principles of oral and maxillofacial surgery maxillofacial neurologic disorders has promulgated...

Michael MiloroEditor

G. E. Ghali • Peter E. Larsen • Peter D. WaiteAssociate Editors

2004BC Decker Inc

Hamilton • London

PETERSON'S

PRINCIPLES OF

ORAL AND MAXILLOFACIAL

SURGERYSecond Edition

www.allislam.net-Problem

C H A P T E R 4 1

Microneurosurgery

Michael Miloro, DMD, MD

Injuries to the terminal branches of thetrigeminal nerve may occur commonlyfollowing a variety of routine oral andmaxillofacial surgical procedures, and theoverwhelming majority of these injuriesundergo spontaneous recovery withouttreatment. Third molar surgery is respon-sible for most of the injuries to both theinferior alveolar and lingual nerves. Thereported incidence of nerve injury variesin the literature, but generally both tem-porary and permanent paresthesia mustbe considered. Nerve injury may occur fol-lowing mandibular and maxillary orthog-nathic surgery, maxillofacial trauma, den-tal implant placement, endodontictherapy, facial fractures, and treatment ofpathology. The anatomy of the trigeminalnerve system is unique since it carries, insome branches, both general sensoryinformation and special (eg, taste) sensa-tion. Injury to a nerve may result in neu-roma formation, which can manifest in avariety of clinical signs and symptoms.Nerve injuries are classified by two popu-lar classification schemes, which are basedon the likelihood of an injured nerverecovering spontaneously. A basic under-standing of nerve terminology (Appendix)and normal neural wound healing isessential to most appropriately manageclinical situations.

The initial evaluation of patients withnerve injuries must proceed in an orderlyfashion, with several levels of testing to

determine most accurately the degree ofindividual nerve injury. A standardizedclinical neurosensory test (CNT) may beemployed for most patients; however, someadvanced testing is available for special cir-cumstances. A variety of nonsurgical andpharmacologic treatments are available forthe patient with nerve injury. For mostpatients with dysesthesia, pharmacologictherapy is the mainstay of treatment.

Once the decision is made to proceedwith microneurosurgery, a sequence of sur-gical steps must be followed meticulously.Specific surgical techniques depend onwhich specific nerve is involved, as well asthe extent of the injury. In general,microneurosurgical repair of a trigeminalnerve injury involves neurolysis and prepa-ration of the nerve stumps to perform neu-rorrhaphy. The deleterious effects of ten-sion on a nerve repair site have been welldocumented, so the inability to perform aprimary tension-free repair warrants con-sideration for an autogenous nerve graft oranother option for nerve gap managementsuch as conduit repair. Following micro-neurosurgery, postoperative sensory re-education may play a role in the regenera-tive process. The overall success rates ofmicroneurosurgical repair of the trigeminalnerve vary considerably; however, animportant factor in determining success isthe length of time from injury to repairsince this impacts on the degree of ganglioncell death, wallerian degeneration, and cor-

tical somatosensory reorganization. TheAmerican Association of Oral and Maxillo-facial Surgeons Clinical Interest Group onMaxillofacial Neurologic Disorders haspromulgated certain treatment time rec-ommendations for the patient who sustainsa trigeminal nerve injury.1

The field of microneurosurgery is inits infancy. As more surgeons becomefamiliar with the diagnosis and manage-ment of patients with trigeminal nerveinjuries, more laboratory, radiologic, andclinical information will become availableto guide therapy. Also, residency programswill become more capable of training resi-dents in the principles and practice ofmicroneurosurgery and will thus fosteraccess to this aspect of specialty carethroughout the country and abroad.

DemographicsTrigeminal nerve injuries result from avariety of routine oral and maxillofacialsurgical procedures, such as third molarodontectomy, management of facial trau-ma, orthognathic surgery, endosseous den-tal implant placement, salivary duct andgland surgery, treatment of benign andmalignant lesions of the head and neck,preprosthetic surgery, and endodontic andperiradicular surgery. Complications ofthird molar removal are responsible for themajority of nerve injuries.2 These can occurduring any phase of third molar surgery,including local anesthetic injection, incision


820 Part 6: Maxillofacial Reconstruction

and flap design, the use of a high-speeddrill for bone removal or tooth sectioning,elevation of the tooth with trauma to thelingual soft tissues, socket curettage withexposed neurovascular tissue, removal ofremnants of an assumed “dental follicle”that may contain neural or vascular tissue,the use of medicaments in the extractionsite to aid healing or prevent alveolar osteitis(eg, tetracycline-containing compounds3,4),and the placement of sutures. The effica-cy of lingual nerve retraction duringlower third molar surgery has shownthat although the incidence of tempo-rary lingual nerve paresthesia isincreased owing to a slight stretching ormanipulation (6.4% with retraction vs0.6% without retraction), the differencein long-term dysfunction is not signifi-cant (0.6% with retraction vs 0.2% with-out retraction).5 Other studies haveindicated a temporary paresthesia rate ofapproximately 10 to 15% with lingualnerve retraction and protection, with apermanent rate of < 1%.

The incidence of trigeminal nerveinjury may be estimated based on a reviewof the available literature. Overall the inci-dence of inferior alveolar nerve (IAN)injury from third molar surgery is 0.41 to7.5% and from sagittal split osteotomy is0.025 to 84.6%, whereas the lingual nerveis affected 0.06 to 11.5% of the time fol-lowing third molar removal. However, themore important clinical distinction is todifferentiate temporary from permanentparesthesia rates. For sagittal splitosteotomies, temporary inferior alveolarparesthesia may be as high as 80 to 100%,but permanent rates are < 1 to 5%. Forthird molar surgery, both inferior alveolarand lingual nerve temporary paresthesiasrange from 2 to 6% each, whereas perma-nent rates are approximately 25% of thetemporary rates, or 0.5 to 2% overall.Many risk factors for nerve injury duringthird molar surgery have been reportedand include advanced patient age, femalesex (recent animal studies indicate that

gender may play a role in spontaneousneurosensory recovery following injury),depth of impaction, mesiodistal angula-tion of the tooth (distoangular), lingualangulation of the tooth, integrity of thelingual cortex, the need for tooth section-ing, removal of bone distal to the thirdmolar, and surgeon experience. Certainlythe risk of an IAN injury may be influ-enced by so-called Rood radiographic pre-dictors of potential tooth proximity to theinferior alveolar canal.6 These seven radi-ographic predictors on panoramic radi-ograph may indicate the potential forincreased risk of injury to the IAN, andthey are listed in Table 41-1. In cases witha high index of suspicion of nerve injury(eg, deep impaction, advanced age), inten-tional coronectomy with close observationshould be considered.7 As opposed to therelatively consistent course of the IAN, thelingual nerve position is variable; and it isinjured less often than the IAN followingthird molar surgery.8–12 The position ofthe lingual nerve has been documentedclinically,13 in cadaveric dissections,14,15

and radiologically.16 On average, in thethird molar region, the lingual nerve lies2.5 mm medial to the lingual plate of themandible and 2.5 mm inferior to the lin-gual crest. The lingual nerve may be indirect contact with the lingual plate in25% of cases (Kisselbach and Chamber-lain reported 62%13) and may lie above thelingual crest in 10 to 15% of cases (Kissel-bach and Chamberlain reported 17.6%13)based on an undisturbed radiographicassessment of the nerve.

Mandibular blocks may result in infe-rior alveolar and lingual nerve injuries;however, the incidence is unknown owingto unreported cases. An estimated 1 in100,000 to 1 in 500,000 blocks result inparesthesia. Perhaps the largest study of itskind, Harn and Durham’s study of 9,587mandibular blocks showed a 3.62% inci-dence of temporary paresthesia and a1.8% incidence of long-term paresthesialasting > 1 year.17 Several theories have

been proposed to explain the mechanismof injury. Direct neural trauma is unlikelyowing to abundant interfascicular neuralcomponents resulting in separation of thefascicles by a needle or suture withoutdirect neural disruption.18 The resultantedema may be responsible for the tran-sient paresthesia that resolves sponta-neously. Local anesthetic toxicity may beresponsible for prolonged paresthesia fol-lowing a mandibular block, especially ifthe solution is deposited within the con-fines of the epineurium. Recent reportsindicate that prilocaine and articaine maybe associated with an increased risk oflong-term paresthesia compared withother local anesthetic solutions, but fur-ther investigation is warranted.19–21 Thethird potential mechanism of injuryinvolves the formation of an epineurialhematoma. The epineurium and per-ineurium contain a vast plexus of vesselsthat nurture the neural elements, and aneedle may cause disruption of one ormore vessels. The localized bleeding mostcertainly tamponades itself owing to thesurrounding epineurium, and the pressuremay impinge on select groups of fasciclescontained within the nerve. The resultantclinical signs and symptoms of localizedparesthesia, not involving the entire distri-bution of the inferior alveolar/ mentalnerve, nicely match the expected histolog-ic situation, making this theory plausible.Also, lymphatic drainage of the localizedhematoma over the few days to weeks

Table 41-1 Rood’s Radiographic Predictors of Potential Tooth Proximityto the Inferior Alveolar Canal

1. Darkening of the root2. Deflection of the root3. Narrowing of the root4. Dark and bifid root apex5. Interruption of the white line of the canal6. Diversion of the canal7. Narrowing of the canal

Adapted from Rood JP and Shehab AAN.6


Microneurosurgery 821

following surgery coincides with the clini-cal resolution of symptoms in most cases.The final theory is that of the needle-barbmechanism of injury.22 During a mandibu-lar block injection, the needle may beadvanced to the medial ramus where asmall barb may form at the needle tip. Onwithdrawal, if the needle has passedthrough or in the vicinity of the lingualnerve or IAN, fascicular disruption mayoccur with potentially long-standing clini-cal consequences. Recent trends in ourclinical understanding of injection-relatednerve injuries are the following:

• These injuries are difficult to predictand prevent

• The classic electric-shock sensation isreported uncommonly by patientswho sustain these injuries

• Injection injuries are more likely toresult in dysesthesia than are othercauses of nerve injuries

• There may be a nonanatomic distribu-tion of nerve involvement (includingthe second and third divisions of thetrigeminal nerve)

• Injection injuries occur more com-monly in females

• The lingual nerve, which is stretchedmore upon mouth opening than is theIAN, is more commonly affected

• The majority of cases resolve within 8 weeks, and if paresthesia persists for> 8 weeks, then only one-third ofthose injuries resolve spontaneously

Microneurosurgery is a poor optionfor patients with injection-related nerveinjuries because surgical access is difficult;therefore, most cases are managed withpharmacologic therapy. One of the diffi-culties for microneurosurgeons is differ-entiating a mandibular block injury froma third molar injury to the IAN. On rareoccasions the third molar site of the IANhas been explored and found to be nor-mal, with the assumption that the injuryoccurred as a result of injection ratherthan extraction.23

It is well known that orthognathicsurgery may result in nerve injury. TheIAN is affected more often than is the lin-gual nerve, and rarely the facial nerve maybe affected (0.67% with sagittal splitosteotomy in one study24). Certainly muchis known about the risks of IAN injuryassociated with sagittal split osteotomy, aswell as screw overpenetration injury to thelingual nerve.25,26 Unfortunately, thereported incidence of immediate andlong-term neurosensory deficit varies con-siderably (from < 5% to > 90%) owing topoorly controlled factors inherent in thestudy designs, such as individual operatorvariability and surgeon experience, lack ofstandardization of neurosensory testing,lack of control sites for normal cutaneousfacial sensibility, and variation in the peri-ods of neurosensory testing. Several stud-ies have examined the specific parametersof neurosensory recovery after bilateralsagittal split osteotomy by using objectiveand subjective assessment.27 One studyfound a 39% incidence of neurosensorydysfunction following sagittal ramussurgery,28 and others have shown < 15%dysfunction at 6 months.29 Although theincidence of nerve dysfunction varies,there are well-known risk factors for nerveinjury, including the following30: patientage31; increased length of the surgical pro-cedure; proximal or distal segment frac-ture (“bad splits”); concomitant thirdmolar removal; concomitant genioplastyprocedures; compression during fixation;inadvertent use of chisels; nerve entrap-ment in the proximal segment; nervemanipulation in the area of the osteotomyand, perhaps more significantly, in the lin-gual region during medial dissection(based on intraoperative recordings ofIAN somatosensory evoked potentials)32;the location of the inferior alveolar canalclose to the inferior border; low corpusheight and retrognathism (IAN closer tobuccal cortex)33; and frank nerve transec-tion during surgery. Unfortunately, long-term neurosensory dysfunction following

orthognathic surgery is not generallyamenable to surgical correction. However,most patients tolerate the paresthesia wellfollowing correction of a significantdentofacial deformity. Two caveats are thatpatients tolerate mild paresthesia follow-ing major surgery well (with informedconsent) and that the magnitude of neu-rosensory dysfunction decreases as thetime from injury increases. This certainlyapplies to orthognathic nerve injuries.

Maxillofacial trauma may result ininjury to any of the terminal branches ofthe trigeminal nerve. Mandible fracturesthat violate the IAN canal result in tempo-rary or permanent paresthesia. Treatmentof mandible fractures with inadvertentplacement of screws may cause iatrogenicnerve injury. In general, reduction of thefracture aids in realigning the natural con-duit (ie, the IAN canal) that will help toguide spontaneous neurosensory recoveryeven with a transection injury.

Also, the presence and/or treatment oforal pathologic lesions may result in nerveinjury. The use of Carnoy’s solution (ferricchloride 0.1 g/mL, absolute alcohol 6 mL,chloroform 3 mL, glacial acetic acid 1 mL)following treatment of pathology has beenshown to have a critical exposure time inan animal model of 5 minutes, after whichtime there may be long-term irreversibleneural injury.34,35 Following a resectionprocedure, consideration should be givento immediate or delayed neural recon-struction using autogenous nerve grafts.

Although preprosthetic surgery is per-formed less frequently today than in thepast, procedures such as torus mandibu-laris reduction and vestibuloplasty placethe terminal branches of the mental nerveand infraorbital nerve at risk of injury. Sur-gical repair of small terminal nerve fibers isdifficult and often results in scarring and apoor chance of neurosensory recovery. Themaxilla and mandible are excellent sourcesof autogenous bone grafts; however, theyare not without potential morbidity. Themajority of patients who undergo genial



bone graft harvest complain of desensitiza-tion of the mandibular anterior teeth.Depending on the specific techniqueemployed for posterior mandibular ramusgrafting, the IAN may be at risk of iatro-genic injury. Mandibular endodontic ther-apy and periapical surgery may result in aninjury to the IAN, depending on the prox-imity of the root apex to the canal. Someendodontic filling materials may be neuro-toxic, and to prevent irreversible paresthe-sia that in many cases results in dysesthesia,consideration should be given to promptexploration and débridement of medica-ments that have permeated through theroot apex and are in direct contact with thenerve. Distraction osteogenesis of themandible has been shown to induce tran-sient changes in neuronal conductionwithout significant long-term nerve dys-function.36,37 On a clinical level, a youngerpatient would certainly tolerate a “stretch-type” of injury to the nerve well. Recentdata indicate that with a corticotomy anddistraction rates of 1 mm/d neural changesare unlikely but that rates greater than thismay be deleterious to nerve function; how-ever, more studies are necessary.38

Finally, implant-related injuries to theIAN are common (30–40%) and problem-atic to manage appropriately. Unfortu-nately there is a lack of data regardingappropriate patient assessment and man-agement, with a lack of consensus ontreatment protocols. In the posteriormandible the likely cause of nerve damageis that the initial pilot (depth) drill pene-trates the superior cortex of the canal andviolates the IAN vein (or artery, which isless likely). This results in some bleedingthat, on placement of the implant, tam-ponades itself. The resultant increasedpressure in the closed environment createsa compartment syndrome, with harmfuleffects on neurosensory function. Thistype of injury commonly results in long-term unpleasant altered sensation (dyses-thesia) rather than simple decreased sen-sation (hypoesthesia). The recognition

postoperatively that the patient has pares-thesia and that the implant is within theconfines of the canal warrant the clinicianto consider removal of the implant, withor without immediate replacement with ashorter implant. If, however, the injurywas due to a compartment syndromeeffect, then implant removal withoutreplacement may be prudent. For patientswith persistent paresthesia, referral to amicroneurosurgeon may be warranted.The procedure of IAN repositioning (lat-eralization and transpositioning) is anoption that theoretically would induce a“controlled” injury to the nerve and pro-tect it during implant preparation. Withlateral decortication of the mandible andnerve exposure, a compartment syndromeis not possible. Despite the potentialadvantages of nerve repositioning, there isa high incidence of long-term paresthesiaranging from 0 to 77%, with a mean ofapproximately 30 to 40%.39 With appro-priate surgeon experience, proper patientselection, and informed consent, this pro-cedure remains a viable option in posteri-or mandibular reconstruction.

Trigeminal Nerve Anatomy and PhysiologyA brief review of the trigeminal nerve isnecessary to understand clinical diagnosisand management. The trigeminal nerve(Figure 41-1) is composed of a mesoneuri-um that suspends the nerve within thesurrounding tissues and is continuouswith the outer epineurium that definesand surrounds the nerve trunk. Theepineurium contains a vast plexus of ves-sels called the vasa nervorum, as well aslymphatic channels. The epineurium isdivided into outer and inner epineuriums,and the inner layer is composed of a looseconnective tissue sheath with longitudinalcollagen bundles that protect against com-pressive and stretching forces imposed onthe nerve. Individual fascicles are definedby the perineurium, which is a continua-tion of the pia-arachnoid layer of the cen-

tral nervous system. It functions to pro-vide structural support and act as a diffu-sion barrier, similar to the blood-brainbarrier that prevents the transport of cer-tain molecules. The individual nerve fibersand Schwann cells are surrounded by theendoneurium, which is composed of colla-gen, fibroblasts, and capillaries. There arethree types of neural fascicular patterns:monofascicular (one large fascicle), oligo-fascicular (2–10 fascicles), and polyfascic-ular (> 10 fascicles) (Figure 41-2). Theinferior alveolar and lingual nerves arepolyfascicular in nature. Polyfascicularnerves have abundant interfascicular con-nective tissue—the importance of which isthat needle penetrations rarely causedirect neural trauma and that nerve repairwith realignment of the fascicles is chal-lenging. The nerve is composed of a func-tional unit with differing fiber types thattransmit a variety of information (Table41-2). The A alpha fibers are the largestmyelinated fibers with the fastest conduc-tion velocity; they mediate position andfine touch through muscle spindle affer-ents and skeletal muscle efferents. The Abeta fibers mediate proprioception. Thesmallest myelinated fibers are the A delta

Outer epineurium

Inner epineurium

PerineuriumEndoneurium

Schwann cellSchwann cell

AxonAxon

Fascicle

Unmyelinated fibers Myelinated fiber

FIGURE 41-1 Trigeminal nerve anatomy.



fibers that carry pain (“first” or “fast” pain)and temperature information. The smaller-diameter and slower-conducting unmyeli-nated C fibers mediate “second” or “slow”pain and temperature sensations. TheSchwann cells surround both myelinated(one Schwann cell per nerve fiber) andunmyelinated (one Schwann cell per sev-eral nerve fibers) nerves, and they play amajor role in nerve survival and regenera-tion following injury. Although the myelinsheath may not survive a nerve injury, theSchwann cells do, and they provide a sup-portive role in the production of neu-rotrophic and neurotropic factors (such asnerve growth factor) that enhance neuralrecovery. The nodes of Ranvier are the 0.3to 2.0 µm unmyelinated segments betweenthe myelin sheaths that are responsible forthe diffusion of certain ions that causenerve depolarization and repolarization

and the saltatory conduction of a nerveimpulse along the nerve.

Following nerve injury many changesoccur, but the basic process of nerve heal-ing involves both degeneration and regen-eration (Figure 41-3).40,41 The nerve cellbody responds with an increased metabol-ic phase with a heightened production ofribonucleic acid and breakdown of Nissl’ssubstance for export from the cell body. Atthe site of injury, there is edema and par-ticulate cellular debris. In addition, there isa proliferation of phagocytes, andmacrophages begin to clean the area.Within days there are axonal sprouts thatextend from the proximal nerve stump.Each axon may have as many as 50 collat-eral sprouts. There is proliferation and ahigh level of activity of Schwann cells aswell. These begin to lay down new myelinfor the arrival of the new axons. Addition-

ally, nerve growth factors are producedthat influence the direction of sproutingand guide the new axons into the newly

FIGURE 41-2 Three types of neural fascicular patterns: A, monofascicular; B, oligofascicular; C, polyfascicular. Adapted from Lundborg G. The nerve trunk.In: Lundborg G, editor. Nerve injury and repair. New York: Churchill Livingston; 1998. p. 198.

A B C

Table 41-2 Trigeminal Nerve Fibers

Size Conduction Fiber (µ) Velocity (m/s) Function

A alpha (myelin) 12–20 70–120 Position, fine touchA beta (myelin) 6.0–12 35–170 ProprioceptionA delta (thin myelin) 1.0–6.0 2.5–3.5 Superficial (first) pain,

temperatureC (unmyelinated) 0.5–1.0 0.7–1.5 Deep (second) pain,

temperature

Cell body

Axon

Schwann cell

Endoneurium

Injury site

Macrophages and phagocytes clear debris

Cell body swelling due toincreased metabolic activity

Axonal sprouts

Schwann cells producenerve growth factors

Schwann cells align into bands of Büngner to guide axonal sprouts

FIGURE 41-3 A to E, Neural wound-healing mechanisms.

A

C

B

D

E



formed myelin sheaths, known as thebands of Büngner. In the event that all ofthese interrelated processes occur appro-priately, then spontaneous neural regener-ation occurs. In the event that one or moreof the reparative processes fail, there maybe neuroma formation. A neuroma is sim-ply a disorganized mass of collagen fibersand randomly oriented small nerve fasci-cles (sprouts). Neuromas are classified bygross morphology into the following types(Figure 41-4): amputation (stump) neuro-ma, neuroma-in-continuity (central or

fusiform neuroma), and lateral neuromasthat are either lateral exophytic neuromasor lateral adhesive neuromas.

Nerve Injury ClassificationThere are two acceptable classificationschemes used to describe the histologicchanges that occur following nerve injury.Seddon described a three-stage classifica-tion system in 1943,42 and Sunderlandrevised and further subclassified nerveinjuries into five grades in 1951 (Figure41-5 and Table 41-3).43 A neurapraxia(Seddon) or first-degree (Sunderland)injury is characterized as a conductionblock from transient anoxia owing toacute epineurial/endoneurial vascularinterruption resulting from mild nerve

manipulation (traction or compression),with rapid and complete recovery of sen-sation and no axonal degeneration. Dam-age is confined to within the endoneuri-um. Sunderland further subdividesfirst-degree injuries into types I, II, and III.Type I results from mild nerve manipula-tion with rapid (hours) return of sensa-tion when neural blood flow is restored.Type II is due to moderate traction orcompression with the formation of tran-sudate or exudate fluid and intrafascicularedema, with return of sensation followingedema resolution (days). Type III injuriesresult from more severe nerve manipula-tion that may result in segmental demyeli-nation, with recovery within days toweeks. An axonotmesis (Seddon) corre-

Amputation neuroma

Neuroma-in-continuity

Lateral exophyticneuroma

Periosteum

Lateral adhesive neuroma

FIGURE 41-4 Neuroma types: amputation neuro-ma, neuroma-in-continuity, lateral exophytic neu-roma, lateral adhesive neuroma.

Neurapraxia Axonotmesis Neurotmesis

EpineuriumPerineuriumEndoneurium

Basal laminaAxon

To endoneurium

To perineurium

Through endoneurium

Through perineurium

Through epineurium

First degree

Second degree

Third degree

Fourth degree

Fifth degree

FIGURE 41-5 Nerve injury classifications: A, Seddon classification; B, Sunderland classification.

A

B



sponds to second-, third-, and fourth-degree (Sunderland) injuries, with the dif-ference being the degree of axonal damage.Second-degree injuries are due again totraction or compression that results inischemia, intrafascicular edema, ordemyelination. This damage extendsthrough and includes the endoneuriumwith no significant axonal disorganization.Recovery is slow and may take weeks tomonths, and it may not be complete.Third-degree injuries continue the spec-trum of more advanced injury owing tomore significant neural trauma with vari-able degrees of intrafascicular architectur-al disruption and damage extending to theperineurium. Recovery is variable; it maytake months and be incomplete. Fourth-degree injuries result in damage to theentire fascicle that extends through theperineurium to the epineurium, but theepineurium remains intact. There is axon-al, endoneurial, and perineurial damagewith disorganization of the fascicles.Spontaneous recovery is unlikely, but min-imal improvement may occur in 6 to 12 months. Finally, neurotmesis (Seddon)and fifth-degree (Sunderland) injuriesresult from complete or near completetransection of the nerve with epineurialdiscontinuity and likely neuroma forma-tion. Spontaneous neurosensory recoveryis unlikely. For completeness, in 1988 Del-lon and Mackinnon described a sixth-degree injury, which recognizes that manynerve injuries exhibit features of differentdegrees of injury according to Sunderland(Table 40-4).44 The Seddon and Sunder-

land classification schemes attempt to cor-relate histologic changes with clinical out-come (see Table 41-3).

Clinical Neurosensory TestingThe patient who sustains an injury to thetrigeminal nerve may present with a vari-ety of signs and symptoms. These may bedivided into nonpainful anesthesia,hypoesthesia, hyperesthesia, or painfulanesthesia (anesthesia dolorosa), hypoes-thesia, or hyperesthesia (allodynia—painfrom a nonpainful stimulus—or hyper-pathia—increased pain owing to a painfulor nonpainful stimulus). The history usu-ally indicates the etiologic event, and thechief complaint may include the followingdescriptive terms: numbness, itchy, crawl-ing, stretched, drooling, painful, tingling,tickling, pulling, burning, stinging, pinsand needles, hot sensation, cold sensation,inability to feel food on lip, inability totaste, inability to shave, inability to smile,and loss of consortium. The history ofpresent illness should be explored in depth

with a description of the onset and pro-gression of symptoms, change in symp-toms, treatment received and response,aggravating and alleviating factors, andpresent symptoms.

The McGill Pain Questionnaire(MPQ) may be used to assess pain andaltered sensation, and it is a useful tool formonitoring progression of neurosensoryrecovery. The MPQ uses three classes ofdescriptive words to assess the level of dys-function and interference with activity:sensory class (temporal, spatial, thermal,punctate, incisive, constrictive, tractionpressure), affective class (tension, fear,autonomic properties, punishment), andevaluative class (patient perception). Per-haps the simplest and most reliable mea-sure of subjective patient assessment is theuse of a visual analog scale. Generally, thisis a 10 cm five-degree scale, with a degreemarked every 2.5 cm (Figure 41-6). This isa useful tool for monitoring subjectiveimprovement. It must be remembered thatsubjective and objective nerve testings are

Table 41-3 Nerve Injury Classifications: Seddon versus Sunderland

Seddon Sunderland Histology Outcomes

Neurapraxia First degree No axonal damage, no demyelination, Loss of sensation, rapid recoveryno neuroma (days to weeks), no microneurosurgery

Axonotmesis Second, third, and More axonal damage, demyelination, Loss of sensation, slow incomplete recoveryfourth degrees possible neuroma (weeks to months), possible

microneurosurgeryNeurotmesis Fifth degree Severe axonal damage, epineurial Loss of sensation, spontaneous recovery

discontinuity, neuroma formation unlikely, microneurosurgery

Table 41-4 Sunderland Grade and Recovery Patterns

Degree of Injury Recovery Pattern Rate of Recovery Treatment

First degree Complete Fast (days to weeks) NoneSecond degree Complete Slow (weeks) NoneThird degree Variable Slow (weeks to months) Possible nerve

explorationFourth degree None Unlikely recovery MicroneurosurgeryFifth degree None No recovery MicroneurosurgerySixth degree* Varies† Varies† Varies†

*Sixth-degree injury data from Dellon AL and Mackinnon SE44

†Depending on specific injury pattern.



rarely at the same level. For example, inone study of nerve testing following sagit-tal split osteotomy, the subjective neu-rosensory deficit was 26.0%, whereas theobjective tests revealed an 89.5% deficit.45

Treatment planning decisions must bebased on an assessment of both the sub-jective and objective testing results. Also, aradiographic assessment may reveal priorradiographic predictors of root proximityto the canal, retained root fragments, dis-tal bone removal, or the presence of for-eign bodies in extraction sites.

Clinical examination begins withinspection of the oral cavity, which mayshow signs of self-induced trauma, a lin-gually placed third molar incision scar, oratrophic changes of the tongue fungiformpapillae.46 Palpation may induce a Tinel’ssign, which is a provocative test of regen-erating nerve sprouts that it is performedby light palpation over the area of sus-pected injury. This maneuver elicits a dis-tal referred “tingling” sensation at the tar-get site. This sign is thought to indicatesmall-diameter fiber recovery; however, itis poorly correlated with functionalrecovery and is often confused with neu-roma formation. To perform the CNTappropriately, the patient should be seat-ed comfortably in a quiet room, and thespecific testing procedures should beexplained clearly to the patient, with con-firmation that there is an understandingof what the patient is being asked to doand what possible responses are accept-able. The specific tests are performed

with the patient’s eyes closed, and thecontralateral uninjured side serves as thecontrol, when appropriate.

The CNT is performed at three levels:A, B, and C (Table 41-5).47 The CNTinvolves a dropout algorithm that attemptsto correlate the results of the test with thelevel of nerve injury (Figure 41-7). If theresults of level A testing are normal, thenthe CNT is terminated and the patient isconsidered normal; this would correspondto a Sunderland first-degree injury. Anabnormal result at level A indicates theneed to proceed to level B testing. If theresults of level B testing are normal, thenthe patient is considered mildly impaired(Sunderland second-degree injury). If levelB results are abnormal, then level C testingis performed. If level C results are normal,then the patient is moderately impaired(Sunderland third-degree injury). If level Cresults are abnormal, then the patient isconsidered severely impaired (Sunderlandfourth-degree injury). If the patient’s testresults are abnormal at levels A, B, and Cand there is no response to any noxiousstimulus, the patient is considered com-pletely impaired (Sunderland fifth-degreeinjury). Level A testing includes brush-stroke directional and static two-point dis-criminations. These tests assess function ofthe larger myelinated A alpha and betafibers. These fibers are the most sensitive tocompression and traction injuries; there-fore, the CNT is terminated if level A isnormal. Brush-stroke directional discrimi-nation is performed with a fine sable or

camel hair brush. The brush is stroked gen-tly across the area of involvement at a con-stant rate, and the patient is asked to indi-cate the direction of movement (ie, to theleft or right) and the correct number ofpatient statements out of 10 is recorded.Two-point discrimination is performed ina static fashion (vs a moving two-point dis-crimination) and with blunt tips to avoid Adelta and C fiber stimulation. This test canbe performed with any device that is capa-ble of allowing the distance between twopoints to be measured consistently (eg, aBoley gauge). The closest distance (in mil-limeters) at which the patient can consis-tently discern the two points is recorded. Atlevel B testing, contact detection is per-formed with Semmes-Weinstein monofila-ments or von Frey hairs, which, again,assess the A beta fiber integrity and func-tion. These devices are acrylic resin or plas-tic transparent/translucent rods with nylonfilaments of varying diameters. The stiff-ness of each filament determines the forcenecessary to deflect or bend the filament.The narrowest diameter filament thatrequires the least amount of force to deflectthat is detected consistently is recorded. Atlevel C testing, pinprick nociception andthermal discrimination assess the smaller Adelta and C fibers, which are most resistantto injury. Pinprick nociception may be per-formed simply with a 30-gauge needle;however, a pressure sensitive device is moreappropriate. Thermal discrimination maybe performed with suprathreshold meth-ods using ice or ethyl chloride or hot wateron a cotton swab, but other options are

1Completeabsence ofsensation

2Almost no sensation

3Reducedsensation

4Almostnormalsensation

5Fullynormalsensation

Right

1Completeabsence ofsensation

2Almost no sensation

3Reducedsensation

4Almostnormalsensation

5Fullynormalsensation

Left

FIGURE 41-6 Visual analog scale.

Table 41-5 Clinical Neurosensory Testing

Subjective assessment: visual analog scale

Objective assessmentLevel A: static two-point discrimination,

brush-stroke directional discrimination

Level B: contact detectionLevel C: pinprick nociception, thermal

discrimination

Please indicate with an “X” on each of the two lines your perception of your current level of sensation.



available. Minnesota thermal disks made ofcopper, stainless steel, glass, and polyvinylchloride can be used.

Although the tests employed in theCNT are considered objective tests, theyare, in reality, subjective since they requirea patient response. There are few purelyobjective tests of nerve function available,and these include trigeminal somatosen-sory evoked potentials and magneticsource imaging.48 Unfortunately, thesetests are not readily available and are notconsidered a part of the routine assess-ment of a nerve-injured patient. Also,there is little data on the trigeminal nerve

and the patterns of responses based onspecific injuries.

Finally, taste can be assessed by a vari-ety of means, but generally it is performedas either whole-mouth or localized testing.Solutions such as 1 M sodium chloride(salt), 1 M sucrose (sweet), 0.4 M aceticacid (sour), and 0.1 M quinine (bitter)may be used. There are many difficultieswith taste assessment in the patient with alingual nerve injury. The perception oftaste alteration is extremely variable andhas little correlation with the degree of lin-gual nerve injury. For example, a patientwith a fourth- or fifth-degree lingual nerve

injury may not report any taste alterationsubjectively but may test abnormally withdifferent solutions. The complex sense oftaste is mediated not only by the chordatympani branch of the facial nerve but alsothrough feedback mechanisms in thenasopharynx, oropharynx, and hypophar-ynx, as well as the nucleus tractus solitar-ius in the brainstem.49 Regarding lingualnerve repair, objective and subjective neu-rosensory recovery also is inconsistent.50

Diagnostic nerve blocks can be a usefulcomponent of the patient evaluation whendysesthesia or unpleasant sensations pre-dominate the clinical scenario. The primarypurpose of the diagnostic block is to local-ize the source of pain and determine theprognosis for recovery following eitherpharmacologic or surgical therapy. Thepreferred local anesthetic solution is of alow concentration (eg, 0.25% lidocaine) toselectively block the smaller A delta and Cfibers while not affecting the larger myeli-nated fibers. If the low concentration failsto relieve the pain, a higher concentration isused in the same location. Diagnosticblocks begin peripherally and proceed cen-trally with constant reassessment of thearea of involvement both objectively andsubjectively. If patients present with symp-toms consistent with sympathetically medi-ated pain or causalgia, a stellate ganglionblock may be performed. These symptomsindicate a problem not amenable to periph-eral microneurosurgery. Other pain syn-dromes that generally are not relieved withdiagnostic nerve blocks include anesthesiadolorosa and deafferentation pain; thesealso are not managed surgically but, rather,pharmacologically.

Nonsurgical TreatmentPharmacologic management of peripheralnerve injuries is reserved for patients whopresent with unpleasant abnormal sensa-tions or dysesthesia. In the majority ofcases, pharmacologic treatment should bemanaged with a consultation from an expe-rienced individual such as a neurologist or

Normal

Mildlyimpaired

Abnormal

Impaired

Abnormal

Moderatelyimpaired

Abnormal

↑Threshold↓Response No response

Severely impaired Anesthetic

Contact detection(level B)

Pain sensitivity(level C)

Normal

Moderatelyimpaired

Brush stroke direction and two-point discrimination

(level A)

Normal

FIGURE 41-7 Algorithm for objective clinical neurosensory test.



facial pain specialist. Many systemic (Table41-6) and topical (Table 41-7) medicationsare available.51 Whereas the systemic drugsmay have significant side effects, topicalagents offer the advantages of little systemicabsorption, possibly only minor irritation(which can be relieved with a period ofabstinence), and over-the-counter avail-ability in many cases. There are also manycombinations of topical agents that can beused, such as a eutectic mixture of localanesthetics (EMLA) that contains 2.5%lidocaine and 2.5% prilocaine. Many of thetopical agents are prepared in a pleuroniclecithin organogel base. For most oral sur-geons long-term pharmacologic manage-ment is not part of their routine practice, sothe prompt referral to a microneuro-surgeon or neurologist may offer the bestchance for long-term success. Considera-tion may be given to a trial of a topical

agent such as capsaicin cream 0.025% tidand/or a systemic medication with few sideeffects, such as baclofen 10 mg tid orgabapentin 100 mg tid.

Some oral surgeons manage perioper-ative paresthesia following third molarremoval or implant placement with ashort course of corticosteroid therapy inan attempt to decrease perineural edema.Although there is little evidence to suggestthat systemic steroids actually provide anyeffect, the use of steroids when a nerveinjury occurs, indicates that the surgeonhas recognized a problem and has taken anaction to improve outcome, which isadvantageous when considering medico-legal involvement issues.

Perhaps the most important consider-ation should be prompt referral, whenindicated, to a specialist for pharmacologicor surgical management of the patientwith a nerve injury. The indications forreferral include but are not limited tothose listed in Table 41-8.

In the past, prior to consideration ofsurgical management, a variety of neuro-ablative techniques have been used to man-age painful neuropathies. Some of theseinclude radiofrequency thermal neurolysis,cryoneurolysis, and alcohol and glycerolinjections at the site of injury as well as atthe gasserian ganglion. Based on the com-plications and recurrence rates of dys-esthesia, caution should be employed when

considering these options.52,53 The use of alow-level laser (gallium-aluminum-arsenide, wavelength 820 nm) has promisein the area of neural healing. Several stud-ies have shown improvement in objectiveand subjective neurosensory recoverieswith the use of laser therapy in some of themore difficult cases, such as long-standinginjuries, orthognathic IAN paresthesia,and prolonged dysesthesia unresponsive topharmacologic or surgical therapy.54–56

However, the current limited availabilityof the low-level laser and the lack ofapproval by the US Food and DrugAdministration preclude its routine usefor patients with nerve injuries.

Treatment AlgorithmsThe decision to proceed with microneuro-surgery must be made following a carefulpatient assessment over a defined periodof time. The dilemma is that sufficienttime must be given to allow for sponta-neous neurosensory recovery but thatprompt surgical intervention may affordthe best chance for recovery. Time is a crit-ical issue for three main reasons. First, atthe site of injury, distal nerve degeneration(wallerian degeneration—named forAugustus Waller in 1892) occurs owing tothe interruption of axonal transport. Thisprogressive loss of neural tissue may com-promise future repair attempts. Second, atthe nerve cell bodies there is ganglion celldeath that occurs early following injury.57

Third, as the time from nerve injuryincreases, there is a higher likelihood thatcentral cortical changes may occur, andthese would make peripheral repair inef-fective.58 As a result, if 30 to 50% of gan-

Table 41-7 Topical Medications

Category Example

Topical anesthetics 5% viscous lidocaine gel; 20% benzocaine gel;2.5% lidocaine with 2.5% prilocaine

Neuropeptides Capsaicin cream (0.025% or 0.075%)Nonsteroidal anti-inflammatory drugs Ketoprofen 10–20% PLO base;

diclofenac 10–20% PLO baseSympathomimetics Clonidine 0.01% PLO base or patchN-methyl-D-aspartate blocking agents Ketamine 0.5% PLO baseAnticonvulsants Carbamazepine 2% PLO baseTricyclic antidepressants Amitriptyline 2% PLO baseAntispasmodics Baclofen 2% PLO base

PLO = pleuronic lecithin organogel.

Table 41-8 Microneurosurgeon Referral Indications

Observed nerve transectionComplete postoperative anesthesiaPersistent paresthesia (lack of improvement

in symptoms) at 4 wkPresence or development of dysesthesia

Table 41-6 Systemic PharmacologicAgents

Local anestheticsCorticosteroidsNonsteroidal anti-inflammatory agentsAntidepressantsNarcotic analgesicsAnticonvulsantsMuscle relaxantsBenzodiazepinesAntisympathetic agents



glion cells have undergone necrosis, thebest possible success rate from surgicalrepair may also be 30 to 50%.

Microneurosurgery is indicated forpersistent paresthesia that fails to improveover successive examinations. Thisincludes both subjective and objectiveassessments. Surgery is not indicated if

there is continued improvement at eachsubsequent assessment. The current rec-ommendations are to consider surgery forthe lingual nerve within 1 to 3 months fol-lowing the injury, and for the IAN within3 to 6 months following the injury (Figure41-8). The rationale for the difference intime is that the IAN lies within a bony

Transection or Sunderland fourth or

fifth degree (3rds, BSSO)

AvulsiveClean

Immediate primaryrepair

Delayed primaryrepair

(14–21 days)

NST NST

NST

Consider surgery,as indicated

Chemical(RCT, tetracycline)

NST

Consider surgery,as indicated

Compression (root tip, implant, mandible fracture)

Stretch or Sunderlandfirst to third degree

Observed nerve injury

NST Immediate decompression

Immediatedébridement

Unobservednerve injury

NST

Inferior alveolar nerveLingual nerve

Surgery1–3 mo

Surgery3–6 mo

FIGURE 41-8 Nerve treatment algorithms: A, unobserved nerve injury; B, observed nerve injury. BSSO = bilateral sagittal split osteotomy; NST= neurosensory testing; RCT = root canal therapy.

A

B

canal that can guide spontaneous regener-ation, so more time is allotted for thatprocess, whereas a lingual nerve injuredwithin soft tissue does not have a “physio-logic conduit” to guide regeneration. Ingeneral, the oral surgeon should have follow-up examinations with the patientover a period of approximately 4 weeks. Ifthere is persistent paresthesia or a worsen-ing of symptoms, referral should be madeto a microneurosurgical specialist.

For an unobserved nerve injury, theplan should be to continue neurosensorytesting for 1 month and then to refer forsurgery in the 1- to 3-month (lingualnerve) or 3- to 6-month (IAN) time peri-ods. For an observed nerve injury, treat-ment should focus on the specific etiology.For a suspected traction injury (Sunder-land first-, second-, and third-degreeinjuries), the patient should be tested for 1 month for signs of expected spontaneousrecovery. In the case of nerve compression,immediate decompression should be con-sidered. This includes removal of a rootdisplaced into the IAN canal, removal orreplacement when there is evidence ofimplant impingement within the confines



of the IAN canal, or reduction and align-ment of a displaced posterior mandiblefracture including the IAN canal. Neu-rosensory testing should be performed fol-lowing decompression, and microneuro-surgery should be considered as indicated.Chemical injuries should be débridedpromptly. For observed transectioninjuries (Sunderland fourth- or fifth-degree injuries), an immediate primaryrepair may be performed for a clean tran-section injury (eg, scalpel transection). Foran avulsive injury (eg, lingual nerve entan-gled in a bur), consideration is given to adelayed primary repair performed at 3 weeks following the injury. This allowstime for the proximal and distal nervestumps to define the degree of injury, andto determine whether the surroundingenvironment is conducive to nerve surgery,when there are high levels of neurotropicand neurotrophic factors. After surgery,patients should be followed up with repeatneurosensory testing.

The success rates of microneurosurgi-cal reconstruction following nerve injuryare variable in the literature. This is due tomany factors including the lack of stan-dardization with the following59: age, theetiology of injury, the time of delay frominjury to repair, specific surgical techniquesused, the length of the nerve gap, themethod of neurosensory examination, theuse of normative values for control sites,follow-up period variability, and criteria todefine success (Table 41-9). A global reviewof the literature might indicate a successrate of 30 to 50% following microneuro-surgery, including direct and gap repairs. Ingeneral, direct repair is preferred over gaprepair (eg, using an autogenous nerve graft)and has higher reported success rates.60

Perhaps the largest study to date indicatesan overall “success” rate of 76.2% in 521 patients.61 The success criteria weredefined as light touch detected > 80% ofthe time and a 30% decrease in postopera-tive pain level. The study results suggestedsome important trends in outcome.

Hypoesthetic injuries improved better fol-lowing microneurosurgery than did hyper-esthetic injuries, the lingual nerve recoveredbetter than did the IAN overall, and therewas a decrease in success associated with adelay of > 6 months. A recent report of51 microneurosurgical reconstructions(direct and gap repairs) found that 10patients subjectively reported goodimprovement, 18 patients some improve-ment, 22 patients no improvement, and 1 patient reported feeling worse followingsurgery.62 This indicates that 55% ofpatients showed some improvement. Inanother study of 53 surgical patients, with amean follow-up of 13 months, light touchimproved from 0 to 51% and pinprick noci-ception improved from 34 to 77%. Patientsalso experienced improved taste and anincreased number of fungiform papillae,and there was a decrease in incidence ofaccidental tongue biting. Interestingly, therewas no correlation of success with delayfrom time of injury to repair. No patientbecame completely normal, and there wasno reduction in dysesthesia; however, mostpatients considered the surgery worthwhile.There is certainly a need for standardizationin all aspects of evaluation and managementof microneurosurgical patients.

Surgical TreatmentMicroneurosurgical reconstructioninvolves a sequence of surgical proceduresincluding exposure, dissection, assess-ment, manipulation, and repair. Many ofthe techniques of trigeminal nerve repairfollow those of hand surgery and use sim-ilar instruments. In general, surgical loupemagnification (×3.5 magnification) is ade-quate. An operating microscope (×12magnification) is cumbersome and diffi-cult to use with a transoral exposure,although it may be more useful with atransfacial approach.

ExposureSurgical access to the lingual or IAN maybe accomplished transfacially or transoral-

ly. The transfacial approach affords wideexposure and access; however, it necessi-tates a facial incision with subsequent scarformation. The intraoral approach pro-vides a more difficult surgical access andrequires more diligence in microsurgery inthe posterior regions of the oral cavity, butit avoids a facial incision. The decisionregarding surgical access depends on anindividual patient’s anatomy, the site ofnerve injury, planned surgical procedures,patient preference, and surgeon’s skill andexperience.

External NeurolysisMicrodissection of the nerve once exposedinvolves liberation of the nerve from thesurrounding tissues to facilitate inspection.For the lingual nerve this procedure mayinvolve the release of the nerve from a lat-eral adhesive neuroma in the area of thelingual plate in the third molar region,whereas for the IAN a corticotomy is gen-erally required for external neurolysis. Sev-

Table 41-9 Classification of SensoryRecovery

Grade (Stage) Recovery of Sensibility

S0 No recoveryS1 Recovery of deep cutaneous painS1+ Recovery of some superficial painS2 Return of some superficial pain

and tactile sensationS2+ S2 with over-responseS3* Return of some superficial pain

and tactile sensation without over-response; two-point discrimination > 15 mm

S3+ S3 with good stimulus localization; two-point discrimination = 7–15 mm

S4 Complete recovery, S3+;two-point discrimination = 2–6 mm

*S3 score indicates significant clinical recovery (WyrickJD, Stern PJ. Secondary nerve reconstruction. HandClin 1992;8:587).

Adapted from Mackinnon SE. Surgical management of theperipheral nerve gap. Clin Plast Surg 1989;16:587.



eral techniques have been described for lat-eral decortication in the area of the thirdmolar for IAN exposure, and these rangefrom a simple nerve transpositioning to amodified buccal corticotomy or a unilater-al sagittal split ramus osteotomy (Figure41-9).63 The location of the injury and thesurgeon’s preference frequently dictate thespecific approach used. The lingual nerve isusually exposed via a modified incisionused for third molar surgery with a sulcu-lar lingual extension (Figure 41-10). Forthe infraorbital nerve, external neurolysismay be performed secondary to reductionand fixation of a displaced zygomatico-maxillary complex fracture impinging onthe neurovascular bundle at the infraor-bital foramen. It has been suggested thatexternal neurolysis may provide definitivetreatment for a nerve injury if the nervecompression is < 25% of the normal diam-eter, if the paresthesia is of short duration(< 6 mo), and if there is no evidence ofneuroma formation.64

Internal NeurolysisThe term internal neurolysis refers to sur-gical manipulations within the epineuri-um to prepare the nerve for repair. Sophis-ticated maneuvers may compromise repairby unnecessary removal of tissue and

FIGURE 41-9 Exposure techniques for the IAN: A, Lateral decortication of the mandible; B, withexposure of the inferior alveolar neurovascular bundle. C, Sagittal ramus osteotomy with anteriorextension via lateral decortication to the mental foramen. D, Lateral mandibular decortication.E, Bone removal with chisels. F, Wide exposure of the neurovascular bundle.

A

B

D

C

E F

Distal nerve

Neuroma of right lingual nerve

Distal nerve

Proximal nerve

Sural graft

FIGURE 41-10 Lingual nerve exposure. A, Incision design via a distobuccal extension and lingual gingival sulcus approach. B, Right lingual nerve exposure with neu-roma. C, Right lingual nerve repair with an interpositional nerve graft.

A B C



induction of cicatrix formation owing toexcessive manipulation. Several types ofinternal neurolysis have been described,including epifascicular epineurotomy, epi-fascicular epineurectomy, and interfascic-ular epineurectomy (Figure 41-11). Thefirst two prepare the epineurium forrepair; any interfascicular surgery maycause further fascicular disruption andscarring. Extensive internal neurolysisprocedures should be used with caution.

Nerve Stump PreparationPerhaps the most critical portion of thesurgical procedure involves the inspectionof the proximal and distal nerve stumpsvia magnification. The preparation of thenerve stumps follows exposure; there mayalready be an existing discontinuity from atransection injury. When a neuroma ispresent, meticulous excision is required(Figure 41-12). It must be recognized thatwith any neuroma, the clinical appearanceof neuronal edema or atrophy is less thanthe internal fascicular changes (see Figure41-12A). Failure to resect enough nervetissue to reach normal fascicles results in afailure of neurosensory recovery. Once thenerve is divided, if necessary, into proxi-mal and distal stumps, care must be takento resect small (1 mm) portions of thenerve trunk in both directions (see Figure

41-12B) until healthy glistening whitemushrooming fascicles are seen to herni-ate through the edges of the epineurium(see Figure 41-12C).

ApproximationThe trigeminal nerve is similar to otherperipheral nerves in that it does not toler-ate tension well; therefore, tension-free clo-sure is mandatory.65 The deleterious effectsof tension result from vascular compro-mise and subsequent fibrosis at the nerverepair site. Approximation is the act of

bringing the nerve stumps into contact andassessing the degree of tension that is pre-sent. At the time of approximation a deci-sion must be made regarding whether touse an interpositional graft. In general,mobilization with primary epineurialrepair is possible for lingual nerve gaps < 10 mm and for IAN gaps < 5 mm.

CoaptationCoaptation is the process of aligning theproximal and distal nerve stumps into thepremorbid cross-sectional fascicular ori-

Epineurotomy

Epineurectomy

FIGURE 41-11 Internal neurolysis: A, epifascicular epineurotomy; B, epifascicular epineurectomy; C, interfascicular epineurectomy. A and B adapted from LaBancJP. Reconstructive microneurosurgery of the trigeminal nerve. In: Peterson LJ, Indresano AT, Marciani RD, Roser SM. Principles of oral and maxillofacial surgery. Vol2. Philadelphia: J.B. Lippincott Company; 1992. p. 1067.

A B C

1 mm

1 mm

FIGURE 41-12 Nerve stump preparation.A, Neuroma; resection at the “clinical margin” ofthe neuroma fails to complete nerve preparation.B, Neuroma resection in 1 mm increments. C,Mushrooming fascicle.

A

B C



entation. This is a difficult maneuver witha polyfascicular nerve that has undergoneany degree of distal nerve changes indiameter or fascicular pattern. This step isusually not performed painstakingly intrigeminal nerve repair because of thecomplex polyfascicular pattern.

NeurorrhaphyNeurorrhaphy is the act of nerve suturingfor both direct and gap repairs. The trigem-inal nerve is repaired using epineurialsutures, not perineurial sutures (Figure41-13). Generally, an 8-0 monofilamentnonresorbable nylon suture is chosensince a resorbable material would invokeinflammation and disturb the area ofanticipated neural healing. At least twosutures are used per anastomosis site toprevent rotation, but not more than threeor four sutures should be used per anasto-mosis. The first suture is placed on themedial side of the anastomosis since it ismore difficult to access. The epineurium ispierced with the needle 0.5 to 1.0 mmfrom the edge of the nerve. The secondsuture is placed 180˚ from the first suture,and then an assessment is made regardingthe need for more sutures.

Nerve GraftsWhen neurorrhaphy is not possible with-out tension and a nerve gap exists, aninterpositional graft must be consideredfor indirect neurorrhaphy.66 The optionsfor autogenous nerve grafting include butare not limited to the sural nerve, thegreater auricular nerve, and possibly themedial antebrachial cutaneous nerve.67

The sural nerve is the preferred nerve forgrafting since it most appropriatelymatches the nerve diameter and the fasci-cular number and pattern of the trigemi-nal nerve (Table 41-10).68 The area of thenerve superior to the lateral malleolusexhibits less branching than at or belowthe lateral malleolus. The sural nerve, ormedial sural cutaneous nerve, is a branchof the sacral plexus (S1, S2) and suppliessensory information to the posterior lowerextremity and the dorsolateral foot. Suralgrafts up to 20 cm in length are possible,and patients tolerate the donor site deficitwell.69 The greater auricular nerve is apoor choice for trigeminal repair. As abranch of the cervical plexus (C1, C2), thegreater auricular nerve supplies sensationto the pre- and postauricular regions, thelower third of the ear, and the skin overly-ing the posteroinferior border at the angleof the mandible. Patients are generally notamenable to sacrificing one facial regionfor another. Additionally, the small diame-ter of the nerve makes it useful only whenused as a cable graft (Figure 41-14). Thesole advantage of a greater auricular graftover a sural graft is in situations when itcan be harvested via the same incision foranother procedure, such as the repair of an

extraoral mandibular fracture or manage-ment of pathology. The basic premise withgraft repair is that the graft supplies theSchwann cells and growth factors neces-sary to support and encourage axonalsprouting through the graft toward thetarget site.

Entubulation TechniquesIn an attempt to avoid donor site morbidi-ty, a variety of entubulation techniqueshave been proposed to create conduits dur-ing nerve regeneration (Figure 41-15).These conduits involve both autogenousand alloplastic materials (Table 41-11). Theautogenous options include vein,70–72 colla-gen,73,74 and muscle grafts.75 Alloplastic

FIGURE 41-13 Direct epineurial neurorrhaphy.

Table 41-10 Size of Donor Nerve Grafts Relative to Injured Nerve

Donor Nerve

Sural Greater Auricular Greater Auricular Injured Nerve (2.1 mm) (1.5 mm) Cable (3.0 mm)

Inferior alveolar (2.4 mm) 88% 63% 125%Lingual (3.2 mm) 66% 47% 94%

Adapted from Brammer JP and Epker BN.68

FIGURE 41-14 Greater auricular nerve cable graft.

FIGURE 41-15 Entubulation (conduit) nerverepair.



materials include polyglycolic acid,76 poly-meric silicone,77 and expanded polytetra-fluoroethylene.78–81 It appears that the useof these alloplastic materials has a highsuccess in the animal model but poor clin-ical outcomes. Further investigation is war-ranted as new materials are developed.

Postsurgical ManagementIn the majority of cases, patients experiencea variable period of complete anesthesiafollowing nerve repair. In general, nerveregeneration progresses at approximately 1 mm/d (about 3 cm/mo) from the cellbody to the target site. For example, with adirect IAN repair, the approximate distancefrom the trigeminal ganglion to the lowerlip and chin is 10 cm; therefore, completenerve regeneration takes about 100 days or12 weeks following repair. With graft repairthe time frame is lengthened owing toslowed regeneration through the graft site,but recovery is variable. A poor outcomefollowing microneurosurgery may precludefuture surgical options; therefore, the bestchance for microneurosurgical success is atthe first (and most likely, the last) surgicalintervention.

Medicolegal IssuesOral and maxillofacial surgeons currentlypractice during a time of “malpractice cri-sis,” and nerve injuries secondary to thirdmolar removal account for a large propor-

tion of the complaints.82 Based on theinformation contained in this chapter andrecent trends in malpractice, all oral andmaxillofacial surgeons should have a min-imum of understanding of the diagnosisand management of nerve injuries accord-ing to the so-called legal parameters ofcare.83 These are summarized as follows:

• Spontaneous sensory recovery occursin most but not all patients. It is diffi-cult to predict early, it may not be“complete,” and it may not be to thepatient’s satisfaction. Nerves in softtissue (lingual nerve) have a lower rateof spontaneous regeneration than dothose in bony canals (IAN)

• All nerve injuries should be document-ed and evaluated with a history, exami-nation, and neurosensory testing(objective and subjective). The injuryshould be classified (Seddon or Sun-derland). In cases of observed orknown nerve injury, prompt referralfor microsurgery provides the bestopportunity for sensory recovery

• Repeat examinations at frequent inter-vals may be necessary. Patients shouldbe followed up for at least 1 month.Complete recovery in 1 month indi-cates neurapraxia, and no furthertreatment is indicated. Neurosensorydysfunction that lasts > 1 month indi-cates a higher-grade injury with uncer-tain spontaneous neurosensory recov-ery. Microneurosurgical consultationshould be considered

• Nerve injuries that show improvement(objective and/or subjective) may befollowed up expectantly. Onceimprovement stops for a period oftime, it usually does not begin again

• Most nerve injuries resolve within 3 to9 months, but only if improvementbegins prior to 3 months. Patientswho are anesthetic at 3 months usual-ly do not achieve significant neurosen-sory recovery. Prompt microsurgery isusually indicated

• Patients with partial sensory loss and/orpainful sensations that they find unac-ceptable should be considered formicrosurgery if objective and subjectivefindings have not improved or returnedto normal by 4 months. Microsurgicaldelay decreases the chance of successbecause progressive distal nerve degen-eration and/or the development of acentral pain syndrome occur

• Some painful neuropathies may bemanaged nonsurgically under thesupervision of a microneurosurgeonor other experienced individual (eg,neurologist)

• Angry uninformed patients withnerve injuries are less likely to improvewith any treatment, surgical or nonsur-gical. A discussion regarding optionsand the risk of nerve injury should beprovided so that the patient can giveinformed consent. Local anestheticinjections carry a risk of nerve injury

• Early surgical intervention (ie,at 3–4 mo)is more likely to produce neurosensoryimprovement than is late intervention.Surgery delayed beyond 12 months isseriously compromised by distal nervedegeneration and the development ofchronic pain syndromes

• Surgery is more likely to improveresponses to objective sensory testingand/or to reduce functional impair-ment than it is to reduce pain or sub-jective feelings of numbness

References1. American Association of Oral and Maxillofa-

cial Surgeons. Parameters and pathways:clinical practice guidelines for oral andmaxillofacial surgery (AAOMS ParPath 01),Version 3.0. J Oral Maxillofac Surg 2001;59Suppl.

2. Pogrel MA, Thamby S. The etiology of alteredsensation in the inferior alveolar, lingual,and mental nerve as a result of dental treat-ment. J Calif Dent J 1999;27:531, 534–8.

3. Zuniga JR, Leist JC. Topical tetracycline-induced neuritis: a case report. J Oral Max-illofac Surg 1995;53:196.

4. Leist JC, Zuniga JR. Experimental topical

Table 41-11 Materials for Entubulation (Conduit) Repair

Autogenous materialsCollagenMuscleFasciaVein

Alloplastic materialsPolyglycolic acidPolyesterPolytetrafluoroethylene (PTFE)Expanded PTFE Silicone, polymeric silicone



tetracycline-induced neuritis in the rat. JOral Maxillofac Surg 1995;53:427.

5. Pichler JW, Beirne OR. Lingual flap retractionand prevention of lingual nerve damageassociated with third molar surgery: a sys-tematic review of the literature. Oral SurgOral Med Oral Pathol Oral Radiol Endod2001;91:395.

6. Rood JP, Shehab AAN. The radiological predic-tion of inferior alveolar nerve injury duringthird molar surgery. Br J Oral MaxillofacSurg 1990;28:20.

7. Pogrel MA, Lee JS, Muff DF. Coronectomy inlower third molar removal. J Oral Maxillo-fac Surg 2003;61 Suppl 1:25.

8. Alling CC. Dysesthesia of the lingual and infe-rior alveolar nerves following third molarsurgery. J Oral Maxillofac Surg 1986;44:454.

9. Gulicher D, Gerlach KL. Sensory impairment ofthe lingual and inferior alveolar nerves fol-lowing removal of impacted third molars.Int J Oral Maxillofac Surg 2001; 30:306.

10. Carmichael FA, McGowan DA. Incidence ofnerve damage following third molarremoval: a West Scotland Oral SurgeryResearch Group study. Br J Oral MaxillofacSurg 1992;30:78.

11. Valmaseda-Castellon E, Berini-Aytes L, Gay-Escoda C. Lingual nerve damage after thirdlower molar surgical extraction. Oral SurgOral Med Oral Pathol Oral Radiol Endod2000;90:567.

12. Valmaseda-Castellon E, Berini-Aytes L, Gay-Escoda C. Inferior alveolar nerve damageafter lower third molar surgical extraction: aprospective study of 1117 surgical extrac-tions. Oral Surg Oral Med Oral Pathol OralRadiol Endod 2001;92:377.

13. Kisselbach JE, Chamberlain JG. Clinical andanatomic observations on the relationshipof the lingual nerve to the mandibular thirdmolar region. J Oral Maxillofac Surg 1984;42:565.

14. Pogrel MA, Renaut A, Schmidt B, Ammar A.The relationship of the lingual nerve to themandibular third molar region: an anatom-ic study. J Oral Maxillofac Surg 1995;53:1178.

15. Holzle FW, Wolff KD. Anatomic position of thelingual nerve in the mandibular third molarregion with special consideration of an atro-phied mandibular crest: an anatomicalstudy. Int J Oral Maxillofac Surg 2001;30:333.

16. Miloro M, Halkias LE, Slone HW, ChakeresDW. Assessment of the lingual nerve in thethird molar region using magnetic reso-nance imaging. J Oral Maxillofac Surg1997;55:134.

17. Harn SD, Durham TM. Incidence of lingualnerve trauma and postinjection complica-tions in conventional mandibular blockanesthesia. J Am Dent Assoc 1990;121:519.

18. Pogrel MA, Bryan J, Regezi J. Nerve damageassociated with inferior alveolar nerveblocks. J Am Dent Assoc 1995;126:1150.

19. Pogrel MA, Thamby S. Permanent nerveinvolvement resulting from inferior alveo-lar nerve blocks. J Am Dent Assoc 2000;131:901.

20. Pogrel MA, Schmidt BL, Sambajon V, et al. Lin-gual nerve damage due to inferior alveolarnerve blocks: a possible explanation. J AmDent Assoc 2003;134:195.

21. Van Eeden SP, Patel MF. Letter: prolongedparaesthesia following inferior alveolarnerve block using articaine. Br J Oral Max-illofac Surg 2002;40:519.

22. Stacy GC, Hajjar G. Barbed needle and inex-plicable paresthesias and trismus after den-tal regional anesthesia. Oral Surg Oral MedOral Pathol 1994;77:585.

23. Pogrel MA, Schmidt BL. Trigeminal nervechemical neurotrauma from injectablematerials. Oral Maxillofac Surg Clin NorthAm 2001;13:247.

24. Behrman S. Complications of sagittal osteoto-my of the mandibular ramus. J Oral Surg1972;35:554.

25. Hegdvedt AK, Zuniga JR. Lingual nerve injuryas a complication of sagittal ramus osteoto-my. J Oral Maxillofac Surg 1990;48:647.

26. Schow SR, Triplett RG, Solomon JM. Lingualnerve injury associated with overpenetra-tion of bicortical screws used for rigid fixa-tion of a bilateral sagittal split osteotomy. JOral Maxillofac Surg 1996;54:1451.

27. August M, Marchena J, Donady J, Kaban L. Neu-rosensory deficit and functional impairmentafter sagittal ramus osteotomy: a long-termfollow-up study. J Oral Maxillofac Surg1998;56:1231.

28. Westermark A, Bystedt H, von Konow L. Infe-rior alveolar nerve function after mandibu-lar osteotomies. Br J Oral Maxillofac Surg1998;36:425.

29. Karas ND, Boyd SB, Sinn DP. Recovery of neu-rosensory function following orthognathicsurgery. J Oral Maxillofac Surg 1990;48:124.

30. Teerijoki-Oksa T, Jaaskelainen SK, Forssell K, etal. Risk factors of nerve injury duringmandibular sagittal split osteotomy. Int JOral Maxillofac Surg 2001;31:33.

31. Nishioka GJ, Zysset MK, van Sickels JE. Neu-rosensory disturbance with rigid fixation ofthe bilateral sagittal split osteotomy. J OralMaxillofac Surg 1987;45:20.

32. Jones DL, Wolford LM. Intraoperative record-

ing of trigeminal evoked potentials duringorthognathic surgery. Int J Adult OrthodonOrthognath Surg 1990;5:167.

33. Hallikainen D, Iizuka T, Lindqvist C. Cross-sectional tomography in evaluation ofpatients undergoing sagittal split osteoto-my. J Oral Maxillofac Surg 1992;50:1269.

34. Frerich B, Cornelius C-P, Wietholter H. Criticaltime of exposure of the rabbit inferior alve-olar nerve to Carnoy’s solution. J Oral Max-illofac Surg 1994;52:599.

35. Loescher AR, Robinson PP. The effect of surgi-cal medicaments on peripheral nerve func-tion. Br J Oral Maxillofac Surg 1998;36:327.

36. Block MS, Daire J, Stover J, Matthews M.Changes in the inferior alveolar nerve fol-lowing mandibular lengthening in the dogusing distraction osteogenesis. J Oral Max-illofac Surg 1993;51:652.

37. Hu J, Zou S, Tang Z, et al. Response of Schwanncells in the inferior alveolar nerve to dis-traction osteogenesis: an ultrastructuraland immunohistochemical study. Int J OralMaxillofac Surg 2003;32:318.

38. Hu J, Tang Z, Wang D, Buckley MJ. Changes inthe inferior alveolar nerve after mandibularlengthening with different rates of distrac-tion. J Oral Maxillofac Surg 2001;59:1041.

39. Louis P. Inferior alveolar nerve transpositionfor endosseous implant placement: a pre-liminary report. Oral Maxillofac Surg ClinNorth Am 2001;13:265.

40. Zuniga JR. Normal response to nerve injury:histology and psychophysics of degenera-tion and regeneration. Oral Maxillofac SurgClin North Am 1992;4:323.

41. Muller HW, Stoll G. Nerve injury and regener-ation: basic insights and therapeutic inter-ventions. Curr Opin Neurol 1998;11:557.

42. Seddon JJ. Three types of nerve injury. Brain1943; 66:237.

43. Sunderland S. A classification of peripheralnerve injuries produced by loss of function.Brain 1951;74:491.

44. Dellon AL, Mackinnon SE. Basic scientific andclinical applications of peripheral nerveregeneration. Surg Annu 1988;20:59.

45. Coglan KM, Irvine GH. Neurological damageafter sagittal split osteotomy. Int J OralMaxillofac Surg 1986;15:369.

46. Zuniga JR, Cheng N, Miller I, Phillips C.Regeneration of taste receptors and recov-ery of taste after lingual nerve repair. J OralMaxillofac Surg 1994;52 Suppl 2:128.

47. Zuniga JR, Meyer RA, Gregg JM, et al. Theaccuracy of clinical neurosensory testingfor nerve injury diagnosis. J Oral MaxillofacSurg 1998;56:2.

48. McDonald AR, Roberts TPL, Rowley HA,



Pogrel MA. Noninvasive somatosensorymonitoring of the injured inferior alveolarnerve using magnetic source imaging.J Oral Maxillofac Surg 1996;54:1968.

49. Scrivani SJ, Moses M, Donoff, RB, Kaban LB.Taste perception after lingual nerve repair.J Oral Maxillofac Surg 2000;58:3.

50. Hillerup S, Hjorting-Hansen E, Reumert T.Repair of the lingual nerve after iatrogenicinjury: a follow-up study of return of sen-sation and taste. J Oral Maxillofac Surg1994;52:1028.

51. Padilla M, Clark GT, Merrill RL. Topical med-ications for orofacial neuropathic pain: areview. J Am Dent Assoc 2000;131:184.

52. Gregg JM, Small EW. Surgical management oftrigeminal pain with radiofrequency lesionsof peripheral nerves. J Oral Maxillofac Surg1986;44:122.

53. Fardy MJ, Patton DW. Complications associat-ed with peripheral alcohol injections in themanagement of trigeminal neuralgia. Br JOral Maxillofac Surg 1994;32:387.

54. Khullar S, Emami B, Westermark A, Haanes H.Effect of low-level laser treatment on neu-rosensory deficits subsequent to sagittalramus osteotomy. Oral Surg Oral Med OralPathol Oral Radiol Endod 1996;82:132.

55. Khullar S, Brodin E, Barkvoll B, Haanes H. Pre-liminary study of low-level laser treatmentof long-standing sensory aberrations of theinferior alveolar nerve. J Oral MaxillofacSurg 1996;54:2.

56. Miloro M, Repasky M. Low-level laser effect onneurosensory recovery after sagittal ramusosteotomy. Oral Surg Oral Med Oral PatholOral Radiol Endod 2000;89:12.

57. Zuniga JR. Trigeminal ganglion cell response tomental nerve section and repair in the rat. JOral Maxillofac Surg 1999;57:427.

58. Pons TP. Massive cortical reorganization aftersensory deafferentation in adult macaques.Science 1991; 252:1159.

59. Dodson TB, Kaban LB. Recommendations formanagement of trigeminal nerve defects

based on a critical appraisal of the litera-ture. J Oral Maxillofac Surg 1997;55:1380.

60. Smith KG, Roninson PP. An experimentalstudy of three methods of lingual nervedefect repair. J Oral Maxillofac Surg 1995;53:1052.

61. LaBanc JP, Gregg JM. Trigeminal nerve injuries:basic problems, historical perspectives, earlysuccesses, and remaining challenges. OralMaxillofac Surg Clin North Am 1992;4:277.

62. Pogrel MA. The results of microneurosurgeryof the inferior alveolar and lingual nerve. JOral Maxillofac Surg 2002;60:485.

63. Miloro M. Surgical access for inferior alveolarnerve repair. J Oral Maxillofac Surg1995;53:1224.

64. Joshi A, Rood JP. External neurolysis of the lin-gual nerve. Int J Oral Maxillofac Surg 2002;31:40.

65. Millesi H, Terzis JK. Nomenclature in periph-eral nerve surgery. Clin Plast Surg1984;11:3.

66. Eppley BL, Snyders RV. Microanatomic analy-sis of the trigeminal nerve and potentialnerve graft donor sites. J Oral MaxillofacSurg 1991;49:612.

67. McCormick SU, Buchbinder D. Microanatom-ic analysis of the medial antebrachial cuta-neous nerve as a potential donor nerve inmaxillofacial grafting. J Oral MaxillofacSurg 1994;52:1022.

68. Brammar JP, Epker BN. Anatomic-histologicsurvey of the sural nerve: implications forinferior alveolar nerve grafting. J Oral Max-illofac Surg 1988;46:111.

69. Miloro M. Subjective outcomes following suralnerve harvest. J Oral Maxillofac Surg2002;60 Suppl 1:75.

70. Miloro M. Inferior alveolar nerve regenerationthrough an autogenous vein graft. J OralMaxillofac Surg 1996;54:65.

71. Pogrel MA, Maghen A. The use of autogenousvein grafts for inferior alveolar and lingualnerve reconstruction. J Oral MaxillofacSurg 2001;59:985.

72. Miloro M. Discussion: the use of autogenousvein grafts for inferior alveolar and lingualnerve reconstruction. J Oral MaxillofacSurg 2001;59:988.

73. Kitahara AK, Suzuki Y, Qi P. Facial nerve repairusing a collagen conduit in cats. Scand JPlast Reconstr Surg Hand Surg 1999;33:187.

74. Eppley BL, Delfino JJ. Collagen tube repair ofthe mandibular nerve: a preliminary inves-tigation in the rat. J Oral Maxillofac Surg1996;46:41.

75. DeFranzo AJ, Morykwas MJ, LaRosse JR.Autologous denatured muscle as a nervegraft. J Reconstr Microsurg 1994;10:145.

76. Mackinnon SE, Dellon AL. Clinical nervereconstruction with a bioabsorbable poly-glycolic acid tube. Plast Reconstr Surg1990;85:419.

77. Eppley BL, Snyders RV, Winkelmann T. Effica-cy of nerve growth factor in regeneration ofthe mandibular nerve: a preliminary report.J Oral Maxillofac Surg 1991;49:61.

78. Miloro M, Macy J. Expanded polytetrafluo-roethylene entubulation of the rabbit infe-rior alveolar nerve. Oral Surg Oral MedOral Pathol 2000;89:292–8.

79. Miloro M, Halkias L, Mallery S, et al. Low levellaser effect on neural regeneration in Gore-Tex tubes. Oral Surg Oral Med Oral PatholOral Radiol Endod 2002;93:27–34.

80. Pitta MC, Wolford LM, Mehra P, Hopkin J. Useof Gore-Tex tubing as a conduit for inferioralveolar and lingual nerve repair: experi-ence with 6 cases. J Oral Maxillofac Surg2001;59:493.

81. Pogrel MA, McDonald AR, Kaban LB. Gore-textubing as a conduit for repair of lingual andinferior alveolar nerve continuity defects: apreliminary report. J Oral Maxillofac Surg1998;56:319.

82. Lydiatt DD. Litigation and the lingual nerve.J Oral Maxillofac Surg 2003;61:197.

83. Deegan AE. The numbing truth. Monitor1998;9:1.



APPENDIX Nerve Terminology Review*allodynia: Pain due to a stimulus that does not normally provoke pain.analgesia: Absence of pain in the presence of stimulation that would normally be painful.anesthesia: Absence of any sensation in the presence of stimulation that would normally be painful or

nonpainful.anesthesia dolorosa: Pain in an area or region that is anesthetic.atypical neuralgia: A pain syndrome that is not typical of classic nontraumatic trigeminal neuralgia.axonotmesis (Seddon) or second- sthrough fourth-degree injuries (Sunderland): Nerve injury characterized by axonal injury with subsequent degeneration

and regeneration.causalgia: Burning pain, allodynia, and hyperpathia after a partial injury of a nerve.central pain: Pain associated with a primary central nervous system lesion (spinal cord or brain trauma, vascular lesions, tumors).chemoreceptor: A peripheral nerve receptor that is responsive to chemicals, including catecholamines.deafferentation pain: Pain occurring in a region of partial or complete traumatic nerve injury in which there is interruption of afferent impulses by

destruction of the afferent pathway or other mechanism.dysesthesia: An abnormal sensation, either spontaneous or evoked, that is unpleasant. All dysesthesias are a type of paresthesia but not all paresthesias are

dysesthesias.endoneurium: A connective tissue sheath surrounding individual nerve fibers and their Schwann cells.epineurium: A loose connective tissue sheath that encases the entire nerve trunk.fascicle: A bundle of nerve fibers encased by the perineurium.hyperalgesia: An increased response to a stimulus that is normally painful.hyperesthesia: An increased sensitivity to stimulation, excluding the special senses (ie, seeing, hearing, taste,

and smell).hyperpathia: A painful syndrome characterized by increased reaction to a stimulus, especially a repetitive

stimulus. The threshold is increased as well.hypoalgesia: Diminished pain in response to a normally painful stimulus.hypoesthesia: Decreased sensitivity to stimulation, excluding the special senses (ie, seeing, hearing, taste,

and smell).mechanoreceptor: A peripheral nerve receptor preferentially activated by physical deformation from pressure and associated with large sensory axons.mesoneurium: A connective tissue sheath, analogous to the mesentery of the intestine, that suspends the nerve trunk within soft tissue.monofascicular pattern: Characteristic cross-section of a nerve containing one large fascicle.neuralgia: Pain in the distribution of a nerve or nerves.neurapraxia (Seddon) or first-degree injury (Sunderland): Nerve injury characterized by a conduction block, with rapid and virtually complete return

of sensation or function and no axonal degeneration.neuritis: A special case of neuropathy now reserved for inflammatory processes affecting nerves.neurolysis: The surgical separation of adhesions from an injured peripheral nerve.neuroma: An anatomically disorganized mass of collagen and nerve fascicles, and a functionally abnormal region of a peripheral nerve resulting from a failed

regeneration following injury.neuropathy: A disturbance of function or a pathologic change in a nerve.neurotization: Axonal invasion of the distal nerve trunk.neurotmesis (Seddon) or fifth-degree injury (Sunderland): Nerve injury characterized by severe disruption of the connective tissue components of the nerve

trunk, with compromised sensory and functional recovery. Third-degree injury: Characterized by axonal damage and a breach of the endoneurial sheath,resulting in intrafascicular disorganization. The perineurium and epineurium remain intact. The mechanism is typically traction or compression.Fourth-degree injury: Characterized by disruption of the axon, endoneurium, and perineurium, resulting in severe fascicular disorganization. The epineurium remains intact. Possible mechanisms include traction, compression, injection injury, and chemical injury. Fifth-degree injury: Characterized bycomplete disruption of the nerve trunk with considerable tissue loss. Possible mechanisms include laceration, avulsion, and chemical injury.

nociceptor: A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged.oligofascicular pattern: Characteristic cross-section of a nerve containing 2 to 10 rather large fascicles.paresthesia: An abnormal sensation, either spontaneous or evoked, that is not unpleasant. A global term used to encompass all types of nerve injuries.perineurium: A thick connective tissue sheath surrounding fascicles.polyfascicular pattern: Characteristic cross-section of a nerve containing > 10 fascicles of different sizes, with a prevalence of small fascicles.protopathia: The inability to distinguish between two different modes of sensation, such as a painful and nonpainful pinprick.sympathetically mediated pain: A general term that refers to a family of related disorders including causalgia, reflex sympathetic dystrophy, minor causalgia,

Sudeck’s atrophy, and postherpetic neuralgia, which may be sympathetically maintained.synesthesia: A sensation felt in one part of the body when another part is stimulated.wallerian degeneration: The distal degeneration of the axon and its myelin sheath following injury.

*Adapted from LaBanc JP, Gregg JM. Glossary. Trigeminal nerve injury: diagnosis and management. Oral Maxillofac Surg Clin North Am 1992;4:563.


principles of oral and maxillofacial surgery maxillofacial neurologic disorders has promulgated...

Documents