Pathogenesis of Postoperative Oral Surgical Pain: Neurophysiology of Postoperative Pain

In: Anesthesia

30 Sep 2009

Neurophysiology of Postoperative Pain

Acute pain, the pain felt at the moment of injury, results from activation of the nociceptive sensory endings in the affected tissues. This direct nociceptive activation is usually gone within minutes after withdrawal of the noxious stimulus, but the resulting pain often lasts much lon ger—from hours to days. In surgery the nociceptive input (indirect) continues in the presence of extensive chemically sensitized traumatized tissues. In the case of third-molar surgery, this nociception may last for many hours, long after the local anesthetic used for the surgery has worn off. Very often the offset of the local anesthetic coincides with the peak release of important pain mediators such as prostaglandins and bradykinin.

The pain that lasts hours to days after surgery is not a direct result of the initial impact but a later development of a series of changes in the peripheral tissues themselves and the associated trigeminal nucleus (*Generic Tegretol controlling certain types of seizures and relieving pain in patients with nerve pain in the face, jaw, tongue, or throat). Hyperalgesia and allodynia often aggravate pain for variable periods of time after surgery. Pain that is induced by normally nonpainful stimuli (allodynia) or abnormally intense pain elicited by noxious stimuli (hyperalgesia) may be the consequence of the increased sensitivity of the nociceptors (peripheral sensitization) or may be due to an increased responsiveness of neurons in the CNS (central sensitization). It is a common clinical experience to see third-molar surgical patients suffering from hyperalgesia and allodynia. The hyperalgesia is present both in the area of direct injury (primary hyperalgesia) and in the surrounding undamaged tissues (secondary hyperalgesia). In these patients, hyperalgesia is characterized by spontaneous pain, a decreased pain threshold, and the increased magnitude of perceived pain for any given stimulus. This may occur even days after the surgery. Hence, methods to prevent or reduce hyperalgesia and allodynia would be of great value in reducing the overall morbidity of this type of surgery.

Peripheral sensitization refers to the events that occur within the injured tissue itself after the injury. The resulting inflammation results in the release of a complex array of chemical mediators. These inflammatory mediators sensitized the nociceptive endings in the tissues, causing them to generate sensory impulses in response to stimuli that would otherwise be too weak. Peripheral sensitization acts almost exclusively on nociceptor endings in peripheral tissues, both A-delta and С fibers. It simply renders them more responsive. The results are tenderness of the mucosa (allodynia and hyperalgesia) and soreness and aching of the tissues, particularly on movement—resulting in trismus after third-molar surgery. Correspondingly, a wide array of effective antiinflammatory agents are available to treat it, most notably nonsteroidal anti-inflammatory drugs (NSAIDs). The use of NSAIDs is based on their ability to inhibit the generation of hyperalgesic molecules in the injured tissues. viagra jelly online

Central sensitization refers to an abnormal amplification of incoming sensory signals in the CNS, particularly in the spinal cord or the trigeminal nucleus (canadian Tegretol used to treat severe pain of the jaw or cheek caused by a facial nerve problem trigeminal neuralgia). The resulting amplification of the sensory signal generated in the postsynaptic spinal neuron sends a pain message to the brain. Central sensitization amplifies the signal of nociceptors, but it also amplifies the signal of low-threshold A-beta sensory fibers. In particular, it causes the A-beta touch input to be felt as pain. Acute painful input consistently triggers central sensitization, particularly impulses carried along nociceptive sensory С fibers. The transmitter substances released from the С fibers include substance P, calcitonin gene-related peptide (CGRP), glutamate, and aspartate. These transmitters react with receptors on the postsynaptic terminal of the central WDR neuron. Receptors for substance P include the NK-1 receptor and for glutamate, the N-methyl D-aspartate (NMDA) receptor. Repeated stimulation is associated with activation of NMDA-glutamate receptors, causing a condition of windup where pain persists beyond the original peripheral stimulus. NMDA receptor activation is associated with metabotrophic changes, including activation of various phospholipases, raised intracellular concentration of calcium, activation of nitric oxide synthase, and induction of early genes. These events may result in permanent neuroplastic changes. Usually, peripheral sensitization and central sensitization occur together. The concept of preemptive analgesia (analgesic intervention before nociception) may be particularly useful here because it can potentially prevent induction of central sensitization after injury by blocking the arrival of a nociceptive input to the spinal cord. Preemptive analgesia also may potentially prevent peripheral sensitization by preventing the formation of hyper-algesic molecules in the injured tissues.

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Blog invites submissions of review articles, reports on clinical techniques, case reports, conference summaries, and articles of opinion pertinent to the control of pain and anxiety in dentistry.


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