Mandibular Nerve Neurosensory Impairment Following Dental Implant Surgery_ Management and Protocol

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TABLE OF CONTENTS Aug 2012 - 0 comments

Mandibular Nerve Neurosensory Impairment Following DentalImplant Surgery: Management And Protocol

By: Carl E. Misch DDS, MDS and Randolph Resnik DMD, MDS

2012-08-01
http://www.oralhealthgroup.com/issues/toc.aspx?edition=8/1/2012


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Sensory impairment of the skin and mucosa innervated by branches of the trigeminal nerve is a potential concern in association with dental implant surgery.The most common nerves traumatized in implant dentistry are the inferior alveolar nerve (IAN) and its mental branch. Other nerves at risk include the lingualnerve, long buccal nerve and the infraobital nerve because of the anatomic location of these structures. Neurosensory impairment may occur during allphases of dental implant surgery, including anesthetic administration, incis ions, soft tissue reflection, osteotomy preparation, bone augmentation, implantplacement, suturing and/or soft t issue swelling after surgery. The reported incidence of such nerve injuries following dental implant procedures is highlyvariable (0%-44%).1-5

When a nerve injury occurs, the dentist should be able to recognize the type and extent of injury and provide the most appropriate post-operative care.Traumatic and iatrogenic nerve complications may involve total or partial nerve resection, crushing, s tretching, or entrapment injuries. The resulting sensorydeficits may range from a non-painful minor loss of sensation to a permanent and severe debilitating pain dysfunction. Presently, no standardized protocolexists for the dentist in the management of nerve injuries after implant surgery. Yet, surveys at the Misch International Implant Institute indicate 87% of dentists have encountered situations of neurosensory impairment within their practices.6 Yet , no organized approach to evaluate and/or treat this conditionhas been presented. The purpose of this paper is to present guidelines for the dentist in the diagnosis and possible management of mandibular nerveneurosensory deficits (including referral) following dental implant surgery that i s dependent on the his tory, type, and nature of the injury.

PERIPHERAL NERVE ANATOMY/HISTOLOGYThe trigeminal nerve is the largest of the cranial nerves and has three major divisions: the opthalamic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). A nerve outside of the central nervous system is called a peripheral nerve. The mandibular nerve is a peripheral nerve which is the largest of thetrigeminal branches and, as previously stated, i s t he most common branch that is involved with neurosensory disturbances following dental implant surgery.This division carries sensory information from the lower lip, chin, lower teeth (and associated soft tissues), the mandibular bone, and parts of the externalear.

The mandibular nerve also contains motor fibers for supply of the muscles of mastication, tensor tympani muscles of the ear and tensor veli palatine

muscles of the soft palate.6 However, these motor branches and many of the sensory fibers to the external ear are not injured during implant surgery, sincethe motor fibers are separated from V3 prior to its exit from the foramen ovale of the skull and many of the sensory fibers enter the nerve above the lingula of the ramus. A V3 injury in implant surgery usually occurs after the nerve enters the lingula of the mandibular ramus and anywhere along its pathway in thebody and/or its exit from the mental foramen.

The histology of the mandibular nerve consists of connective tissue and neural components. The smallest functional unit in the trigeminal nerve is the nervefiber. These nerve fibers can be either myelinated or unmyelinated. Myelinated nerve fibers, the most abundant, consist of a single axon that is encasedindividually by a single Schwann cell. The individual nerve fibers and Schwann cells are surrounded by a protective endoneurial connective tissue layer (endoneurium), which is made up of a basal lamina, collagen fibers and endoneurial capillaries.7


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The individual nerve fibers of the trigeminal nerve are situated in multiple groups termed fascicles. Surrounding the bundles of fascicles is a thin, dense,multilayered connective tissue sheath called the perineurium. The perineurium maintains intrafascicular pressure and acts as a diffusion barrier in theprotection of the individual fibers. If any of these extra neural tissues are injured, impaired neural transmission of the individual nerve fibers may result in asensory dis turbance.11 The neurosensory impairment is dependent on the extent of damage to the individual tissue type.

A main concern related to injury of the IAN is the altered sensory functions (i.e. touch, pressure, temperature or pain) following implant related surgeries.Loss of sensation of the cheek and/or mandibular lip may lead to traumatic injury to the soft tis sues during chewing and mastication and may affect theability to drink. Significant pain may also be associated with these sensory functions, which may be debilitating to the patient.

TERMINOLOGY OF SENSORY DISTURBANCESThe literature related to peripheral nerve injuries is abundant; however there exists great variation in the nomenclature used to describe the clinical signs andsymptoms. Several common terms are used, often with overlapping meanings. The most commonly used term to describe an altered sensation i sparesthesia. For years, paresthesia has been used to describe any altered sensation including pain, numbness, tingling, aching, warmth, cold, andburning.12 Recently, the Association for the Study of Pain has s tandardized a nomenclature sys tem that defines the most frequently used neurosensorydescriptive terms.13 There now exists three distinct categories with related subcategories describing neurosensory deficits. The most significant change isparesthesia which is limited to an altered sensation that is not unpleasant. Dysesthesia is defined as any altered sensation that is unpleasant. Anesthesiais the total loss of feeling or sensation. These three main categories are used to describe, diagnose and treat (including referral) the nerve injury in theprotocol suggested in this paper. Table 1 describes the most commonly used terms for neurosensory deficits. (Table 1).

RELATED HOST AND LOCAL FACTORSMany factors, both local and host-related, will determine the neurologic response to an injury. The type of injury is the most significant local factor relating tothe neurologic response. In general, injuries that occur at the proximal site of the peripheral nerve are more significant (i.e. ramus region) than those thatoccur at dis tal si tes (i.e. the mental foramen area). The more proximal the nerve injury site, the higher the risk of trigeminal ganglion cell damage and the

initiation of retrograde differentiation effects into the central nervous system.16

Less traumatic injuries often are associated with early paresthesia or dyses thesias. When a nerve is stretched or compressed, the perineurium will protectthe nerve fibers within the fascicles. With greater tension, the fascicles will begin to elongate, thus elevating the intrafascicular pressure. Further pressurewill lead to axon damage and if elongation is greater than 30%, structural failure with possible severance may occur.17 Partial or incomplete nerve injurieswill have different responses than complete nerve lacerations or resect ions. In contrast, more severe injuries are initially anesthetic lesions with poor orofacialfunction and associated referred, radiating forms of paresthesia. Although they may not be painful initially, they may eventually lead to formation of dysfunctional chronic neuroma formation.18,19


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The most significant host factors related to implant dentistry are the patients age and gender. It is well documented, for all types of nerve injuries that bothfemales and increasing age are at greater risk of neurosensory deficits.20,21 In older individuals, cell body regeneration has been shown to be slower andless dramatic than in younger individuals.

PHARMACOLOGIC THERAPYThe pharmacologic therapies for acute nerve injuries include the use of corticosteroids and non-steroidal anti-inflammatory agents. The use of adrenocorticosteroids (e.g., Dexamethasone) has been shown to minimize neuropathy following nerve injuries if administered in high doses within one weekof injury.22,23 Additionally, adrenocorticosteroids have been shown to inhibit axon sprouting centrally and ectopic discharges from injured axons andprevention of neuroma formation.24,25 Dexamethasone (812 mg) is specifically recommended because of its greater anti- inflammatory effects incomparison to other corticosteroids.26,27 It has been advocated that a tapering dose of a corticosteroid for 57 days be prescribed following trigeminal nerveinjury.28

Further pharmacologic therapy inc ludes the use of Nonsteroidal Ant i-Inflammatory agents (NSAIDs). NSAIDs have been shown to be excellent inhibitors of prostaglandin synthesis from damaged peripheral nerve endings.29 Prostaglandins released as a result of peripheral nerve damage sensitize peripheralnociceptor fibers and central spinal tract neurons.30 Accordingly, maintaining therapeutic blood levels of NSAIDs as an adjunct to the corticosteroid usagefor one to three weeks after the injury i s highly beneficial for the acute and intermediate stages of trigeminal nerve recovery.31 Since any altered sensationmay be due to an inflammatory reaction, a post-operative course of steroid treatment followed by a high dose of nonsteroidal anti-inflammatory medication(such as ibuprofen 600 to 800 milligrams three times per day for three weeks) is used as soon as possible following any nerve injury. If necessary at two tothree weeks after the injury on the basis of a repeated neurosensory examination, the c linician can prescribe an additional three weeks of nonsteroidal anti-inflammatory drug treatment, i f no signs of gastric dis turbances are present.

Additional pharmacologic agents that have been advocated include antidepressants, anticonvulsants, antisympathetic agents and topical medications.Precaution should be taken with these types of pharmacologic treatments as they should be prescribed and managed by a clinician familiar with the side

effects of these drugs and experienced in treatment of nerve injuries.

INITIAL MANAGEMENT OF NEUROSENSORY IMPAIRMENTVarious surgical and pharmacologic treatments have been advocated in the literature for nerve injury with varying degrees of success.30 The management of the neurosensory deficits presented in this paper (Table 2) should first include recognition and documentation of the type of injury and associated s igns andsymptoms. Initially, phys iologic and pharmacologic nonsurgical therapies are indicated followed by surgical evaluation and/or treatment.


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If the patient experiences an electric shock feeling to the tongue (lingual nerve) or chin, lip, and/or gingival region (IAN), the anesthetic needle may haveperforated the nerve. This is more an issue for the lingual nerve, since it is smaller in diameter. Although more than 75% of altered feelings from this type of nerve injury resolves within threeweeks when this happens, a pharmacologic protocol of immediate dexamethasone 4 mg/ml injection into the site, followedby three days of decreasing corticost eroid doses is beneficial (Fig. 1).

If, during surgery, known or observed trauma (including traction or compression of the nerve trunk) has occurred, the topical application of Dexamethasone issuggested. One to two ml of the intravenous form of Dexamethasone (4mg/ml) may be topically applied for 1-2 minutes32 (Figs. 2-4). The direct applicationof adrenocorticosteroids will reduce neural inflammation and reduce compression from swelling, which may enhance recovery from neurosensory deficits. Nomorbidity has been associated with topical s teroid application at the nerve injury si te, yet significant improvement in post surgery recovery has beenobserved. This is followed by a six day regimen of oral dexamethasone (4 mg two tabs AM for three days, one tab AM for three days). If known nerve trunktransection is clinically observed during the surgery, immediate referral to a nerve repair specialist is highly recommended.

The most important physiologic therapy at the time of surgery includes removal or repositioning of any irritant (implant, bone screw) in close approximationto the neurovascular bundle. A radiograph or CT scan immediately after implant placement is warranted to insure the nerve is not violated. If a post operativeradiograph indicates the implant may encroach upon the IAN, it may be removed, a steroid introduced into the ost eotomy site and then a shorter lengthimplant replaced in the same s ite in a more ideal location.32 No bone grafting materials should be placed in the osteotomy site, since it may invade themandibular canal and interfere with nerve repair.

Cryotherapy should be applied extraorally to most any implant or bone graft s ite, but especially when nerve injury is suspect. The paraneural tissues shouldhave ice applied intensely for the first 24 hours post operatively and then episodically for the first week. Cryotherapy has been shown to minimize s econdarynerve injury from edema-induced compression, decrease the metabolic degeneration rate of trigeminal ganglion cells from undergoing degeneration, and slowpotential neuroma formation.33 Ice, when applied to the t issues, has been shown to s ignificantly improve postsurgical recovery.

POST-OPERATIVE MANAGEMENT OF MEUROSENSORY DEFICITS

Neurosensory Testing When the dentist discovers a neurosensory deficit has occurred (often at the suture removal) a comprehensive sensory evaluation should be completed. Thepurpose of this initial examination is to ascertain whether a sensory deficit ex ists , to define and quantify the extent of nerve injury, record a baseline for recovery, and to determine if referral for microneurosurgery is indicated.11


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There are several accepted protocols for neurosensory testing. Ideally, a range of tests are performed ranging from light mechanical to noxious stimuli. Theauthors have advocated two categories of clinical neurosensory test ing, nociceptive and mechanoreceptive. Each test is specific for various neural receptorsand axons. The responses are recorded and quantitatively compared with responses from contralateral uninjured tissues (control). The following are the morecommon test s suggested for the neurosensory evaluation:

NociceptivePin-Prick Test : A 27-gauge needle is utilized to test for pressure detection and anesthesia/paresthesia/dysthesia. A cosmetic pencil is used for mappingand photographs are used to evaluate the recovery period (Fig. 5).

Temperature Sensitivity Tests : Ice chips or ethyl chloride spray and a heated mirror handle (warmed to 43 degrees) are used to determine the patientsability t o feel cold and hot. Alternatively, test t ubes may be filled with hot (43C) water and/or cold water.

Mechanoceptive Tests :Static Touch Detection Tests : A cotton tip applicator is used to determine sensation.

Direction of Movement Test : The sensory modalities of mandibular nerve fibers are touch and vibration. A soft brush is used (with the patients eyes c losed)to determine the patients ability to detect both sensation and direction of movement.

Two-Point Discrimination Tes t : With the patients eyes closed, the patients ability to discriminate varying distances between two points is determined. Acaliper with the ability to vary the distance between two points can be used. The normal distance at which most patients can discriminate two separatepoints is 6 mm.34

If the initial exam is within one week of the surgery, a course of steroids (decadron) is prescribed followed by three weeks of high dose NSAIDs (600 mg 800 mg ibuprofen). If paresthesia is reported after a two week period, only high doses of NSAIDs should be prescribed (600 mg to 800 mg ibuprofen TID for three weeks). If necessary, an additional three weeks of NSAIDs may be prescribed. If paresthesia i s present, the neurosensory exam is repeated every twoto three weeks. The patient should be periodically re-examined to evaluate if nerve repair is occurring, signified by reduced symptoms and less soft tissuearea involvement. Neurosensory improvement most often occurs by two to three months. If significant sensation has not improved by three to four monthsafter the surgery, the prognosis typically is poor.


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REFERRAL OF NEUROSENSORY DEFICITSIn certain situations, patients need to be referred to a practitioner experienced in nerve injury assessment and repair (Table 2). As previously mentioned, if known transection of the nerve occurs during surgery, Dexamethasone should be applied and following surgery, an immediate referral to a specialis t inmicrosurgical repair. Likewise, if the patient has dysesthesias or complete anesthesia at t he initial exam after surgery, the patient should be referred to anerve specialist. Prompt surgical intervention may allow for the best chance of neurosensory recovery.

The decision post operatively to refer should be based on the patients signs and symptoms and the type of injury. A paresthesia should be given sufficienttime for neurosensory recovery. However, referral to a nerve injury specialist is suggested after three months if the paresthesia has not improved during thistime frame.

Additional physiologic therapies have shown successful results in the treatment of nerve impairments, and include transcutaneous electric nerve stimulation(TENS),35 acupuncture36 and low-level laser therapy.37 It i s suggested these physiologic therapies be used as indicated by a nerve specialis t.

Various techniques to surgically treat nerve impairments have been advocated with varying results. This includes decompression, direct anastamosis ,38

autogenous nerve grafts,39 and alloplastic grafts.40 Successful surgical intervention, when indicated, is generally agreed to be most predictable if performedprior to the onset of Wallerian degeneration (approximately three months).28 This early, aggressive treatment may prevent transition to chronic refractoryneuropathies.41,42

SUMMARYThe suggested treatment of mandibular nerve neurosensory deficit is summarized in Table 2. The protocol during surgery is divided into two aspects: nerveinjury suspected (most often after a radiograph is made), or known nerve transection during surgery. Corticosteroids, NSAIDs, and cryotherapy areprescribed following surgery. The post operative protocol is divided into the one week, initial treatment and the 12 week period. During this time frame aparesthesia is documented and mapped every two to three weeks to monitor the condition. NSAIDs are prescribed for up to three weeks after the initial

corticosteroid therapy. If dyses thesias or anesthesia is found at the initial post operative appointment, a referral to a nerve specialis t is suggested. Referral isalso suggested to a specialist in nerve damage after three months if the paresthesia is not improved.

CONCLUSIONWith the popularity of dental implants and associated bone grafting, peripheral trigeminal nerve branch impairments may become more frequent. It is notexpected that the practitioner make a definite neurosensory diagnosis. However, one must be sufficiently knowledgeable in the causes , prevention andtreatment of such injuries to make an appropriate diagnosis and t reatment and timely referral when necessary. Neurosensory changes in the orofacial regionon rare occasions may be devastating. A protocol has been presented which emphasizes early treatment with a wide range of modalities and guidelines for treatment based on type and degree of neurosensory impairment. OH


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*Clinical Professor, Temple University, PA, +Misch International Implant Institute, Beverly Hills, MI Private Practice, Beverly Hills, MI

Private Practice, Pittsburgh, PA Faculty, Misch Implant Institute, Beverly Hills, MI. Oral Health welcomes this original article. REFERENCES

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13. Classification of Chronic Pain, Second Edition: International Association for the Study of Pain Task Force on Taxonomy, ed.: H Merskey and N. Bogduk.IASP Press IASP Council in Kyoto, November 29-30-2007.

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29. Devor, M.: Pathophysiology of damaged peri pheral nerves. In Wall PD, Melzack, R. (eds): Textbook of Pain, ed 2. London, Churchill Livingstone, 63-66,1989.

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9/11/13 Mandibular Nerve Neurosensory Impairment Foll owing Dental Implant Surg ery: Management And Protocol


37. Poole, TE., Holland, I., Peterson, LJ.: Clinical efficacy of low level laser treatment of oro-facial neurosensory deficits, J Oral Maxillofac Surg, 51 (suppl.3), 182-186, 1993.

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Photos

Larger photo & full captionFile size: 452.9 KB (900px X 587px)Caption: Figure 1: Dexamethasone 4m g/ml (in tra venous form) may...

Larger photo & full captionFile size: 525.5 KB (900px X 655px)Caption: Figure 2. Dexamethasone 4 mg/ml may be used to bathe th...
http://viewphoto%28900%2C655%2C%27/daily_images/1001604108-1001604145.jpg','Figure%202.%20Dexamethasone%204%20mg/ml%20may%20be%20used%20to%20bathe%20the%20IAN%20after%20injury.','');http://viewphoto%28900%2C655%2C%27/daily_images/1001604108-1001604145.jpg','Figure%202.%20Dexamethasone%204%20mg/ml%20may%20be%20used%20to%20bathe%20the%20IAN%20after%20injury.','');http://viewphoto%28900%2C587%2C%27/daily_images/1001604108-1001604144.jpg','Figure%201:%20Dexamethasone%204mg/ml%20(in%C2%ADtra%C2%ADvenous%20form)%20may%20be%20used%20after%20an%20electric%20shock%20feeling%20during%20an%20injection.','');


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Larger photo & full captionFile si ze: 223.2 KB (900px X 659px)Caption: Figure 3. A post operative radiograph (the day of surge...

Larger photo & full captionFile size: 227.9 KB (900px X 675px)Caption: Figure 4. After the dexamethasone treatment, the implan...

Larger photo & full captionFile size: 279.9 KB (900px X 600px)Caption: Figure 5. Pin-Prick Test: A 27-guage needle is used to ...

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Mandibular Nerve Neurosensory Impairment Following Dental Implant Surgery_ Management and Protocol

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