FACIAL PAIN: A 21st CENTURY GUIDE

For People with Trigeminal Neuralgia Neuropathic Pain

10.4 Trigeminal Neuropathic Pain and Dental Issues

Gary D. Klasser (Doctor of Dental Surgery USA)

The International Association for the Study of Pain (IASP) defines neuropathic pain as “pain caused by a lesion or disease of the somatosensory nervous system.”1 Alternatively, Costigan et al provide a definition describing neuropathic pain as a dysfunctional pain which involves “amplification of nociceptive signaling in the absence of either inflammation or neural lesions.”2 This dysfunctional pain represents a malfunction (considered a disease unto itself ) of the somatosensory nervous system, involving both spontaneous and stimulus-dependent pain (evoked by both low- and high-intensity stimuli). This type of pain has no known biologically adaptive characteristics as does nociceptive pain (provides a warning signal to protect against potential or further tissue damage). Trigeminal neuropathic pain (TNP) is a dysfunctional pain that may originate and involve one or more branches (V1: ophthalmic; V2: maxillary; V3: mandibular) from the sensory distribution of the trigeminal nerve (cranial nerve V). For simplicity and clinical purposes, TNP may be classified based upon a temporal component and therefore divided into continuous and episodic (intermittent periods of pain) types of pain. Continuous neuropathic pains have their origin in neural structures and are experienced as a constant, ongoing, and unremitting pain. Patients usually have varying and fluctuating intensities of pain, often without total remission. The pain is often sensed in odontogenic structures or in those that surround these structures and has been previously referred to as atypical odontalgia3 or phantom toothache.4 In some cases, there may be a sympathetic component associated with this pain.5 According to the International Classification of Headache Disorders (ICHD-3), these types of pain have currently been categorized as persistent idiopathic facial pain (Figure 10.4A) or painful posttraumatic trigeminal neuropathy6 (Figure 10.4B).

Figure 10.4A: Diagnostic criteria for idiopathic facial pain according to the ICHD.

Figure 10.4B: Diagnostic criteria for painful posttraumatic trigeminal neuropathy according to the ICHD.

Episodic TNP is characterized by sudden volleys of electric-like, severe, shooting pain lasting only a few seconds to several minutes and is referred to as neuralgia (e.g., trigeminal or glossopharyngeal neuralgia). Often there exists a perioral or intraoral trigger zone, whereby nontraumatic stimuli such as light touch elicits a severe paroxysmal pain.7 Interestingly, anesthetic blocking of the trigger zone may eliminate the paroxysmal episodes during the period of anesthesia. There are also inflammatory conditions associated with neural tissues, and these are labeled as neuritis (e.g., acute herpes zoster). Unfortunately, due to the lack of recognition and understanding of these dysfunctional neuropathic conditions among dental practitioners, they often lead to a misdiagnosis or an incomplete diagnosis, resulting in the delivery of well-intentioned invasive procedures that may unfortunately be misdirected, incomplete, or ineffective.8 In a retrospective study involving 64 TNP patients, 71% reported initial consultation with a dentist for their pain complaint, with 79% receiving dental interventions that were ineffective in pain resolution.9

Dental Issues

  1. Clinical implications. First and foremost, it is imperative the dental practitioner establish a differential diagnosis to rule out pain of dental soft tissue or pathologic (peripheral or central) origin. Therefore, the first step in diagnosis is performing a comprehensive history and clinical/imaging examination. Once the diagnosis of TNP is determined, no further dental procedures should be performed unless specific findings of dental pathosis(es) are identified. The dental practitioner then must decide whether to treat these individuals or provide a referral to a healthcare professional who understands these types of conditions. Furthermore, individuals experiencing TNP will inevitably require dental treatment either on an acute basis or for the routine maintenance of oral health. However, due to the fear of reigniting the original pain or amplifying the current pain, they may neglect these procedures. Unfortunately, this may lead to progressive dental disease, with the additional consequence of barrages of nociceptive input into an existing dysfunctional nervous system. Effective oral health maintenance may reduce the need for invasive dental treatments, with the additional benefit of reducing the risk of complications associated with TNP. When invasive procedures are required, it is of the utmost importance for the dental team to recognize and understand these issues and to select the least invasive approaches to treatment.10,11
  2. Patient scheduling. The goal of every practitioner should be to provide maximum comfort during and following the procedure. The intensity of TNP often has a tendency to fluctuate throughout the day; therefore, dental appointments may be best planned during periods of the lowest pain intensity or periods of remission (as is possible with TN).

Dental procedures should be performed when medication used in the management of these conditions is at its peak level of effectiveness, which requires a thorough understanding of the characteristics of the medication(s) being used to manage pain.

  • Local anesthetic and preemptive analgesia. The administration of local anesthetic and the use of needles, although routinely performed on a daily basis and rarely associated with complications, may be a source of pain exacerbation in TNP patients.12,13 Furthermore, consideration should be given as to the neurotoxicity associated with each local anesthetic agent.12,14–16 Other factors to be considered for choice of local anesthetic are related to its concentration and time of exposure to peripheral neural tissue.17 In order to minimize the risk of an increase in pain, the local anesthetic should be administered carefully, avoiding undue tissue trauma, using agents that have minimal neurotoxic and ischemic potential, with minimal concentrations and exposure times. The use of preemptive analgesia by providing the patient with “booster” doses of antineuropathic medication(s) prior to invasive procedures should be considered.18 The administration of long-acting anesthetic at the end of the procedure should be done to delay postoperative discomfort.19,20 When procedures are performed under general anesthesia, the addition of local anesthesia will reduce or minimize peripheral and central sensitization.18,21,22 Another approach may be the involvement of behavioral medicine to augment pain control or suppression with approaches such as hypnosis and/or relaxation techniques.23
  • Preventive/hygiene procedures. Oral hygiene procedures and techniques may require modifications to minimize stimulation and prevent an increase in the patient’s TNP, and also to prevent avoidance in performing normal daily dental hygiene. Atraumatic oral hygiene may be facilitated by use of an ultrasoft toothbrush and by using a soft foam brush soaked in chlorhexidine.24 Interdental cleaning may be facilitated with an assortment of devices (various floss textures, dental tape, and interdental cleaners). The use of antiseptic/antiplaque alcohol-free mouth rinses, recalcifying and remineralizing agents, and fluoride supplementation (in high-risk patients) delivered in soft custom trays and/or pastes, gels, or rinses should be considered. Professional scaling and prophylaxis should be delivered with care and may require local anesthesia to the areas to be treated to decrease nociception.
  • Conservative rehabilitative interventions. The least invasive approach for rehabilitation should be considered. Prevention as discussed above is the first choice. Examples of approaches that may have lower risk in aggravation of pain include crown amputation and retaining roots rather than extraction, site selection for implants outside of the immediate zone of TNP, and use of a removable prosthesis rather than fixed prosthetic devices which could also serve as a vehicle for application of transmucosal medication(s).

Conclusion. Dental practitioners involved with patient care should be able to recognize and understand the concepts of TNP to provide appropriate dental interventions and avoid any undesirable complications. To provide the best quality of dental care for this unique patient population, factors such as communication among all health practitioners and the patient, appreciation and respect for the individual experiencing TNP, and understanding the patient’s tolerance for procedures must be incorporated into the overall management plan, which may be multidisciplinary and multimodal in nature.

References

  1. IASP Taxonomy Working Group. In: International Association for the Study of Pain. IASP Publications. 2011. https://www.iasp-pain.org/Taxonomy?navItemNumber=5 76#Neuropathicpain. Accessed 16 February 2018.
  2. Costigan M, Scholz J, Woolf CJ. Neuropathic pain: a maladaptive response of the nervous system to damage.
  3. Clark GT. Persistent orodental pain, atypical odontalgia, and phantom tooth pain: when are they neuropathic disorders? J Calif Dent Assoc 2006;34(8):599-609.
  4. Marbach JJ. Phantom tooth pain: differential diagnosis and treatment. N Y State Dent J 1993;59(10):28-33.
  • Vickers ER, Cousins MJ, Walker S, Chisholm K. Analysis of 50 patients with atypical odontalgia. A preliminary report on pharmacological procedures for diagnosis and treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85(1):24-32.
  • Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38(1):1-211.
  • Scrivani SJ, Mathews ES, Maciewicz RJ. Trigeminal neuralgia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100(5):527-38.
  • Truelove E. Management issues of neuropathic trigeminal pain from a dental perspective. J Orofac Pain 2004;18(4):374-80.
  • Ram S, Teruel A, Kumar SK, Clark G. Clinical characteristics, and diagnosis of atypical odontalgia: implications for dentists. J Am Dent Assoc 2009;140(2):223-8.
  • Remick RA, Blasberg B, Barton JS, Campos PE, Miles JE. Ineffective dental and surgical treatment associated with atypical facial pain. Oral Surg Oral Med Oral Pathol 1983;55(4):355-8.
  • Allerbring M, Haegerstam G. Invasive dental treatment, pain reports, and disease conviction in chronic facial pain patients. A retrospective study. Acta Odontol Scand. 1995;53(1):41-3.
  • Hillerup S, Jensen RH, Ersboll BK. Trigeminal nerve injury associated with injection of local anesthetics: needle lesion or neurotoxicity? J Am Dent Assoc 2011;142(5):531-9. 13. Pogrel MA. Permanent nerve damage from inferior alveolar nerve blocks: a current update. J Calif Dent Assoc. 2012;40(10):795-7.
  • Haas DA, Lennon D. A 21-year retrospective study of reports of paresthesia following local anesthetic administration. J Can Dent Assoc 1995;61(4):319-20, 23-6, 29-30.
  • Piccinni C, Gissi DB, Gabusi A, Montebugnoli L, Poluzzi E. Paraesthesia after local anaesthetics: an analysis of reports to the FDA Adverse Event Reporting System. Basic Clin Pharmacol Toxicol. 2015;117(1):52-6.
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