Nerve Injury-!Induced Pain in the Trigeminal System

Abstract

This article reviews some recent findings on peripheral mechanisms related to the development of oro-facial pain after trigeminal nerve injury. Chronic injury-induced oro-facial pain is not in itself a life-threatening condition, but patients suffering from this disorder undoubtedly have a reduced quality of life. The vast majority of the work on pain mechanisms has been carried out in spinal nerve systems. Those studies have provided great insight into mechanisms of neuropathic spinal pain, and much of the data from them is obviously relevant to studies of trigeminal pain. However, it is now clear that the pathophysiology of the trigeminal nerve (a cranial nerve) is in many ways different to that found in spinal nerves. Whereas some of the changes seen in animal models of trigeminal nerve injury mimic those occurring after spinal nerve injury (e.g., the development of spontaneous activity from the damaged axons), others are different, such as the time-course of the spontaneous activity, some of the neuropeptide changes in the trigeminal ganglion, and the lack of sprouting of sympathetic terminals in the ganglion. Recent findings provide new insights that help our understanding of the etiology of chronic injury-induced oro-facial pain. Future investigations will hopefully explain how data gained from these studies relate to clinical pain experience in man and should enable the rapid development of new therapeutic regimes.

Silencing the Kir4.1 Potassium Channel Subunit in Satellite Glial Cells of the Rat Trigeminal Ganglion Results in Pain-Like Behavior in the Absence of Nerve Injury

“…In turn, the increased excitability of primary sensory neurons has been associated with neuropathic pain-like behavior (Fried et al, 2001;Tsuzuki et al, 2003;Cherkas et al, 2004;Robinson et al, 2004). During RNAi, the K ϩ buffering capacity of SGCs (Haydon, 2001; Butt and Kalsi, 2006) would significantly decrease, with a consequent increase in extracellular K ϩ .…”

“…One characteristic of neuropathic pain is its resistance to common analgesics and is currently the focus of intense research aimed at developing alleviating treatments. A contributing factor to the generation of neuropathic pain is a change in the excitability of primary sensory neurons, causing them to become spontaneously active or discharge at a much lower threshold than normal (Fried et al, 2001;Tsuzuki et al, 2003;Cherkas et al, 2004;Robinson et al, 2004). Such hyperexcitability gives rise to paresthesia (prickling or tingling sensation on the skin), shooting pains and allodynia (painful response to nonpainful stimuli) in the cutaneous territory served by the injured nerve.…”

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

“…Trigeminal neuropathies associated with peripheral mechanisms represent a major contribution to orofacial pain after nerve injury [102]. Glia-neuron signaling may therefore not only be important in the spinal nucleus of the trigeminal nerve but also within the trigeminal ganglia that contain the cell bodies of trigeminal afferent neurons.…”

Risk of Ear-Associated Diseases After Zygomaticomaxillary Complex Fracture

“…ZMC-fractured patients may have various presentations, such as soft tissue swelling, edema, ecchymosis, cheek numbness, trismus, diplopia, and epistaxis, depending on the associated injuries. In addition to these, ear-associated problems such as sudden hearing loss [5][6][7], tinnitus [8,9], trigeminal neuralgia [10,11], and vertigo [12,13] have also been reported.…”