Pathogenesis of Postoperative Oral Surgical Pain: Neuroanatomy of Postoperative Pain

In: Anesthesia

29 Sep 2009

Understanding orofacial pain begins with a sound knowledge of the neuroanatomy of the orofacial structures. This section will briefly review the important structures that are basic to the understanding of orofacial pain. Information from the tissues outside the CNS needs to be transferred from the periphery into the CNS and on to the higher centers in the brain stem and cortex for interpretation and evaluation (Figure 1).

The largest and most significant nerve subserving the orofacial structures is the trigeminal nerve. This nerve is the principal innervator of the oral mucosa, teeth, tongue, masticatory muscles, facial skin, and meningeal linings. It is a mixed nerve containing both sensory and motor fibers. The sensory fibers pass from the periphery within the 3 main divisions of the nerve (ophthalmic, maxillary, and mandibular) to their cell bodies in the trigeminal (*Generic Tegretol controlling certain types of seizures and relieving pain in patients with nerve pain in the face, jaw, tongue, or throat.) ganglion situated on the floor of the middle cranial fossa. From the ganglion the sensory nerve fibers pass centrally to the trigeminal nuclei in the brainstem at the level of the pons. In lower-third-molar surgery the mandibular nerve is usually blocked with local anesthetic (canadian Betagan does not have significant local anesthetic effect or intrinsic sympathomimetic activity) to prevent the transmission of nociception to the brain.

Noxious stimuli are detected by the terminal endings of 2 major classes of nociceptive afferent nerve fibers: A-delta (myelinated, fast conducting) and C-fibers (unmyelinated, slow conducting). These nociceptors are distributed throughout the mucosa, skin, periosteum, muscles, and dental pulp. Recent studies emphasize, however, that in the presence of tissue damage or inflammation, the A-beta fibers, which normally only respond to innocuous stimuli, may also become important in nociception.

The first neuron carrying information is called the primary afferent neuron or first-order neuron and receives stimulus from the sensory receptor. For most regions of the body, this impulse is carried by the primary afferent neuron into the CNS by way of the dorsal root to synapse in the dorsal horn of the spinal cord with a second-order neuron. Impulses carried by the trigeminal nerve (Tegretol canadian used to treat severe pain of the jaw or cheek caused by a facial nerve problem (trigeminal neuralgia)) enter directly into the brain stem in the region of the pons to synapse with the trigeminal spinal nucleus. This trigeminal complex extends from the pons to the upper cervical cord and can be subdivided into the main sensory nucleus and the spinal tract nucleus. The spinal tract is subdivided from rostral to caudal into subnucleus oralis, subnucleus interpolaris, and subnucleus caudalis. The subnucleus caudalis has been implicated especially in trigeminal nociceptive mechanisms on the basis of electrophysiological observations of nociceptive neurons. Evidence at this time supports the concept that the subnucleus caudalis is homologous to the substantia gelatinosa (SG) of the spinal cord.

Figure 1. Sensory innervation

Figure 1. Sensory innervation of the orofacial region is predominately carried out by the trigeminal nerve. The first-order neurons have their cell bodies in the trigeminal ganglion. The peripheral processes of these cells innervate the orofacial structures, whereas the central processes enter the brainstem and synapse with the second-order neurons at various levels of the trigeminal brainstem sensory nuclear complex. This complex may be subdivided into the caudal spinal tract nucleus, which transmits pain, and the rostral principal sensory nucleus, which transmits afferent inputs such as touch. Proprioceptive impulses end in the mesencephalic nucleus, which is connected to the motor nucleus. The subnucleus caudalis extends into the cervical spinal cord and merges with the dorsal horn. It possesses gating mechanisms capable of modulating painful stimuli.

Second-order trigeminal neurons project to the thalamus from synaptic junctions with primary afferents in the subnucleus caudalis. As in the dorsal horns, these inter neurons represent 3 types of transmission cells: (a) wide dynamic range (WDR) neurons that respond to both noxious and nonnoxious stimuli, such as touch; (b) nociceptive-specific neurons that respond exclusively to noxious stimuli and receive input from small-diameter A-delta and C-fibers; and (c) low-threshold mechanore-ceptor neurons that normally do not receive nociceptive input but respond to light touch carried by large myelinated A fibers. cialis super active online

Most second-order afferent neurons in the spinal dorsal horn and trigeminal nucleus cross to the contralateral side and ascend to the thalamus by way of the spinothalamic and trigeminothalamic pathways. Axons here then synapse with third-relay fibers (third-order neurons) in the thalamus. Third-order neurons then project to different areas in the sensory cerebral cortex and to the limbic forebrain. These impulses contribute to the sensory-discriminative and affective-emotional component of pain.

Figure 2. Physiological mechanisms

Figure 2. Physiological mechanisms of acupuncture and TENS. (Originally published in Ong KS, Ho VCL. The similarities and differences in the physiological mechanisms of acupuncture and TENS. American Journal of Pain Management 2002; 11(4): 140-148. Copyright 2002 by American Academy of Pain Management; reprinted with permission.) Painful stimulus stimulates the С primary afferent (type IV) nociceptor that projects to substantia gelatinosa (SG) cells in the dorsal horn of the spinal cord; these generate further impulses that pass to, or inhibit, wide dynamic range (WDR) cells whose axons pass up to the cortex in the spinoreticular tract, where they are interpreted as pain. Segmental acupuncture: Acupuncture stimulates the A delta primary afferent pinprick (type III) receptors projecting both to marginal (M) cells, which project up to the cortex in the spinothalamic tract about the pinprick information, and to enkephalinergic stalked (St) cells, which release the enkephalins (ENKs) that inhibit the SG cells, preventing painful stimulus from being transmitted. Heterosegmental acupuncture: The M cells carrying the pinprick information by acupuncture also give off a collateral branch to the periaqueductal gray matter (PAG) in the midbrain. The PAG projects down to the nucleus raphe magnus (nRM) in the medulla oblongata, which sends serotonergic (5 HT) and nonadrenergic (NAD) fibers to the St cells. The St cells inhibit the SG cells by an enkephalinergic mechanism, preventing painful stimulus from being transmitted. The PAG is also influenced by opioid endorphinergic fibers descending from the arcuate nucleus (A) in the hypothalamus, and the hypothalamus in turn receives projections from the prefrontal cortex. The hypothalamus may cause the release of free ENKs into the blood and cerebrospinal fluid from the pituitary gland. The M cells also send branches to the subnucleus reticularis dorsalis (R) in the medulla oblongata, whose descending projections bring about inhibition of noxious stimulus arriving at the SG cells in the spinal cord. This is the diffuse noxious inhibitory control (DNIC) theory mechanism. Transcutaneous electrical stimulation (TENS) mechanism: TENS stimulates the A beta primary afferent tactile (type I) receptors, which project to the dorsal column and to the SG cells through an intemeuron. Inhibition of the SG cells through the release of gama-aminobutyric acid (GABA) prevents noxious stimulus from being transmitted further. This is believed to be the principal mechanism of TENS. Dorsal column stimulation (DCS) may also lead to stimulation of the PAG in the midbrain and in turn activates the nRM, causing it to send monoaminergic fibers to the St cells in the spinal cord. levothyroxine 100 mcg

There is evidence of a difference in the CNS structures that is associated with the sensory and emotional aspects of pain. Central sensory and affective pain processes share common mechanisms in the periphery: A-delta and С fibers serve as nociceptors for both. Differentiation of sensory and affective processes begins at the dorsal horn of the spinal cord. Sensory-discriminative transmission follows the spinothalamic pathways, and transmission destined for affective-motivational processing takes place in the spinoreticular pathways that lead to limbic areas through extensive noradrenargic projections. The limbic system is a set of structures located in the cerebral hemispheres that play an important role in the expression of emotion. The limbic structures consist of the limbic cortex, the amygdala, and the hippocampus.

An anatomically distinct and physiologically selective CNS pain-modulating network has been identified (Figure 2). This network dampens and controls the incoming pain signals. These pain modulation systems can be grouped into 4 regions:
• Spinal level—gating mechanisms at the first synaptic relay in the dorsal horn/spinal tract nucleus, which may inhibit pain signals reaching the central neuron. This mechanism is facilitated by the activity of large A-beta fibers caused by rubbing the affected region.
Stimulation of the A fibers activates the SG cells, which closes the gate for nociceptive impulse. • The periaqueductal gray (PAG) is of great importance for initiating the powerful descending control systems that act on trigeminal and spinal neurons. PAG con¬tains significant quantities of all families of endogenous opioid peptides. In addition, the presence of projections from PAG to the medial thalamus and the frontal cortex raises the possibility of ascending control of nociception. There are afferent fibers from the hypothalamus, the frontal cortex, and the amygdala to the PAG.
• The rostral ventromedial medulla (RVM), which includes the nucleus raphe magnus (nRM) and the reticular substance. It is likely that the descending, pain-modulating action of PAG is relayed through the RVM. Serotonin is the neurotransmitter of this system.
• The dorsal lateral pontomesencephic tegmentum also plays an important role in pain modulation. It contains neurons, which project to the RVM and directly to the dorsal horn. Norepinephrine is the transmitter of this system.
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These pain-modulating systems are responsible for many of the pain management techniques like acupuncture and transcutaneous electrical stimulation (TENS), as shown in Figure 2. Both acupuncture and TENS have been shown in randomized controlled trials to be effective in the reduction of postoperative surgical pain. It has been stated in a systematic review and the NIH Consensus Development Panel on Acupuncture that “there is clear evidence that acupuncture treatment is effective for postoperative dental pain.” It has also been suggested that hypnosis induced analgesia may work through these descending inhibitory systems. Hypnosis is a well-documented psychological tool for inhibiting both clinical and experimental pain. In a study by Rainville et al, hypnotic induction was used to reduce the affective processing of painful stimuli in patients by immersion of the hand in moderately painful hot water. Positron emission tomography studies in these patients showed that this was accompanied by concomitant reduced activity in the anterior cingulate, whereas activity in the primary somatosensory cortex remained unaltered. This study provides anatomical evidence for hypnosis-induced analgesia because the anterior cingulate is the region of the brain implicated in the affective components of pain and the somatosensory cortex is the region implicated in the sensory component of pain.


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