medulla and midbrain periaqueductal gray to engage descending feedback systems that regulate the output from the spinal cord.
Tissue damage leads to the release of inflammatory mediators by activated nociceptors. Pathophysiological studies denote that these fibers express a host of sodium channels acting through G protein–coupled pathways and potassium channels that modulate nociceptor excitability and/or contribute to action potential propagation.
It is at the spinal level that non-nociceptive neurons are recruited by strong nociceptor activation through functional modulation of local circuits. Glutamate/NMDA receptor-mediated sensitization is crucial. Disinhibition is manifested as inhibitory interneurons continuously release GABA and/or glycine to decrease the excitability of lamina I output neurons and modulate pain transmission.
Higher pain intensity and sensitivity are related to decreased regional gray matter volume in distinct brain regions collectively named “the pain matrix”. This brain reorganization is evidenced on functional neuroimaging studies.
Studies offer an opportunity to evaluate polygenic inheritance of pain. These can be roughly divided into three categories of translational application based on the association between the gene and pain phenotype: pain facilitating alleles, pain protective alleles, and alleles related to analgesia.
Multimodal Techniques for Pain Management is mandatory. This includes the administration of two or more drugs that act by different mechanisms for providing analgesia. (which might also be combined with non-pharmacological interventions) might have synergistic effects and more effective pain relief. Either surgical site–specific peripheral regional anesthetic techniques or neuraxial interventions in adults and children are strongly recommended.
A four-point definition has been proposed of Persistent Post-Surgical Pain (PPSP). Postoperative pain qualifies as chronic if: the pain has emerged as a consequence of surgery; its duration is at least two to three months; no other explanation exists for the pain and the pain is not a continuation of a preexisting chronic pain condition for which the surgery was performed.
Several theoretical frameworks have been proposed to explain the physiological basis of pain. The Gate Control Theory is the cornerstone while discussing the anatomy of the pain pathway. Other theories demonstrated that in chronic pain conditions, brain structure and function undergo plasticity proving that cognitive effects can alter sensory discrimination.
Primary afferent nociceptors send a peripheral axon to innervate the skin and a central axon to synapse on second-order neurons in the dorsal horn of the spinal cord or the trigeminal nucleus. They transmit to the somatosensory cortex via the thalamus. Other projection neurons engage the cingulate and insular cortices via connections in the brainstem and amygdale. This ascending information also accesses neurons of the rostral ventral medulla and midbrain periaqueductal gray to engage descending feedback systems that regulate the output from the spinal cord.
Tissue damage leads to the release of inflammatory mediators by activated nociceptors. Pathophysiological studies denote that these fibers express a host of sodium channels acting through G protein–coupled pathways and potassium channels that modulate nociceptor excitability and/or contribute to action potential propagation.
It is at the spinal level that non-nociceptive neurons are recruited by strong nociceptor activation through functional modulation of local circuits. Glutamate/NMDA receptor-mediated sensitization is crucial. Disinhibition is manifested as inhibitory interneurons continuously release GABA and/or glycine to decrease the excitability of lamina I output neurons and modulate pain transmission.
Higher pain intensity and sensitivity are related to decreased regional gray matter volume in distinct brain regions collectively named “the pain matrix”. This brain reorganization is evidenced on functional neuroimaging studies.
Studies offer an opportunity to evaluate polygenic inheritance of pain. These can be roughly divided into three categories of translational application based on the association between the gene and pain phenotype: pain facilitating alleles, pain protective alleles, and alleles related to analgesia.
Multimodal Techniques for Pain Management is mandatory. This includes the administration of two or more drugs that act by different mechanisms for providing analgesia. (which might also be combined with non-pharmacological interventions) might have synergistic effects and more effective pain relief. Either surgical site–specific peripheral regional anesthetic techniques or neuraxial interventions in adults and children are strongly recommended.
Other data
| Title | Chronic Pain as an Outcome of Surgery | Other Titles | الألم المزمن كمحصلة للجراحات | Authors | Mohammed Reda AbdelFattah Mohammed Ashour | Issue Date | 2017 |
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