Neuropathic Orofacial Pain Rafael Benoliel, BDS, LDS RCS Eng a, * , Eli Eliav, DMD, PhD b a Department of Oral Medicine, Hebrew University-Hadassah, POB 12272, Jerusalem, Israel 91120 b Division of Orofacial Pain, Department of Diagnostic Sciences, University of Medicine & Dentistry of New Jersey-New Jersey Dental School, 110 Bergen Street, Newark, NJ 07103, USA Neuropathic pain is initiated by a primary lesion or dysfunction of the nervous system (Table 1) [1]. Neuropathic pain may be triggered by local trauma or systemic disorders, such as dia- betes, that affect structures along the neuraxis from the central nervous system to peripheral structures. Based on symptomatology, neuro- pathic orofacial pain may be divided into two broad categories: episodic and continuous [2]. Episodic neuropathies are characterized by short electrical or sharp pain that may be paroxysmal, as in trigeminal neuralgia. Continuous burning pain is characteristic of posttraumatic neuropathy or inflammation in nerve structures (neuritis). De- pending on the location of the initiating event, neu- ropathic pain may also be classified as peripheral or central. However, persistent peripheral neurop- athies eventually involve maladaptive responses of the central nervous system. Clinical approach to neuropathic pain Occurrence of neuropathic pain may be spon- taneous (stimulus-independent) or touch-evoked (stimulus-dependent), and these episodes may be superimposed on a background of constant pain. Typically neuropathies include positive (eg, hyper- algesia; see Table 1) or negative (eg, numbness) signs. Some sensory signs and symptoms, particu- larly thermal or mechanical allodynia, are frequently associated with neuropathic pain. As- sessment of sensory changes is best performed by quantitative sensory testing (QST), usually using sophisticated equipment. However, when advanced QST equipment is unavailable, a simple pin, blunt instrument, warmed and cooled imple- ments, and cotton wool may be used. This information may be complemented by mapping of areas with sensory changes; these should be documented with sketches or photographs and should be part of the patient evaluation and follow-up (Fig. 1A). Quantitative sensory testing QST uses noninvasive assessment and quanti- fication of normal and abnormal responses of the nervous system to various stimuli. External stim- uli are usually mechanical, thermal, or electrical; each selectively activates different sensory nerve fibers (eg, heat activates C-fibers and cold stimuli and punctuate mechanical stimuli activate A- delta-fibers and electrical stimuli A-beta fibers). Clinical relevance Extensive mechanical nerve damage is charac- terized by myelinated and unmyelinated nerve fiber hyposensitivity, clinically characterized by elevated detection thresholds to heat, electrical, and mechanical stimulation [3]. Partial damage may be followed by either hypo- or hypersensitiv- ity [3]. In contrast, other specific nociceptive processes may provide a different, identifiable sen- sory signature. For example, neuritis (perineural inflammation) is characterized, particularly dur- ing its early phase, by a reduced detection thresh- old (hypersensitivity) in large myelinated A-beta nerve fibers [4,5]. Additionally, a measurable re- duction in the interval between detection and pain thresholds has been shown to characterize centrally mediated pain conditions. Thus, data * Corresponding author. E-mail address: benoliel@cc.huji.ac.il (R. Benoliel). 1042-3699/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.coms.2007.12.001 oralmaxsurgery.theclinics.com Oral Maxillofacial Surg Clin N Am 20 (2008) 237–254