Traumatic Dysesthesia of the Trigeminal Nerve Dermot Canavan. B Dent Sc Traumatic injury to the peripheral nerves often results in persistent Postdoctoral Resident discomfort. Substance P has been tmpUcated as a mediator of pain Department of Orofaciai Pain School of Dentislry and depletion of this neurotransmitter has been shown to reduce University of California. Los Angeles pam. Subjects suffering from traumatic dysesthesia of the trigemt- Los Angeles, California nal nerve were treated with capsaicm, a substance P depleter with significant long-term effects. This form of therapy may he used Steven B. Graff-Radford. DDS mdiridtuilly or in combination with other pharmacologie mtervefi- Assistant Research Dentist ttons in the treatment of traumatic trigeminal dysesthesia. Department of Orofacial Pain J OROFACIAL PAIN 1994;S:391-396. University of California. Los Angeles School of Dentistry and Director The Pain Center Cedars Sinai Medical Center Los Angeles, California Barton M. Gratt. DDS Professor Section of Oral Radiology School of Dentistry University of Califomia. Los Angeles raumatic injury of peripheral nerves in humans may resuit in Los Angeles, California pain, dysesthesias, paresthesias, and skeletomotor and autonomie disturbances.' These complaints are often self- Correspondence to: T limiting, but in a certain population, pain or discomfort may per- Dr Steven Grai^-Radford sist. This pain poses a significant clinical management problem. Department of Orofaciai Pain Dysesthesia is usually defined as an unpleasant abnormal sensation, School of Dentistry either elicited or spontaneous.' Paresthesia, in contrast, has been University of California. Los Angeles defined as any abnormal sensation, such as burning, prickling, or CHS 43-009 formication, that is not unpleasant.- Both of these conditions are Los Angeles, California 90024 commonly associated with in|ury to sensory pathways in either the peripheral or central nervous system. The dysesthesia that accom- panies traumatic injury to peripheral nerves has been attributed to deafferentation and hyperactivity of spinal/central pain transmis- sion neurons.' Minor tissue damage associated with pain, without obvious nerve damage, may also lead to the development of the clinical characteristics of a neuropathy.' Although large afferent fibers may show pathologic changes as a result of trauma, small unmyelinated fibers are invariably affected.' Traumatized afferent neurons may generate activity through four possible mechanisms; (Í) neuroma; (2) neurogenic inflammation; (3) trauma; and (4) sympathetically maintained pain. Abnormal sensations resulting from neural injury are therefore the "conse- quence of disorder of the central control systems that establish the normal routing and amphfication of sensory signals.'"' Neurotransmitters are required for the ongoing activation and processing of nociception. Depending on the site of injury or the mechanism producing the pain, different neurotransmitters have been implicated. Substantial evidence exists implicating the neu- ropeptide substance P as one of the transmitters in nociceptive pathways.' It has been proposed that the release of substance P from nociceptors following tissue injury contributes to the spread of neurogenically mediated hyperalgesia and vasodilatation. Substance P, in combination with compounds released irom dam- Journal of Orofacial Pain 391 Can a van aged tissues, can further sensitize or activate noci- referred to The Pain Center, Cedars Sinai Medical ceptor afférents. Endogenous neuropeptides, par- Center, where a comprehensive clinical evaluation ticularly substance P,'*"" have been implicated in was carried out. The oral, stomatognathic (tem- the inflammation and pain of arthritic condi- poromandibular joint), myofascial, and cervical tions,'-" In the rat model, substance-P-induced screening examinations were noncontributory. inflammation has been shown to be suppressed by However, the neurologic screening examination capsaicin, which appears to deplete substance P revealed an area of increased sensitivity to light receptors on target tissues. This effect is considered touch bilaterally in tbe mental nerve region which to be long lasting.''' The principal source of cap- reproduced tbe complaint. The recommended ther- saicin (trans-S-methyl-N-vanillyl-6-nonenamide) is apy was a tricyclic antidepressant in combination capsicum, the common pepper plant," with a topical capsaicin (Zostrix), Desipramine Recent reports suggested that the depolarizing hydrochloride was started at 10 mg at bedtime and effect of capsaicin is selective for C-fiber poly- then gradually increased to 30 mg. It was initially modal nociceptor afférents and involves opening a suggested that the patient should apply the cap- saicin cream five times a day in the affected area nonselective cation channel.'" Thus the selective for 7 days, then three times a day for an additional nature of capsaicin's influence on C-fiber activity 3 weeks. A topical anesthetic was offered in com- suggests tbat it may be useful in treating pain con- bination with the capsaicin to enhance compliance. ditions triggered by C-fiber input. The efficacy of At 1-year follow-up, the patient reported no pain capsaicin m the management of postmastectomy and continued with 10 mg of nortriptyline hydro- pain syndrome,'' postherpetic neuralgia,'^ cluster chloride and a single use of capsaicin per day. headaches,''' diabetic neuropathy,^" and phantom limb pain^' has been evaluated. Persistent dysesthesia following neural trauma has been reported as a complication of orthog- Case 2 nathic surgery, implant placement, third-molar removal, endodontic therapy, and routine dental A é2-year-old woman, a homemaker, presented procedures,--"" The present report describes the use with bilateral continuous pain in her chin and jaw. of capsaicin as an adjunctive treatment of postsur- The pain was variable in intensity, and at times she gical sensory disturbance involving the trigeminal had a tingling tightness or burning sensation in her nerve. The use of capsaicin was helpful in treating chin. The discomfort had hecn present for 2 years facial dysesthesia after trauma as in the three case following surgery for mandibular advancement reports presented. and mandibular osteotomy. No aggravating fac- tors were described. Aspirin, ice, and heat had been tried with little benefit. She was referred to Case 1 The Pain Center, Cedars Sinai Medical Center, where a comprehensive chnical evaluation was car- A 70-year-old woman, a retired school teacher, ried out. The oral, stomatognathic (temporo- presented with bilateral mandibular stiffness in the mandibular joint), myofascial, and cervical screen- mental nerve distribution. The stiffness was con- ing examinations were noncontributory. The tinuous and associated with pain of moderate neurologic screening examination of cranial nerves intensity. The pam was aggravated by changes in II to Xil was noted to be within normal limits, temperature and relieved by ibuprofen. The prob- with the exception of a decreased reaction to pin lem starred after the woman sustained a bilateral prick by approximately 20% in the V3 (mandibu- fractured mandible in the mental nerve region dur- lar) distribution of the trigeminal nerve. This ing a motor vehicle accident. Initially, a plastic sur- decreased reaction to pin prick was restricted to geon reduced the fracture. She was then referred to the mental nerve distribution bilaterally. An area a dentist who believed that a bone graft was neces- of increased reactivity to light touch was noted in sary before the placement of dentai implants. This the left mental nerve distribution and along the was done by an oral surgeon who placed a stabiliz- right border of tbe lower lip. The treatment recom- ing plate on the left side of the mandible. Later, mended was capsaicin (Zostrix) applied topically three dental implants were placed to support a on the affected site, five times a day for 1 week, complete mandihular denture. The patient's jaw and three times a day thereafter. In addition, the stiffness and pain had continued throughout this patient was placed on a low dose of desipramine time. Because of the pain, the patient was unable hydrochloride to enhance pain relief. At 6-month to masticate properly on the right side. She was follow-up, the patient had no pain and continued 392 Volume 8, Number 4, 1994 Cansvan to use 10 mg of desipramine hydroch!oride and region. The pretreatment AT values (area tempera- capsaicin daily. ture differences from side ro side) ranged from +0.7''C to +l.rG. Posttreatment thermograms, which were also obtained from all three patients, Case 3 demonstrated decreased heat emission foiiowing cessation ofthe pain. In the affected regions ofthe A retired man, aged 67 years, presented with a face, AT values ranged from .*- 0.2°C to +0.4°C. All bilateral continuous dull aching pain in the preau- three patients had been instructed not ro use cap- ricular region. This pain e?itended to the inferior saicin for 24 hours prior to their thermography half of each ear. The patient also complained of examinations. Figure 1 is an example of a pretreat- continuous tenderness behind the upper half of the menr lateral facial thermogram demonstrating a right ear. The condition had a sudden onset fol- "hot" area (3 cm x 3 cm, yellow area with red ring) lowing face-lift surgery 18 months previously. A over the left cheek of the face. This area was mea- postoperative infection in the left preauricular area