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CURRENT THERAPY

J Oral Maxillofac Surg66:513-522, 2008

Temporal Bone Fractures: A Review forthe Oral and Maxillofacial Surgeon

Michael Gladwell, DMD,* and Christopher Viozzi, DDS, MD†

Fracture of the temporal bone is, by definition, a fracture of the skull base. Even though the oral andmaxillofacial surgeon (OMS) may not provide definitive management of temporal bone fractures or theirsequelae, a working knowledge of this area is important for any surgeon participating in the care ofpatients with craniomaxillofacial trauma, because temporal bone fractures are often associated withinjuries to other areas of the craniomaxillofacial skeleton and because these fractures are relativelyfrequent. In many centers, particularly community hospitals, the OMS may be the primary provider ofcare for facial trauma and will treat patients with clinical or radiographic evidence of temporal bonefractures. Immediate access to other specialists to manage or observe these injuries may not be possible,making the OMS responsible for early evaluation and management.This article briefly reviews the epidemiology of temporal bone injuries, as well as the pertinent anatomy,radiographic imaging findings, and ancillary testing maneuvers. It then presents a more detailed descrip-tion of the various clinical findings and the associated management strategies. It concludes with adiscussion of the subset of temporal bone fractures involving the temporomandibular joint.© 2008 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 66:513-522, 2008
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pidemiology

Skull fractures affect 23% to 66% of patients withead trauma,1,2 with 21% of these patients sufferingrauma to the skull base.3 Trauma to the skull base is common component of head injuries, particularlylunt head trauma. In adults, up to 75% of patientsith a skull base fracture have a temporal bone frac-

ure as a component of the injury.4-6 Multiple impor-ant anatomic structures are affected by these injuries,ncluding the facial nerve, middle and inner ear, andntracranial contents; thus, these are serious injuries,

ith the potential for significant long-term sequelae.Risk factors for and causes of temporal bone fractures

re similar to those in any patient with head injury:ounger age, male gender, motor vehicle accidents, falls,

*Resident, Department of Surgery, Division of Oral and Maxillo-

acial Surgery, Mayo Clinic, Rochester, MN.

†Consultant, Department of Surgery, Division of Oral and Maxil-

ofacial Surgery, Mayo Clinic, and Assistant Professor of Surgery,

ayo Clinic College of Medicine, Rochester, MN.

Address correspondence and reprint requests to Dr Viozzi: Mayo

linic, Department of Surgery, Division of Oral and Maxillofacial

urgery, 200 First Street SW, Rochester, MN 55905; e-mail: viozzi.

[email protected]

2008 American Association of Oral and Maxillofacial Surgeons

278-2391/08/6603-0015$34.00/0

coi:10.1016/j.joms.2007.08.039

513

ecreational injuries, and assaults. Penetrating trauma islso a relatively frequent cause of temporal bone frac-ure. Other unusual reported causes of temporalone injury include lightning strikes, chiropracticanipulation, and even flying fish.7-9

natomy

The skull base is composed of the occipital bone, 2emporal bones, the sphenoid bone, and the frontalone. A skull base fracture may involve only 1, sev-ral, or all of these bones.The temporal bone itself is composed of 5 parts:

he squamous, petrous, mastoid, and tympanic por-ions, as well as the styloid process (Fig 1). Thequamous portion is smooth and convex; the tempo-alis muscle attaches to this region. The zygomaticrch projects forward from the inferior part of thequamous portion, giving rise to the articular tubercleust anterior to the glenoid fossa. The fossa is boundedosteriorly by the tympanic portion of the temporalone, the bony external auditory canal. The pyramid-haped petrous portion of the temporal bone isedged between the sphenoid and occipital bone at

he base of the skull. Through it pass many importanttructures, including the carotid canal, internal jugu-ar vein, and facial nerve (Fig 2).

Fractures of the temporal bone have generally been
lassified into 2 types, longitudinal and transverse,
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514 TEMPORAL BONE FRACTURES

ndicating the relationship of the fracture line to theong axis of the petrous portion of the temporal bone.ongitudinal fractures begin at the squamous portionf the temporal bone, run through the external audi-ory canal, then turn anteriorly toward the foramenacerum. The middle ear is spared in this type ofracture, because the fracture traverses lateral or an-erior to the otic capsule (Fig 3). Transverse fracturesegin from the foramen magnum, run through thetic capsule containing the middle ear structures, thenurn anteriorly toward the foramen lacerum (Fig 4).

The reported incidence of these fracture patterns isariable. Studies citing the radiographic incidence ofach fracture type span a time period during whichdvances in imaging technology have led to muchore detailed radiographic images and thus differ-

nces in the frequency of each radiographic diagno-is. Some fractures are not purely of a single type, butather are a combination of longitudinal and trans-erse. As a general rule, classic longitudinal fractureccounts for about 80% of cases, with the remaining0% tranvserse fractures.10-14

Longitudinal fractures are most frequently causedy a lateral blow to the skull in the parietal region.ransverse fractures are more commonly caused by

ntense blows to the occipital region or by a directrontal injury. The latter are more frequently seriousr fatal injuries. A fracture with significant comminu-ion or fracture lines running in both longitudinal and

FIGURE 1. Temp

ladwell and Viozzi. Temporal Bone Fractures. J Oral Maxillofa

ransverse directions is termed a mixed fracture. u

Because studies have suggested that the traditionallassification system may not predict the presence ofequelae, such as facial nerve injury or cerebrospinaluid (CSF) leak, alternatives to the traditional classifi-ation scheme have been developed. One alternativecheme that has demonstrated better correlationlassifies fractures based on whether they are oticapsule–sparing or otic capsule–violating.15 Othersave suggested that fracture classifications should in-lude more specifics regarding fracture location, be-ause of the difficulty in describing many fractures asither longitudinal or transverse,10 or should describeractures in a manner that correlates with the optimalurgical approach to repair the facial nerve.16

linical Examination andeneral Findings

Before the development and widespread use ofomputed tomography (CT), temporal bone fracturesere diagnosed on the basis of history of head injury

ccompanied by otorrhea, hemotympanum, and fa-ial paralysis.17 Nonobtunded patients with temporalone fractures may complain of such symptoms asertigo, nausea and vomiting, facial muscle weakness,MJ discomfort or dysfunction, and hearing loss orhanges. Evaluating an obtunded patient with a sus-ected temporal bone fracture is problematic, partic-

ne, lateral view.

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GLADWELL AND VIOZZI 515

Clinical signs may include ecchymosis, particularyn the periorbital region due to anterior or middleranial fossa trauma (“raccoon eyes” sign), or in theostauricular region due to bleeding from the mastoideins or postauricular artery (Battle’s sign). CSF otor-hea or rhinorrhea is a frequent finding, occurring in0% of temporal bone fractures.Hemotympanum is a very common finding in both

racture patterns, and, if hemorrhage from the exter-al auditory canal (EAC) is severe, can indicate injuryo the carotid artery. Facial nerve function should beully assessed and documented. Sensorineural or con-uctive hearing loss also is commonly found.

maging Studies

Today, CT scanning is performed routinely to eval-

FIGURE 2. Skull b


ate head-injured patients and is part of the routine i

nitial workup and treatment of polytrauma patients.t is routinely ordered to rule out life-threateningntracranial hemorrhage. Temporal bone fracture isrequently first noted during this routine head CTxamination. The need for subsequent, more highlyetailed CT imaging of the temporal bone should beuided by the subsequent evaluation of the patient; fornstance, a patient with conductive hearing loss with novidence of facial nerve injury, CSF leak, or nystagmusoes not necessarily need further CT evaluation.

ther Diagnostic Maneuvers

Formal facial nerve testing and audiologic testingre additional tests that may be of use in evaluatingnd treating temporal bone injuries. Audiology is ofarticular use in a patient with suspected inner ear

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onductive hearing loss, allowing time for the hemo-ympanum to resolve. Facial nerve testing is indicatedn a patient with delayed facial nerve palsy, becausehis patient may benefit from surgical decompressionf the facial nerve, although this treatment is contro-ersial. Electroneuronography (ENoG) and nerve ex-itability testing (NET) can be performed to docu-ent the degree of facial nerve dysfunction.

pecific Clinical Findings andanagement Correlations

HEARING LOSS

This common complication is noted in the largeajority of patients with temporal bone fractures and

uggests that audiometry is appropriate for any pa-ient with a temporal bone fracture. Fracture patternictates the auditory structures involved, and thus theype of hearing impairment noted. Because the moreommon longitudinal fracture traverses the EACsparing the middle/inner ear), it produces hemotym-anum, typically with conductive hearing loss. Thisan be due to the hemotympanum itself behind theympanic membrane (TM), or from TM perforation orssicular chain disruption (particularly in cases ofrolonged conductive loss). In contrast, transverse

ractures can violate the otic capsule and result in

FIGURE 3. Longitudinal fracture traversing


evere sensorineural hearing loss (Fig 5). The mem- t

ranous labyrinth can be subjected to concussivenjuries or direct injury with disruption.

ManagementConductive hearing loss generally resolves over

ime (usually within 3 to 4 weeks). Pure hemotympa-um generally resolves without sequelae within thisime period as well, as the blood behind the TMissipates. In other cases, the TM itself is directly

njured or perforation is observed. Again, many (up to0%) of these cases of conductive hearing loss willesolve within 4 weeks. If conductive hearing lossersists to 3 months, then myringoplasty (for smallerforations) or formal tympanoplasty (for larger per-

orations or in cases where myringoplasty has failed)ay be performed. In myringoplasty, the edges of theerforation are freshened, and a paper patch or steri-trip is placed over the perforation to promote heal-ng. Tympanoplasty involves an incision to gain ac-ess to the medial or lateral portion of the TM. A graft,ost commonly an autogenous graft of postauricular

ascia, is placed over the defect. Occasionally, allo-rafts are used. This procedure is successful in 90% to5% of patients, with revisions carrying high successates as well.

Persistence of conductive hearing loss after multi-le attempts at repair suggests ossicular chain disrup-

al auditory canal but sparing otic capsule.

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s thus considered appropriate. High-resolution CTcans can detect ossicular chain disruption,4,18 indi-ating the need for prosthetic reconstruction of thessicle or ossicles. In general, an approach that leavess much of the functional, undamaged ossicles asossible and uses the lightest-weight prosthetic mate-ial available produces the best audiologic outcomes.here are many variations in technique and materials;ecisions should be guided by the portion of thessicular chain requiring reconstruction.19

There is no effective medical treatment for sensori-eural hearing loss (SNHL), which results from damageo the cochlea or nerve pathways to the brain. A study ofearing loss from temporal bone fracture found thathereas 80% of cases of conductive hearing loss from a

ongitudinal fracture resolved spontaneously; no case ofotal SNHL from a transverse fracture showed improve-ent over time.20 SNHL not only involves a reduction in

ound level, but also can affect speech intelligibility andnderstanding. Treatment for SNHL is rehabilitative

FIGURE 4. Transverse frac


ith hearing aids or cochlear implants. S

VERTIGO

Vertigo refers to the sensation of spinning or whirl-ng resulting from a disturbance in balance. The pa-ient’s sensation of such movement is termed sub-ective vertigo, and the perception of movement inurrounding objects by the patient is termed objectiveertigo. The vestibular system is responsible for inte-rating sensory stimuli utilizing visual inputs, sensorynputs from the vestibular system, and proprioceptivenputs from other body structures. This complex pro-ess of neural inputs is integrated to provide theubject with position sense. Vestibular symptoms sec-ndary to temporal bone injury can result from vari-us causes, including direct otic capsule injury, con-ussive injury to the labyrinth, brainstem/nucleinjury, and perilymphatic fistula (PLF). Taken as a

hole, the incidence is variable, reported as rang-ng between 24% to 78% of patients with temporalone fractures.21,22 Persistent vertigo with fluctuating

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etween the perilymph-filled inner ear structures andhe air-filled middle ear structures.

ManagementVestibular symptoms with disequilibrium generally

mprove as activity resumes. Vestibular rehabilitationnvolves exercises aimed at stressing the vestibularystem so as to encourage compensation and acceler-te recovery. Specific techniques for this may includeawthorne-Cooksey exercises and other activities

hat create sensory inputs that tax the visual, vestib-lar, and proprioceptive neural systems to integrate

nputs in a functional way. Over time, these exercisesmprove the dysfunctional vertiginous response of theatient’s balance system to both noxious vertigo-in-ucing inputs and, more importantly, nonnoxious ev-ryday activities. The prognosis for full recovery isxcellent in most patients.PLF occurs most commonly at the round or ovalindow. The usual manifestations are sudden or pro-

ressively fluctuating vertigo with SNHL; other possi-le symptoms are a sensation of aural fullness andinnitus. The treatment for PLF is controversial. Somef these communications are thought to heal without

ntervention over time.23,24 Nonsurgical treatmentsnclude maintaining bed rest, elevating the head ofhe bed, using stool softeners, avoiding the Valsalvaaneuver, and administering sedative agents. The de-

nitive treatment for PLF is surgical exploration, iden-ification of the fistula, and closure of the commu-icating defect. In nontraumatic cases of PLF, the

IGURE 5. Axial view of right temporal bone fracture crossing middlear structures.

ladwell and Viozzi. Temporal Bone Fractures. J Oral Maxillofacurg 2008.

ecision to pursue surgical treatment can be difficult, i

ue to the varying presentations, some of which areery subtle. The decision to pursue surgery is oftenore clear-cut in a patient with a clear history of

emporal bone trauma and symptoms of PLF.The technique for PLF repair includes development

f a tympanomeatal flap to permit visualization of theound and oval window niche. The surgical site ishen observed for clear fluid, which may indicate theresence of perilymph. False-positive identification isossible because of the presence of transudates fromhe middle ear, and even the presence of irrigatinguids. Perilymph is one of the few body fluids thatontains �2-transferrin, but identifying this fluid intra-peratively is not feasible at the present time. Thetility of other maneuvers to aid in the identificationf perilymph, including Trendelenberg positioning,

ntraoperative Valsalva maneuver, and internal jugularein compression, is not clear at present.PLF repair is accomplished by placing a graft over

he leak. If no obvious leak is seen, then the footplatend round window are covered with a graft, on thessumption that this is the most likely area for theeak. Various graft materials have been and are cur-ently used, including fat, fascia, perichondrium, andarotid-masseteric fascia. Fat is no longer used, due toigh failure rates.25 Many surgeons will perform graft-

ng in cases with no obvious leak seen at surgeryprophylactic grafting). Postoperative care includesinimizing intracranial pressure by avoiding Valsalvaaneuvers, heavy lifting, or a head-down position.

tool softeners are used, and antinausea medicationsay be needed.26

CEREBROSPINAL FLUID LEAK

CSF leakage may be noted both from the ear andose in skull base injuries. Diagnosis is based onhysical findings, as well as accurate identification ofhe leaked fluid. Past diagnostic tests for CSF leakagencluded the halo sign and double-ring test. Separa-ion of CSF from serum is suggestive but not conclu-ive for the presence of CSF. Glucose content also isnreliable for testing for CSF, with a reported false-ositive rate of 45% to 75%.27,28 The �2-transferrinest evaluates fluid for the presence of a protein foundxclusively in CSF and perilymph but not in blood,asal secretions, or middle ear secretions. This testas been found to be 100% sensitive and 95% specific

n identifying CSF leakage.27

Leaks can present in a delayed fashion, and posi-ional changes can increase or decrease the amount ofuid leak. The incidence of CSF leaks is generally lowhen taking all skull fractures as a group,29 but the

ncidence in temporal bone fractures has been re-orted to range from 11% to 45%.1,30,31 If there isoubt regarding the validity of CSF leakage, the fluid

s collected and sent for �2-transferrin evaluation.

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ManagementBecause most CSF leaks will close spontaneously,32

edical management is always attempted first. Gen-ral measures used to encourage resolution of CSFeaks include bedrest and head elevation. Use of aumbar drain to decrease circulating CSF may be help-ul, as can maneuvers to avoid increasing pressureithin the subarachnoid space (such as stool soften-

rs to avoid straining, acetazolamide to decrease CSFroduction, and head elevation).13,27 Patients inhom a craniotomy has been performed to treat

ntracranial hemorrhage generally already have an in-raventricular drain in place, and so do not also needlumbar drain.The risk of meningitis is low in cases of CSF leak

hat ceases spontaneously within 7 days post-trauma3%), rising to 23% in cases where the leak persists forore than 7 days.32 The use of prophylactic antibiot-

cs remains controversial.33,34 Some contend that therophylactic doses of antibiotics typically given are

nsufficient to treat meningitis and may mask a sub-linical infection and possibly even create resistantrganisms, whereas others contend that prophylacticntibiotic use does indeed prevent meningitis. Onearge series of head-injured patients with CSF otorrheaound that 20% developed meningitis without the usef prophylactic antibiotics.35 The most common or-anisms causing meningitis in this situation includeneumococcus spp, Staphylococcus spp, Streptococ-us spp, and Haemophilus influenzae. In contrast,ther series have shown lower rates of meningitisith otorrhea.29

CSF leaks that persist longer than 2 to 3 weeks areost likely to require surgical repair. The surgical

pproach depends on the status of the patient’s hear-ng. In a patient with functional hearing, a combined

iddle-fossa craniotomy–transmastoid approach withepair is indicated, whereas in a patient without func-ional hearing, obliteration of the ear with a transmas-oid approach, fat graft, and plugging of the Eusta-hian tube can be performed.

FACIAL NERVE INJURY

The incidence of facial nerve injury is 10% to 25% inongitudinal fractures and 38% to 50% in transverseractures.1 Clinical findings will include single-sidedacial musculature paralysis including the forehead,ecreased ipsilateral salivation and lacrimation, de-reased ipsilateral taste in the anterior two thirds ofhe tongue, and hyperacusis.

Causes of injury include edema, intraneural hema-oma, transection, and bony impingement on theerve. As discussed earlier, it is important to identifyatients with immediate or delayed facial nerve palsy,ecause this is one of the few indications for rapid
urgical management. Because many of these patients f
ave sustained a severe head injury or are comatose,his identification can be challenging. The House-rackman system of grading facial nerve injuries isost commonly used to describe the extent of injury

nd can help predict the likelihood of spontaneousecovery of facial nerve function (Table 1).36

Rapid loss of facial nerve function (immediate toithin the first few hours of injury) is likely due to

ransection, whereas delayed loss is more likely dueo edema from fracture, with progressive compres-ion within bone resulting in loss of function. High-esolution CT scanning is the gold standard for im-ging the facial nerve in temporal bone trauma;adolinium-enhanced magnetic resonance imagingay be useful in some patients to help localize the

ite of injury. Possible patterns of enhancement in-lude no enhancement, focal enhancement, and dif-

Table 1. HOUSE-BRACKMAN FACIAL NERVEINJURY SCALE

rade 1: Normal facial nerve functionrade 2: Mild facial nerve dysfunctionGross

1. Slight weakness on close examination2. Synkinesis slight

Rest: Normal symmetry and toneMotor examination

1. Forehead: moderate to good function2. Eyes: complete closure with minimum effort3. Mouth: slight asymmetry

rade 3: Moderate facial nerve dysfunctionGross:

1. Obvious difference between sides (not disfiguring)2. Synkinesis noticeable


1. Forehead: slight to moderate movement2. Eyes: complete closure with effort3. Mouth: slightly weak with maximal effort

rade 4: Moderately severe facial nerve dysfunctionGross

1. Obvious weakness2. Disfiguring asymmetry


1. Forehead: no motor function2. Eyes: incomplete closure3. Mouth: asymmetric with maximal effort

rade 5: Severe facial nerve dysfunctionGross: Barely perceptible motionRest: AsymmetryMotor examination

1. Forehead: no motor function2. Eyes: incomplete closure3. Mouth: slight movement

rade 6: Total facial nerve paralysis

OTE. Data from Dahiya et al.30

ladwell and Viozzi. Temporal Bone Fractures. J Oral Maxillofacurg 2008.

use enhancement. Focal enhancement has been

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hown to accurately predict the location of directerve injury.37

Audiologic testing also is important in patients withacial nerve injuries. In patients in whom surgicalxploration for transection is being contemplated,earing status is a crucial factor in determining theptimal surgical approach; therefore, preoperativeocumentation of audiologic status is crucial.The pathophysiology of the injury varies widely.ne study of 28 longitudinal fractures with facialerve injury found that 14 of the injuries were intra-eural hematomas, 7 were transactions, and 7 wereue to bony impingement on the nerve by fractureegments without transection.38 Other studies sug-est that bony impingement is the most commonssue.39

ManagementThe treatment of facial nerve injuries is based on

he degree of injury (paresis vs paralysis), as well ashe timing of onset of the weakness.38,40,41 The prog-osis for spontaneous recovery without interventionas been studied. Turner42 reported on 69 patientsith traumatic facial nerve paralysis. In the 36 of hisatients who had immediate paralysis, 75% of patientsad good outcomes without intervention and 15%ad no or minimal recovery at 3 months. In the 33atients who had delayed-onset weakness, all but 2ad good outcomes.42 Since this initial study, electri-al nerve studies, including ENoG and NET, haveeen used to evaluate nerve function and guide treat-ent. Studies have found that patients with over 90%

oss of function on ENoG or NET recover poorlyithout surgery, whereas those with better function

ypically do quite well with conservative nonsurgicalreatment.38,43

With this information in mind, the decision to pro-eed with surgery is based on the timing of the pre-entation of weakness and the results of electricalesting. At one end of the injury severity spectrum ishe patient with immediate complete loss of facialerve function, presumably due to transection injuryr other severe injury. This patient likely would ben-fit from immediate exploration. Surgical approachesre based on the presence or absence of SNHL. Pa-ients without functional hearing can be managedith a translabyrinthine approach; those with intactearing are managed with a combined middle fossa–ransmastoid approach, to allow preservation of hear-ng. This latter approach allows visualization of theerve from the brainstem to the geniculate ganglion.pecific procedures performed are based on the find-ngs at surgery and can range from simple decompres-ion to interpositional nerve grafting in cases with
ransection or segmental deficits. Patients with over p
5% degeneration on electrical testing also are candi-ates for surgery.Most clinicians today agree that the patient with

elayed-onset weakness (paresis) of the facial nervean be closely monitored. This injury is presumablyue to edema of the nerve. Many clinicians use ste-oids in the setting of facial nerve injuries, althoughhere is no clear research evidence to support thisractice. Likely, the resulting reduction of secondarywelling and surrounding edema provides improvedealing conditions.

TEMPOROMANDIBULAR JOINT CORRELATIONS

Injury to the temporal bone portion of the cranio-andibular articulation (glenoid fossa or articular em-

nence) is of particular interest to the OMS, because its a common component of temporal skull injuriesnd a common reason for consultation to the OMS.njuries can involve fracture of the glenoid fossa orrticular eminence.

Isolated fracture of the glenoid fossa has been re-orted without condylar fracture or displacement.44

his is often seen as a component of skull base inju-ies, particularly high-energy injuries with significantomminution. In this instance, the fracture is notecessarily caused by the condylar head impactinghe fossa, but more likely propagates throughout thekull base with the energy dissipating from a lateral orccipital blow. Many of these injuries are noted as

ncidental findings on head CT in an obtunded patientith severe closed/open head injury. Solitary fracturef the articular eminence also has been reported.45-47

gain, injury can result from either impact of theondylar head or propagation along fracture lines.The condylar process of the mandible can be dis-

ocated into the middle cranial fossa as a componentf this type of injury.48-54 This pattern of fracture isost common in the pediatric population, due to

everal factors. Anatomic studies have shown that inhildren, the relatively thinner fossa and the less well-eveloped medial and lateral poles that produce aounded condylar head increase the risk of puncturef the condyle through the fossa.55,56

In their review of temporal bone fractures, Ortt al17 found involvement of TMJ structures in theracture pattern in 43% of cases. Avrahimi57 reportedMJ trismus, inability to chew, and localized pain in 6atients with temporal bone fractures, with CT scansemonstrating instability of the fractured portion ofhe petrous temporal bone. The patients in that studyecovered their normal range of motion and functionithin 6 to 8 months, presumably due to stabilizationf the petrous temporal bone as a result of healingver that period.57

Injury to the temporal bone during surgery for
ost-traumatic ankylosis also has been reported, with

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ransection of the intratemporal facial nerve occur-ing during osteotomies to free ankylosed condylaregments from the glenoid fossa, articular eminence,r zygomatic bones.58

ManagementFracture of the fossa with condylar displacement

as been managed with approaches ranging fromttempts at closed reduction to a combined maxillo-acial–neurosurgical approach with direct visualiza-ion of the displaced condyle, reduction, possibleeconstruction of the glenoid fossa, and appropriateostsurgical treatment to prevent ankylosis. An algo-ithmic approach to management was outlined byroetsch et al,59 who advocated attempted closed

eduction under general anesthesia with postopera-ive CT to confirm appropriate reduction and any newntracranial injuries. Craniotomy is indicated for pa-ients with preoperative neurologic abnormalities at-ributable to the intrusion of the condyle into theranial vault, associated facial fractures, delayed treat-ent, and failed closed reduction. Some researchers

dvocate immediate reconstruction to prevent con-ylar dislocations, restore posterior facial height,nd restore joint function.59 Various materials haveeen used, including alloplasts and autogenousone.55,56,60

Management of isolated glenoid fossa fracturesithout condylar intrusion involves pain control,anagement of occlusal discrepancies, and physio-

herapy to prevent decreased mandibular range ofotion. In our experience, malocclusion is uncom-on in a typical fossa fracture, noted as an incidental

nding on head CT; many of the affected patientsave significant head injuries and are obtunded. In theeurologically intact patient, slight malocclusions dueo edema or joint effusion frequently will settle within

to 7 days, with a return to premorbid occlusion. Ifhis does not occur, then a brief period of maxillo-andibular fixation (7 to 10 days), followed by night-

ime elastics and daytime physiotherapy (bite-repro-ucing exercises), generally provides adequatereatment. Use of a Therabite appliance is also reason-ble to allow a return to normal mandibular range ofotion.Articular eminence fractures, if displaced, may pre-

lude normal excursive movement of the disk–con-yle complex. However, the degree of injury requiredo produce such a displacement is significant, andany of these patients are obtunded or do not survive

ue to concomitant intracranial injuries. Conservativeonoperative management should be used in mostases. In a patient who eventually recovers but hasimited mandibular range of motion due to impinge-

ent on an inferiorly displaced articular eminence,
sseous recontouring to reduce the eminence in the
tandard fashion can be considered to improve mouthpening. This can be delayed until the patient recov-rs from the initial injuries. Minor displacements mayespond well to Therabite physiotherapy. Again, at allimes, the decision to intercede operatively should beuided by the other components of the temporalone fracture and other craniofacial injuries, as wells the patient’s injury pattern and overall prognosis.

As stated at the beginning of this article, temporalone fractures are frequent components of cranio-axillofacial trauma. Although most OMSs do notrovide definitive management of these injuries, hav-

ng a working knowledge of them is important. Inany centers, particularly community hospitals, theMS may be the primary provider of care for facial

rauma and will encounter patients with clinical oradiographic evidence of temporal bone fractures.ccess to other specialists may not be immediatelyvailable, thereby placing at least some responsibilityn the OMS for early evaluation and treatment ofhese injuries.

cknowledgment

The authors thank Robert F. Morreale, MST, CMI, Director ofedical Illustration and Animation, Mayo Clinic, for his expertise

nd meticulous preparation of the illustrations used in this article.

eferences1. Nosan DK, Benecke JE Jr, Murr AH: Current perspective on

temporal bone trauma. Otolaryngol Head Neck Surg 117:67,1997

2. Steadman JH, Graham JG: Head injuries: An analysis and fol-low-up study. Proc R Soc Med 63:23, 1970

3. Jennett B, Teasdale G, Fry J, et al: Treatment for severe headinjury. J Neurol Neurosurg Psychiatry 43:289, 1980

4. Hasso AN, Ledington JA: Traumatic injuries of the temporalbone. Otolaryngol Clin North Am 21:295, 1988

5. Wiet RJ, Valvassori GE, Kotsanis CA, et al: Temporal bonefractures: State-of-the-art review. Am J Otol 6:207, 1985

6. Cannon CR, Jahrsdoerfer RA: Temporal bone fractures: Reviewof 90 cases. Arch Otolaryngol 109:285, 1983

7. Stuart PJ, Bernstein T: A case of subdural hematoma and tem-poral bone fracture as complications of chiropractic manipu-lation. J Emerg Med 7:615, 1989

8. Youngs R, Deck J, Kwok P, et al: Severe sensorineural hearingloss caused by lightning: A temporal bone case report. ArchOtolaryngol Head Neck Surg 114:1184, 1988

9. Goldenberg D, Karam M, Danino J, et al: Temporal bone frac-ture following blunt trauma caused by a flying fish. J LaryngolOtol 112:959, 1998

0. Ghorayeb BY, Yeakley JW: Temporal bone fractures: Longitu-dinal or oblique? The case for oblique temporal bone fractures.Laryngoscope 102:129, 1992

1. McGuirt WF Jr, Stool SE: Temporal bone fractures in children:A review with emphasis on long-term sequelae. Clin Pediatr(Phila) 31:12, 1992

2. Nicol JW, Johnstone AJ: Temporal bone fractures in children: Areview of 34 cases. J Accid Emerg Med 11:218, 1994

3. Shapiro RS: Temporal bone fractures in children. OtolaryngolHead Neck Surg 87:323, 1979

4. Williams WT, Ghorayeb BY, Yeakley JW: Pediatric temporalbone fractures. Laryngoscope 102:600, 1992

5. Ishman SL, Friedland DR: Temporal bone fractures: Traditional
classification and clinical relevance. Laryngoscope 114:1734,2004

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6


6. Yanagihara N, Murakami S, Nishihara S: Temporal bone frac-tures inducing facial nerve paralysis: A new classification andits clinical significance. Ear Nose Throat J 76:79, 1997

7. Ort S, Beus K, Isaacson J: Pediatric temporal bone fractures ina rural population. Otolaryngol Head Neck Surg 131:433, 2004

8. Zimmerman RA, Bilaniuk LT, Hackney DB, et al: Magneticresonance imaging in temporal bone fracture. Neuroradiology29:246, 1987

9. Bojrab DI, Causse JB, Battista RA, et al: Ossiculoplasty withcomposite prostheses: Overview and analysis. Otolaryngol ClinNorth Am 27:759, 1994

0. Tos M: Prognosis of hearing loss in temporal bone fractures. JLaryngol Otol 85:1147, 1971

1. Griffiths MV: The incidence of auditory and vestibular concus-sion following minor head injury. J Laryngol Otol 93:253, 1979

2. Tuohimaa P: Vestibular disturbances after acute mild headinjury. Acta Otolaryngol Suppl 359:3, 1978

3. Glasscock ME 3rd, Hart MJ, Rosdeutscher JD, et al: Traumaticperilymphatic fistula: How long can symptoms persist? A fol-low-up report. Am J Otol 13:333, 1992

4. Glasscock ME 3rd, McKennan KX, Levine SC: Persistent trau-matic perilymph fistulas. Laryngoscope 97:860, 1987

5. Seltzer S, McCabe BF: Perilymph fistula: The Iowa experience.Laryngoscope 96:37, 1986

6. Weider DJ: Treatment and management of perilymphatic fis-tula: A New Hampshire experience. Am J Otol 13:158, 1992

7. McGuirt WF Jr, Stool SE: Cerebrospinal fluid fistula: The iden-tification and management in pediatric temporal bone frac-tures. Laryngoscope 105:359, 1995

8. Yamamoto Y, Kunishio K, Sunami N, et al: Identification of CSFfistulas by radionuclide counting. AJNR Am J Neuroradiol 11:823, 1990

9. Raaf J: Posttraumatic cerebrospinal fluid leaks. Arch Surg 95:648, 1967

0. Dahiya R, Keller JD, Litofsky NS, et al: Temporal bone fractures:Otic capsule sparing versus otic capsule violating clinical andradiographic considerations. J Trauma 47:1079, 1999

1. Kelly K, Tami T: Temporal bone and skull base trauma, inJackler R, Brackman D (eds): Neurotology. St Louis, MO,Mosby, 1994, p 1127

2. Brodie HA, Thompson TC: Management of complications from820 temporal bone fractures. Am J Otol 18:188, 1997

3. Ignelzi RJ, VanderArk GD: Analysis of the treatment of basilarskull fractures with and without antibiotics. J Neurosurg 43:721, 1975

4. Rathore MH: Do prophylactic antibiotics prevent meningitisafter basilar skull fracture? Pediatr Infect Dis J 10:87, 1991

5. Canniff JP: Otorrhoea in head injuries. Br J Oral Surg 8:203,1971

6. House JW, Brackmann DE: Facial nerve grading system. Oto-laryngol Head Neck Surg 93:146, 1985

7. Haberkamp TJ, Harvey SA, Daniels DL: The use of gadolinium-enhanced magnetic resonance imaging to determine lesion sitein traumatic facial paralysis. Laryngoscope 100:1294, 1990

8. Fisch U: Facial paralysis in fractures of the petrous bone.Laryngoscope 84:2141, 1974

9. Lambert PR, Brackmann DE: Facial paralysis in longitudinaltemporal bone fractures: A review of 26 cases. Laryngoscope94:1022, 1984

0. Coker NJ, Kendall KA, Jenkins HA, et al: Traumatic intratem-poral facial nerve injury: Management rationale for preserva-
tion of function. Otolaryngol Head Neck Surg 97:262, 1987
1. McKennan KX, Chole RA: Facial paralysis in temporal bonetrauma. Am J Otol 13:167, 1992

2. Turner J: Facial palsy in closed head injuries: Prognosis. Lancet1:756, 1944

3. Lieberherr U, Schwarzenbach D, Fisch U: Management of se-vere facial nerve paralysis in the temporal bone: A review of 82cases, in Sixth Annual Symposium on the Facial Nerve. Amster-dam, the Netherlands, Kugler and Gagdini, 1990, p 285

4. Iannetti G, Martucci E: Fracture of glenoid fossa followingmandibular trauma. Oral Surg Oral Med Oral Pathol 49:405,1980

5. Keith O, Jones GM, Shepherd JP: Fracture of the articulareminence: Report of a case. Int J Oral Maxillofac Surg 19:79,1990

6. Radecki CA, Wolf SM: Solitary fracture of the articular emi-nence. Oral Surg Oral Med Oral Pathol 69:768, 1990

7. Tay AB, Peck RH: Solitary fracture of the articular eminence: Acase report. J Oral Maxillofac Surg 59:808, 2001

8. Spanio S, Baciliero U, Fornezza U, et al: Intracranial dislocationof the mandibular condyle: Report of two cases and review ofthe literature. Br J Oral Maxillofac Surg 40:253, 2002

9. Barron RP, Kainulainen VT, Gusenbauer AW, et al: Fracture ofglenoid fossa and traumatic dislocation of mandibular condyleinto middle cranial fossa. Oral Surg Oral Med Oral Pathol OralRadiol Endod 93:640, 2002

0. Melugin MB, Indresano AT, Clemens SP: Glenoid fossa fractureand condylar penetration into the middle cranial fossa: Reportof a case and review of the literature. J Oral Maxillofac Surg55:1342, 1997

1. van der Linden WJ: Dislocation of the mandibular condyle intothe middle cranial fossa: Report of a case with 5-year CTfollow-up. Int J Oral Maxillofac Surg 32:215, 2003

2. Christiansen RL: Condylar penetration into the middle cranialfossa. J Craniomandib Disord 3:100, 1989

3. Sandler NA, Ozaki WH, Ochs MW, et al: Intracranial reductionof an intact mandibular condyle displaced into the middlecranial fossa. J Oral Maxillofac Surg 54:506, 1996

4. Copenhaver RH, Dennis MJ, Kloppedal E, et al: Fracture of theglenoid fossa and dislocation of the mandibular condyle intothe middle cranial fossa. J Oral Maxillofac Surg 43:974, 1985

5. Cillo JE, Sinn DP, Ellis E 3rd: Traumatic dislocation of themandibular condyle into the middle cranial fossa treated withimmediate reconstruction: A case report. J Oral Maxillofac Surg63:859, 2005

6. da Fonseca GD: Experimental study on fractures of the man-dibular condylar process (mandibular condylar process frac-tures). Int J Oral Surg 3:89, 1974

7. Avrahami E: CT of intact but nonfunctioning temporomandib-ular joints following temporal bone fracture. Neuroradiology36:142, 1994

8. Unlu RE, Uysal AC, Alagoz MS, et al: An unusual complicationof condylectomy: Fracture of the temporal bone and intratem-poral facial paralysis. J Craniofac Surg 16:185, 2005

9. Koretsch LJ, Brook AL, Kader A, et al: Traumatic dislocation ofthe mandibular condyle into the middle cranial fossa: Report ofa case, review of the literature, and a proposal managementprotocol. J Oral Maxillofac Surg 59:88, 2001

0. Long X, Hu C, Zhao J, et al: Superior dislocation of mandibularcondyle into the middle cranial fossa: A case report. Int J Oral
Maxillofac Surg 26:29, 1997