Temporal Bone Fractures 

Updated: Nov 21, 2017
Author: Antonio Riera March, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA 



The temporal bone is the most complex bone in the human body. It houses many vital structures, including the cochlear and vestibular end organs, the facial nerve, the carotid artery, and the jugular vein. A temporal bone fracture can involve none or all of these structures. Associated trauma to other cranial nerves (other than the facial nerve; ie, VI [abducens], IX [glossopharyngeal], X [vagus] and XI [spinal accessory] can also cause paralysis.

The temporal bone is a very thick and hard structure located in the base of the skull. The base of the skull has multiple foramina, as seen in the images below, creating areas of decreased resistance susceptible to traumatic injury. Therefore, fractures that involve the temporal bone continue along the skull base with a pattern that follows the weakest points of the anatomy.

Internal aspect of the skull base: arcuate eminenc Internal aspect of the skull base: arcuate eminence (AE), cochlea (C), foramen magnum (FM), internal auditory canal (IAC), foramen lacerum (L), foramen ovale (O), foramen rotundum (R), foramen spinosum (SP), sigmoid sinus (SS), transverse sinus (TS), vestibular system (V).
External aspect of the skull base: carotid canal ( External aspect of the skull base: carotid canal (C), condyle (CO), foramen magnum (FM), jugular foramen (J), foramen lacerum (L), foramen ovale (O), pterygoid plates (P), styloid foramen (S), foramen spinosum (SP).

The spectrum of temporal bone trauma is extremely varied, ranging from minor concussion without functional deficits to severe blunt or penetrating trauma with multifunctional deficits that involve the auditory and vestibular nerves, the facial nerve, and the intracranial contents. The clinical presentations specifically related to temporal bone trauma include facial nerve paralysis (partial or complete), hearing loss (conductive, sensorineural, or mixed), vertigo, dizziness, otorrhagia, cerebrospinal fluid (CSF) otorrhea, tympanic membrane perforation, and hemotympanum and canal laceration.

Temporal bone fracture is a frequent manifestation of head trauma. Most cases of temporal bone fracture involve severe body and/or head trauma. In the adult population, approximately 90% of temporal bone fractures are associated with concurrent intracranial injuries and 9 % with cervical spine injuries.[1] Therefore, management of the temporal bone trauma may not be the first priority. However, the initial assessment of the temporal bone trauma in the emergency department by the emergency personnel and the trauma team is critically important.

Usually, the otolaryngology-head and neck surgeon is called in for consultation when the patient is fully stable, many hours after the traumatic event. This is why the initial assessment in the emergency room is so important and definitely assists in the posterior management, improving function. This is also why a thorough understanding of the etiology, classification, complications, and treatment of temporal bone fractures is mandatory for healthcare professionals involved in the care of individuals with such injuries.


The head is the most frequently injured part of the body. Head injuries occur in approximately 75% of all motor vehicle accidents. Approximately 30% of head trauma cases result in skull fracture. The ear is the most frequently damaged sense organ. Temporal bone injuries reportedly occur in 14-22% of all skull fractures. Motor vehicle accidents are the cause of 31% of temporal bone fractures. Other causes, in descending order of frequency, are physical assaults, falls, motorcycle accidents, pedestrian injuries, bicycle accidents, and gunshot wounds. Men aged 21-30 years comprise the most commonly involved group. The predisposition in males is based on an increased number of males involved in high-risk activities compared with females, rather than on a weakness in their skull structures. Bilateral temporal bone fractures have an incidence of 8-29%.

Recently, temporal bone fractures related to motor vehicle accidents appear to have decrease, temporal bone fractures related to assaults, particularly in large urban populations, appear to have increased.[2, 3]

The pediatric population comprises 8-22% of the entire population of patients with the diagnosis of temporal bone fractures. Temporal bone fractures in the pediatric population are also associated with a high incidence of intracranial complications, approximately 58%, and with facial nerve paralysis, at 3-9%.[2, 4, 5]

The pediatric population has a very similar proportion of motor vehicle accidents (47%) and falls (40%), as described in the medical literature.[5, 6] Temporal bone fractures are more common in children younger than 6 years. Approximately 75% of the fractures are longitudinal, and 25% are transverse[7] . The otic capsule is spared in 90% and is involved in 10%.[7] Intracranial injuries are often with associated hearing loss, which is most likely conductive (56%) followed by sensorineural hearing loss (17%) and mixed hearing loss (10%). However, the facial nerve injury is not frequently affected (3%).[5] Children are very susceptible to trauma, in particular to falls and other accidents. However, if the injury cannot be explained based on the medical history, consideration should be given to the possibility of a nonaccidental cause.


In 1926, Ulrich was the first to classify temporal bone fractures into longitudinal fractures and transverse fractures.[8] Ghorayeb and Yeakley, in their study of 150 temporal bone fractures, found that the vast majority of fractures are actually oblique and quite often mixed.[9] Other classifications are based on otic capsule sparing and otic capsule involvement. An otic capsule–sparing fracture runs anterolateral to the otic capsule and is caused by a blow to the temporoparietal region. An otic capsule–involvement fracture runs directly into the otic capsule, damaging the cochlea and semicircular canals, and is caused by a blow to the occipital region (see Table 2). In the adult group the mentioned classifications are useful in predicting otologic sequelae but cannot predict neurologic, neuro-otologic, or skull base complications.[1]

In pediatric patients, the temporal system classification of longitudinal/transverse fractures and otic capsule–sparing/otic capsule–disrupting fractures can prognosticate the sequelae of sensorineural hearing loss, the latter being more accurate in this regard. Conductive hearing loss and/or facial nerve paralysis cannot be prognosticated by either of these classifications.[7]

Another classification system, proposed by Ishman and Friedland, is associated with petrous and nonpetrous involvement, with temporal bone fractures appearing to have a greater correlation with the petrous type and the presence of sensorineural hearing loss, CSF leak, and facial nerve injury.[10]

Despite newer classification systems, Ulrich's original system, due to its simplicity, is still the most commonly used.

The classification models indicated above are arbitrary but indeed useful to predict the pattern of injury. Most temporal bone fractures are completely irregular and not uniform in their pathway, following an oblique or mixed pattern as indicated above. Therefore, rather than the type of fracture, the evaluation of function is the critical issue and is mandatory. The presence or lack of a particular function indicates whether or not the cochlea, middle ear, vestibule, facial nerve, dura, or CNS is damaged, in spite of a demonstrated fracture or the lack thereof.

Longitudinal fractures

Longitudinal fractures comprise 80% of all temporal bone fractures. They are frequently caused by a lateral force over the mastoid or temporal squama, usually produced by temporal or parietal blows. The fracture line parallels the long axis of the petrous pyramid. It starts in the pars squamosa (mastoid or external auditory canal), as seen in the images below, and extends through the posterosuperior bony external canal, continues across the roof of the middle ear space anterior to the labyrinth, and ends anteromedially in the middle cranial fossa in close proximity to the foramen lacerum and ovale.

Internal aspect of the skull base that represents, Internal aspect of the skull base that represents, in black and blue colors, the pathway of the longitudinal temporal bone fracture lines.
Left temporal bone fracture line crossing the mast Left temporal bone fracture line crossing the mastoid process and into Henle's spine and the external auditory canal (surgeon's view).

The most common course of the fracture is anterior and extralabyrinthine; however, although rare, intralabyrinthine extension is possible.[11] Again, bilateral temporal bone fractures are present in 8-29% of all fractures, according to the medical literature.[12]

Signs and symptoms include bleeding into the ear canal from skin and tympanic membrane laceration, hemotympanum, external auditory canal fractures, ossicular chain disruption that produces conductive hearing loss, and facial nerve paralysis. Twenty percent of longitudinal fractures injure the facial nerve and cause paralysis. The injury site is usually the horizontal segment of the nerve distal to the geniculate ganglion. CSF otorhinorrhea is common but usually temporary. Sensorineural hearing loss may occur as a result of concussive damage. Vertigo occurs but is not related to the severity of the fracture.

Transverse fractures

Transverse fractures comprise 20% of all temporal bone fractures. They are usually caused by a frontal or parietal blow but may result from an occipital blow. The fracture line runs at a right angle to the long axis of the petrous pyramid and starts in the middle cranial fossa (close to the foramen lacerum and spinosum). It then crosses the petrous pyramid transversely and ends at the foramen magnum. It may also extend through the internal auditory canal and injure the nerves directly. The pathways of the transverse temporal bone fracture lines are depicted in the image below.

Internal aspect of the skull base that represents, Internal aspect of the skull base that represents, in black and red colors, the pathways of the transverse temporal bone fracture lines.

Cochlear and vestibular structures are usually destroyed, producing a profound sensorineural hearing loss and severe ablative vertigo. The intensity of the vertigo will decrease after 7-10 days and then continues to decrease steadily over the following 1-2 months, leaving only an unsteady feeling that lasts approximately 3-6 months, until compensation finally occurs. Intense nystagmus (third degree) is present since the initial fracture, with the fast component beating away from the fracture site. The nystagmus is easily seen by the naked eye. Nystagmus also decreases progressively in intensity (third degree, second degree, first degree) and then finally disappears. The image below depicts right temporal bone transverse fracture with severe spontaneous nystagmus.

Right temporal bone transverse fracture with sever Right temporal bone transverse fracture with severe spontaneous nystagmus (third degree) manifesting immediately after trauma. The fast component beats away from the fracture site in all directions of the gaze; the intensity of the spontaneous nystagmus is represented by the different lengths of black arrows. This type of nystagmus is usually seen by the naked eye. According to Alexander's law, the nystagmus increases when the eyes are turned in the direction of the quick component and decreases when the eyes are turned in the direction of the slow component.

Rarely, a mixed hearing loss may occur. Facial nerve injury occurs in 50% of transverse fractures. The injury site is anywhere from the internal auditory canal to the horizontal segment distal to the geniculate ganglion. Pneumolabyrinth may be noted.[13]

Histopathology reveals hair cell loss, ganglion cell loss, and supporting cell loss. In rare cases, labyrinthitis ossificans occurs secondary to the trauma or subsequent infection. This must be kept in mind when one considers the placement of cochlear implants after a temporal bone fracture.

Oblique or mixed fractures

These patterns, which extend both longitudinally and transversely, are common. According to some authors, these patterns occur more often than isolated transverse or longitudinal fractures.[14, 15, 16] . A range of 62-90% of temporal bone fractures were designed as a mixed pattern in medical literature.[2, 3, 17]

Internal aspect of the skull base depicting, in gr Internal aspect of the skull base depicting, in green color, a mixed temporal bone fracture line with both a longitudinal pattern (circle) and a transverse pattern (rectangle).

Table 1. Longitudinal and Transverse Fractures (Open Table in a new window)


Longitudinal Fractures

Transverse Fractures


Approximately 80%

Approximately 20%


Temporal or parietal trauma

Frontal or occipital trauma

CSF otorrhea



Tympanic membrane perforation



Facial nerve damage

20% (most often temporary and frequently delayed in onset)

50% (severe, usually permanent, and immediate in onset)

Hearing loss

Common (conductive type and possibly high tone neurosensorial secondary to concomitant inner ear concussion)

Common (severe sensorineural or mixed)


Common (associated with otorrhagia)

Possible (not associated with otorrhagia)


Common (usually spontaneous, usually less intense [first or second degree] or positional; nystagmus absence also possible)

Common (intense [third degree], spontaneous, fast component beating to the opposite ear, long lasting; positional nystagmus also possible before and after compensation period)





Common (less intense, and/or positional; absence is also possible)

Common (intense, usually associated in the acute phase with nausea and possibly vomiting)


Table 2. Otic Capsule–Sparing and Otic Capsule–Disrupting Fractures (Open Table in a new window)


Otic Capsule Sparing

Otic Capsule Disrupting


Approximately 95%

Approximately 5%


Temporal or parietal trauma

Occipital trauma

Line of fracture

Anterolateral to the otic capsule

Through the otic capsule


  • Squamosa portion of temporal bone

  • Posterosuperior wall of the external auditory canal and tympanic membrane commonly involved

  • Also, mastoid air cells and middle ear

  • Foramen magnum, petrous pyramid, and otic capsule

  • Also jugular foramen, internal auditory canal, and foramen lacerum

  • Tympanic membrane and external auditory canal not usually affected

CSF leak

Middle cranial fossa (tegmen mastoideum, tegmen tympani, middle ear, and external auditory canal or eustachian tube)

Posterior cranial fossa (middle ear, eustachian tube)

Ossicular chain involvement



Hearing loss

Conductive or mixed


Facial paralysis

Less common



Penetrating wounds

Stab and gunshot wounds are the most common penetrating wounds. Most of the patients involved are male and young. Gunshot wounds medial to the geniculate ganglion are usually fatal. The otic capsule may act as a missile deflector, protecting the brain. Associated injuries of cranial nerves (other than the seventh) can occur, as well as intracerebral damage and arterial or venous injury. These account for the most severe temporal bone injuries. Usually the timing of the facial paralysis and its injury location are well known, the result of direct observation or CT findings.

Gunshot wounds to the temporal bone often result in profound sensorineural hearing loss, CSF leak, and facial nerve disruption, which is found in approximately 50% of the patients and requires repair by interposition nerve grafting.

External auditory canal fractures associated with temporal bone trauma

External auditory canal fractures are not common; however, they usually are associated with temporal bone trauma and/or mandibular trauma. If not recognized or treated properly, they can produce hearing loss and canal stenosis as long-term sequelae. External auditory canal fractures are seen in all age groups. Men are more affected than women. The fractures can result from a various types of trauma, such falls, assaults, and motor vehicle or bicycle accidents, all of which are capable of producing mandibular and temporal bone fractures. The external auditory canal is involved in 39% of temporal bone traumas and 3% of mandibular traumas, commonly in association with condylar or subcondylar fractures. The most common presenting sign is blood from the external auditory canal. Examination of the external auditory canal and computed tomography (CT) scanning can assist in the identification of external auditory canal fractures. Treatment involves the removal of blood and blood clots and then packing or stenting the canal. Otic drops can be used in addition to the packing or stenting. Outpatient follow-up is required to avoid hearing loss and canal stenosis.[18]


Patients with temporal bone fractures usually have multiple traumatic injuries.[2] Intracranial and maxillofacial injuries can be associated with severe trauma capable of producing temporal bone fracture. Other associated injuries not related to the head and neck, are also possible, such as, abdominal, thoracic and orthopedic injuries.

In the initial evaluation, the application of Advanced Trauma Life Support protocols is imperative in the assessment and management of these patients. Therefore, stabilization must be accomplished first. Airway management, evaluation of neurological status, hemorrhage, open fractures, and abdominal and chest injuries may delay early diagnosis and treatment of temporal bone injuries. The cervical spine should be evaluated and stabilized before the head is manipulated.

As mentioned in the beginning of this article, otolaryngologists are typically not members of the initial team who treat a patient with a head injury. Therefore, neurosurgeons, neurologists, and emergency physicians should be trained to assess the 2 most important aspects of temporal bone fractures: status of the external canal (checking for blood or CSF) and status of the facial nerve.

The physical examination of the patient with temporal bone trauma should include a complete neuro-otologic examination, as well as a complete nose and throat examination. Look for the impact site on the skull. Examine the patient's eyes for nystagmus; indicate the direction and degree. Severe nystagmus (third degree) often occurs in patients with transverse fractures. Central vertigo may have vertical or direction-changing characteristics that fail to suppress with fixation. On the contrary, peripheral vertigo is horizontal or horizonto-rotatory and suppresses with fixation.

If the patient's condition permits, test the hearing with tuning forks, comparing the bone conduction to air conduction (Weber and Rinne tests). Bedside masking can be done by rubbing a piece of paper against the opposite auricle. Complete vestibular audiometric testing can be performed later because it is not usually necessary in the acute phase. Complete audiological evaluation is mandatory prior to any otologic intervention.

The Battle sign (ecchymosis of the postauricular skin) and the raccoon sign (ecchymosis of the periorbital area) may be noted in either type of fracture.

The auricles are inspected for lacerations and hematomas. Lacerations are closed after cleaning and debridement of exposed cartilage. Hematomas are drained and pressure bolsters placed to prevent reaccumulation of blood.

Taking aseptic precautions, examine the external canal for blood, CSF, or the presence of brain herniation. Observe for external canal lacerations, step deformities, and tympanic membrane lacerations/perforations. Canal fractures typically occur along the scutum and roof of the external auditory canal. Check for hemotympanum.

Do not lavage the ear canal and do not use packing in the canal unless bleeding is difficult to control because either may introduce infection into the cochlea and labyrinth, as well as into the brain and meninges. If profuse hemorrhage cannot be controlled with packing, the patient is taken to the operating room for carotid ligation or to the angiography suite for balloon occlusion.

Severely traumatized ear canals are at high-risk for stenosis or cholesteatoma formation. These patients should be monitored closely for the development of these complications. Early intervention at the first sign of stenosis can prevent a problem that is difficult to treat when the stenosis is mature.

Examine the mandible and mid face for fractures. If the patient is conscious, determine if he or she has vertigo. Examine the facial nerve. Checking for paralysis and determining whether it is of immediate or delayed onset is crucial. This may be difficult to determine if the patient is intubated or comatose or if muscle relaxants have been administered. Painful stimuli may elicit a grimace response, even in comatose patients.

In the patient with facial paralysis or CSF fistula, an audiogram is required before surgical repair because the patient's hearing status dictates the surgical approach.

A prospective study by Montava et al of temporal bone fracture sequelae (39 patients, 45 fractures) found that presentations included the following: balance problems (44%), hypacusis (56%), tinnitus (56%), and facial paralysis (15%). Cochleovestibular sequelae were described as disabling in 75-80% of patients.[19]


In adults and children, temporal bone fractures with otic capsule disruption are severe and more prone to complications (such as facial nerve paralysis, sensorineural hearing loss, conductive hearing loss, CSF otorrhea) and sequelae than are temporal bone fractures with otic capsule sparing.[20]

A study by Schell and Kitsko found that in children with temporal bone fracture–related hearing loss, the majority of those in whom the otic capsule was spared suffered only mild hearing loss and recovered normal hearing levels after a mean of 6 weeks, while 75% of those in whom the fracture disrupted the otic capsule suffered severe hearing loss.[21] The study involved 58 children, with most hearing losses in otic capsule–sparing fractures being conductive and all classifiable hearing losses in otic capsule–disrupting fractures being mixed.[22]



Imaging Studies

Temporal bone injury can be associated with severe trauma to the head, spine, and maxillofacial region; most patients with temporal bone fracture have a CT scan of these.[23]

Contemporary CT imaging will be able to identify temporal bone fractures, including the type and direction, as well as the presence or absence of otic capsular involvement and the involved segment of temporal bone. Axial CT imaging is best to identify fractures with otic capsule involvement. (Pneumolabyrinth is an indication that the otic capsule is involved.) Furthermore, CT scanning will be able to identify complications such as hemotympanum, tympanic membrane perforation, ossicular injury, perilymphatic fistula, CSF leak, cochlea-vestibular injury, facial nerve injury, and vascular injury.

High-resolution CT (HRCT) scanning of the temporal bone is useful in assessing injuries complicated by CSF leak, facial paralysis, or suspected vascular injury. Axial and coronal images are usually obtained with 1-mm sections, as are magnified views of the temporal bone. Bone windows are necessary. Axial high-resolution CT of a fractured right temporal bone is seen below.

Axial high-resolution CT of the right temporal bon Axial high-resolution CT of the right temporal bone that represents a longitudinal fracture line that extends from the roof of the external auditory canal to the middle ear cavity.

HRCT of the temporal bone is indicated if surgical intervention for management of otologic complications is required.

If transient or persistent neurologic deficits are present in a patient with basilar skull fracture, HRCT of temporal bone with CT angiography is indicated to evaluate for petrous carotid injury.

A study by Ulano et al indicated that in trauma cases in which a temporal bone fracture is not visible on CT scanning, the presence of air around the temporal bone and a finding of mastoid air cell or middle ear cavity opacity should raise suspicions for the presence of fracture. The study, which included 152 temporal bone fractures, found air adjacent to the styloid process (94 fractures, 61.8%), in the temporomandibular joint (80 fractures, 52.6%), adjacent to the mastoid process (57 fractures, 37.5%), and along the adjacent dural venous sinus (33 fractures, 21.7%). Moreover, 139 fractures (91.4%) were accompanied by mastoid opacification, and 121 fractures (79.6%) showed opacity of the middle ear cavity. The investigators also found a positive association between complex fracture and pneumocephalus.[24]

Magnetic resonance imaging (MRI) cannot identify temporal bone fracture. MRI has both poor sensitivity and specificity in this respect. It is useful in assessment of the intracranial contents and/or a nerve palsy not explained by the HRCT.[2, 25, 26]  MRI is best to identify bleeding inside the otic capsule. The MRI can demonstrate hemorrhage into the vestibular apparatus, vestibular nucleus, and brainstem. It also can identify nerve compression and herniation of intracranial contents into the mastoid cavity.[2] MRI is also useful prior to neurosurgical intervention for temporal bone fractures, particularly with a middle cranial fossa approach.[25]

See also the Medscape Drugs & Diseases topics Temporal Bone Fracture Imaging and MR Imaging of the Temporal Bone.

Other Tests

Electrodiagnostic tests

Electrodiagnostic testing is used to assess and quantify injury to the facial nerve and to determine status of the facial musculature. The most common tests used today in the evaluation of trauma to the facial nerve are maximum stimulation, nerve excitability, electroneurography, and electromyography.

Maximum stimulation test

This test is based on the observation of twitch of the facial musculature using the Hilger facial nerve stimulator after the third day of the injury, usually between 3-14 days postinjury. It is used only in the case of complete facial nerve paralysis (as determined by the House-Brackmann grading) because of the pain caused by the facial stimulation. Supramaximal stimulation is applied with a maximal tolerated current on the normal side. The affected side is compared with the normal side, using the same stimulating current. An absent or markedly decreased response (barely perceptible movement) indicates a poor and incomplete return of facial nerve function.

Nerve excitability test (minimal nerve excitability test)

This test is similar to the previous test that used the Hilger nerve stimulator after the third day of injury; this test compares the amperage site-to-site necessary to initiate a barely visible response on the affected side. A difference of 3.5 mA or more is significant, carries a poor prognosis, and indicates the need to consider surgical exploration.


Electroneurography (ENOG) is the technique designed by Fisch. It is used every 2 days between the third and the 21st day after the initial trauma. The results are expressed as a percentage of the amplitude of the action potentials on the paralyzed side as compared with the nonparalyzed side. The results correlate well with the percentage of nerve degeneration. According to Fisch, 90% degeneration of the involved nerve is considered significant and represents the threshold for surgical management.[27, 28] .

Fisch has developed accepted indications for surgical management based on the “percentage of nerve degeneration,” advocating exploration and decompression or repair when the ENOG indicates 90% degeneration. In other words, degeneration with 10% or less of nerve function compared with the normal side is considered the critical turning point for surgical management recommendation. Fisch found, histologically, that traumatic .injury at the geniculate ganglion induces retrograde degeneration through the labyrinthine and distal meatal segments of the facial nerve. Fisch believes that fibrosis occurs and blocks regenerating fibers and, therefore, advises early surgery in order to avoid this fibrotic complication within the fallopian canal.

Nosan et al believe that ENOG is of paramount importance in determining the need for and the timing of surgery for facial paralysis after trauma. They believe that ENOG has made the determination of the clinical onset of paralysis less necessary and that patients with delayed paralysis can have more severe injuries than those patients with more rapid ENOG degeneration. They believe that the time of paralysis from onset of injury should not confuse the issue.


Normal resting muscle does not produce spontaneous electrical activity. Spontaneous electromyographic activity (fibrillation potentials) found in the muscle indicates complete denervation. Take into consideration that fibrillation potentials take at least 3 weeks to be detected with electromyography. The presence of voluntary motor units (polyphasic action potentials), on the contrary, is a good prognostic factor and the best indicator that regeneration is taking place.



Medical Therapy

Generally, a patient with delayed facial paralysis is managed conservatively with 10-14 days of systemic corticosteroids unless medically contraindicated. A patient with complete paralysis of immediate onset undergoes initial testing with the nerve Hilger stimulator between days 3 and 7. If no loss of stimulability occurs, patients are observed. If the nerve loses stimulability within one week or more than 90% degeneration on ENOG occurs within 2-3 weeks, the threshold for surgical exploration has been reached.


Common complications of temporal bone fractures include hearing loss, CSF fistula, facial nerve paralysis, external auditory canal stenosis, cholesteatoma formation, and vascular injuries. Hearing loss is the most common complication and can be conductive, sensorineural, or mixed type.

Conductive hearing loss

Conductive hearing loss is frequently observed with longitudinal fractures and is caused by hemotympanum, tympanic membrane perforation, or partial or complete ossicular chain disruption. Ossicular chain dislocation is more common than ossicular chain fracture. Tympanic membrane perforations and hemotympanum usually resolve in 3-4 weeks.

Axial and coronal HRCT scans are helpful for diagnosing ossicular chain dislocation. The most common ossicle involved in temporal bone trauma is the incus because it is less stable, having weak attachments to the malleus and stapes. Furthermore, the malleus is anchored by the tensor tympani muscle and its tendon, and the stapes is anchored by the stapedius muscle and its tendon. They contract during trauma and pull the incus medially. This movement is accentuated by the trauma, causing medial dislocation of the incus.

The following chain abnormalities have been identified with temporal bone fractures:[14, 29]

  • Incudostapedial joint separation: The incudostapedial joint is the most common site of traumatic separation. (82%)

  • Incus dislocation (57%)

  • Fracture of the stapes crura (30%)

  • Fixation of the ossicles in the attic (25%)

  • Incudomalleolar joint separation

Other lesions, such as delayed necrosis of the long process of the incus, dislocation of the stapes footplate, and dislocation of the malleus are possible but are not commonly seen.

Most nondisruptive conductive hearing losses resolve spontaneously. If conductive hearing loss is present at greater than 30 dB after 2 months, consider surgical exploration unless the conductive hearing loss is in the only hearing ear. Middle ear exploration/reconstruction in cases of traumatic etiology achieves better functional results compared with middle ear reconstruction for chronic ear infection.[30]

See also the Medscape Drugs & Diseases article Ossiculoplasty.

Sensorineural hearing loss

Sensorineural hearing loss can occur in temporal bone fractures with involvement of the otic capsule (cochlea, vestibule, and semicircular canal) and/or internal auditory canal. Sensorineural hearing loss can also occur with intralabyrinthine bleeding without evidence of temporal bone fracture. Severe-to-profound sensorineural hearing loss most commonly occurs in patients who have transverse fractures with otic capsule involvement. Partial sensorineural loss is also possible. Mild high-frequency loss (5-kHz notch) may occur in longitudinal fractures from cochlear concussion. Blood products and cellular disruption are present on histopathology associated with sensorineural hearing loss.

On physical examination, spontaneous nystagmus observed by the naked eye is an important clinical sign in the acute phase of temporal bone trauma. It is usually related to a transverse temporal bone fracture with damage to the cochlea and semicircular canals.

Before considering cochlear implant, labyrinthitis ossificans must be considered when bilateral severe sensorineural hearing loss is present. Progressive sensorineural hearing loss has also been reported with and without vertigo. When vertigo is present with fluctuating or progressive loss, traumatic endolymphatic hydrops or perilymphatic fistula is the diagnosis. Autoimmune hearing loss may account for some cases of progressive hearing loss.

Mixed hearing loss

Mixed conductive and sensorineural hearing loss may be difficult to detect in the presence of severe sensorineural hearing loss. Surgical correction is considered when gain from correction of the conductive component is desired.


These conditions are difficult to assess during the acute injury phase because of associated neurologic trauma and/or life threatening injuries. Therefore, the incidence of vertigo has been estimated on a wide spectrum to comprise 24-78% of cases. Spontaneous nystagmus observed by the naked eye is an important clinical sign in the acute phase of temporal bone trauma. It is usually related to a transverse temporal bone fracture with damage to the cochlea and semicircular canals. The spontaneous nystagmus in this instance is a severe one, horizontal or horizonto-rotatory, third degree, and beating to the opposite ear. It represents a peripheral vertigo and it is suppressed or diminished by fixation (nystagmus in central vertigo can have a vertical direction, horizontal, horizonto-rotatory, or a changing direction, and its intensity can be enhanced by fixation).

The accompanying vertigo is also severe, with a spinning sensation, and can be associated with nausea and vomiting. Once the acute phase has passed, the spontaneous nystagmus and vertigo resolve within 3-6 months. At this time, the ENG reveals absent vestibular responses in the affected labyrinth. Spontaneous nystagmus, horizontal or horizonto-rotatory, of lesser degree, not easily seen by the naked eye, can also occur in longitudinal fractures and in general is less severe and intense than that seen in transverse fractures. Also, posttraumatic vertigo is usually found in concussive injuries to the labyrinth associated with temporal bone trauma that does not involve the otic capsule or vestibular apparatus. Note that these injuries may not be observed radiographically, nor does the incidence of vertigo or its intensity and duration correlate well with the severity of the temporal bone injury.

Posttraumatic benign paroxysmal positional vertigo

Posttraumatic benign paroxysmal positional vertigo (BPPV) is common. BPPV is defined by a latent onset of postural related nystagmus and fatiguing which is nonreproducible. In BPPV, a geotropic rotatory nystagmus is elicited with the Dix-Hallpike maneuver. After positioning the injured ear down, a latency period of 10 seconds occurs before the nystagmus is seen. The elicited nystagmus is fixed, horizontal, or horizonto-rotatory and, after a few seconds, fatigues. With repetition, the nystagmus is not reproducible at a point; contrarily, central positional vertigo is a changing-direction nystagmus that has no latency period, is nonfatiguing, and is easily reproducible. Postural vertigo of central etiology could be related to injury or hemorrhage in the brainstem, resulting in dysfunction of the vestibular nuclei.

In both benign paroxysmal positional vertigo and central postural vertigo, the spontaneous nystagmus and vertigo usually resolve over 3-6 months and the remaining symptoms by 10-12 months; however, these symptoms may persist in elderly patients. A combination of both central and peripheral causes are highly possible in the pathophysiology of vertigo after head and temporal bone trauma. Vestibular rehabilitation or canal repositioning may be of value, in particular in BPPV.

Perilymphatic fistula

Perilymphatic fistula may also cause paroxysmal vertigo. The onset of fistula and its symptoms may be delayed. This diagnosis is considered when fluctuating hearing loss and vertigo are present in the near posttraumatic period. A fistula test in the ear canal should not be performed in the acute setting to avoid further trauma or complications. CT images with fractures involving the footplate and round window are compatible with perilymphatic fistula.[31] .Medical treatment initially consists of bed rest, head elevation, and stool softeners. Surgical exploration may be indicated in persistent perilymphatic fistulas.

Traumatic endolymphatic hydrops

Traumatic endolymphatic hydrops as a cause of posttraumatic vertigo has the following etiologies: bony labyrinthine fistula, direct membranous labyrinth injury, injury to the endolymphatic drainage system, or surgical trauma. The onset of traumatic hydrops may be delayed for months or years.

Cerebrospinal fluid fistula

CSF fistula may occur as a result of a dural tear after any type of temporal bone fracture (17%).[14, 32] The leak almost always closes within 4 weeks. The average duration of the leak is approximately 4 days. Longitudinal fractures tend to leak more severely, and this occurs through the middle cranial fossa. Transverse fractures cause leaks through the posterior cranial fossa. The most common sites of fistula are the tegmen tympani and tegmen mastoideum when the leak originates in the middle cranial fossa. Most CSF leaks are obvious by their clear, watery appearance in the immediate posttrauma period. CSF leak may be delayed after the initial trauma in approximately 28% of the cases. CT scanning can assist in the identification of the site of the CSF leak after temporal bone trauma. Coronal and sagittal CT image reconstructions will assist in identifying the location and site of the dural defect.[31] MRI of the brain with contrast can help in the identification of patients with encephaloceles.[31] Pneumatoceles and brain herniations are rare. Pneumatoceles may resolve but will occasionally expand.

CSF contains decreased potassium and protein and elevated glucose concentration levels. Qualitative testing of the fluid for glucose is helpful but lacks specificity. Quantitative testing for potassium, protein, and glucose is more precise. The halo test performed by using a filter paper may be helpful (as the paper separates CSF from blood). Nevertheless, if available, beta2- transferrin assay is the most accurate diagnostic test for CSF.

Otorrhea through a canal laceration or tympanic membrane laceration is usually the presenting symptom, or rhinorrhea may be the only symptom. The rate of flow is increased with exertion or learning forward. CSF can also be observed in the middle ear behind an intact tympanic membrane after the blood is resorbed.

The use of antibiotics in the presence of CSF fistula is controversial. In studies before 1970, MacGee and colleagues reported that 16% of patients who receive prophylactic antibiotics developed meningitis.[33] Rathmore found no difference in the rate of meningitis with or without prophylactic antibiotics.[34] Demetriades and colleagues found that the incidence of meningitis and other co-infections was higher in the group that did not receive prophylaxis.[35] Villalobos et al combined 12 studies (1970-1996) of 1241 subjects and concluded that antibiotic prophylaxis does not appear to decrease the risk of meningitis.[36] To date, no clear answers exist, although the literature generally seems to support prophylactic use of antibiotics in patients with CSF fistulas, particularly in the presence of open laceration or co-infection.

CSF leaks tend to close spontaneously with elevation of the head, bed rest, stool softeners, and cessation of sneezing, straining, and nose blowing. Intermittent lumbar punctures or indwelling lumbar drains may help if the leak persists. However, surgical exploration may be indicated for CSF fistulas that last longer than 14 days.

Radiography is necessary before surgical repair is considered. The usefulness of HRCT and CT cisternography in localizing the site of CSF leaks is debatable, and if the fistula is inactive at the time the localizing technique is used, the CSF leak will not be detected. HRCT scanning alone shows bony defects in 70% of patients with fistulas and is the most specific test. MRI may be the next step. If the fracture is seen but the site of the fistula is not identified, CT cisternography with intrathecal contrast agent (Omnipaque) is the next diagnostic procedure of choice. However, if the bony defect cannot be demonstrated with HRCT scanning, CT cisternography rarely depicts the site of leakage. Intrathecal fluorescein can be used when other tests have failed to detect the site of leakage.[30]

The method of surgical closure of CSF fistulas after temporal bone fractures depends on the location of the fistula, hearing status of both ears, presence of brain herniation through the tegmen, and patency of the external canal.


The risk of meningitis is low (5-11%) in patients with leaks that last less than 7 days.[14, 37] The incidence increases to 33-54% in leaks that last greater than 7 days. This incidence increases with time and is usually related to the duration of the CSF leakage. The risk of meningitis increases in patients who have temporal bone fractures with CSF fistula, open lacerations, and co-infections. Brodie and Thompson found a 20% incidence of meningitis with concurrent infection and 3% incidence in the absence of concurrent infection.[32]  Streptococcuspneumoniae and Haemophilus influenzae are the most common infecting organisms. The incidence of meningitis in patients with posttraumatic CSF fistula treated with prophylactic antibiotics was 2.1%. In those patients who did not receive prophylactic antibiotics, the incidence was significantly higher (8.7%).

Facial nerve paralysis

Facial nerve injuries are more common after transverse fractures of the temporal bone. About 50% of patients with transverse fractures have associated facial nerve paralysis, whereas 20% of patients with longitudinal fractures have associated facial nerve paralysis. The higher incidence of longitudinal (80%) versus transverse fractures (20%) makes facial nerve injuries after longitudinal fractures a more common occurrence. The site of injury of the facial nerve in temporal bone fractures is in the perigeniculate region 82-93% of the time.

In longitudinal fractures, the middle ear is almost always involved, although the otic capsule is spared. The most common site of facial nerve involvement is the horizontal segment of the intratympanic portion. The injury is usually caused by compression and ischemia, rather than disruption. Multiple sites are involved in 20% of cases, usually in the mastoid portion. Onset may be immediate or delayed and partial or complete.

In transverse fractures, otic capsule injury is present. Facial nerve paralysis is usually immediate in onset and complete. Frequently, the nerve is avulsed or severed by the comminuted bone fragments. The usual location of injury is anywhere from the internal auditory meatus to the horizontal segment distal to the geniculate ganglion.

Surgery for facial nerve paralysis can involve decompression of the nerve, nerve anastomosis, nerve grafting, and nerve rerouting, depending on the intraoperative findings.[31]

However, treatment of facial nerve paralysis in temporal bone fractures is controversial, including with regard to the decision to operate, the timing of the operation, and the preferred surgical approach to the injured segment.[38] Furthermore, while some practitioners advocate limited exploration of the facial nerve based on clinical and radiographic information, Fisch advocates total facial nerve exploration and decompression by a middle fossa and transmastoid approach. In patients who have total sensorineural hearing loss, Fisch suggests a translabyrinthine approach.  

Initial evaluation in the emergency department is extremely important because patients with delayed-onset paralysis almost always recover. Therefore, delay in onset is the most important predictive factor for nerve recovery. Those patients with immediate paralysis of an incomplete nature also almost always recover. Incomplete paralysis implies a functional nonsevered facial nerve with good prognosis. Electrodiagnostic testing is usually unnecessary, and these patients should be treated conservatively. Determining whether immediate paralysis is partial may be difficult in the emergency department or ICU. Middle ear and mastoid infection can cause a partially denervated nerve to become totally denervated.

Immediate complete paralysis is usually the result of a severed nerve. Recovery rates are lower for immediate-onset paralysis, a fact that generates the main controversy. Turner treated 30 patients with complete paralysis conservatively and reported good recovery in 63%.[39] Maiman and associates treated 21 patients with complete traumatic facial paralysis and reported full recovery in 52% and partial recovery in 43%.[40] When these recovery rates are compared with the expected recovery rate of 55% with facial nerve decompression, decompression surgery does not appear to be indicated. Determining if the facial nerve is severed is difficult and sometimes impossible without surgical exploration.

Generally, surgery for facial nerve paralysis is selected in patients with complete, immediate nerve paralysis and/or in patients with clear progression of loss of function, with nerve degeneration detected with the assistance of electrodiagnostic studies. Surgery should be performed in the case of 90% nerve degeneration detected by ENOG, whether the paralysis is immediate or delayed. Electrodiagnostic studies help the clinician to differentiate “degeneration” and “percentage of degeneration” on the traumatized side as compared with the normal side.

Although not well established, surgical decompression done in the initial 14 days leads to the best response with respect to facial nerve function. If performed up to 3 months after the initial trauma, it can improve nerve function in approximately 50% of patients. In patients with otic capsule temporal bone fractures who still have serviceable hearing capacity, a middle fossa/transmastoid/supralabyrinthine approach is taken. In patients with otic capsule involvement with profound sensorineural hearing loss or anacusis, the translabyrinthine route is the best approach to directly access the entire intratemporal facial nerve course. In otic capsule sparing with conductive hearing loss and a well-aerated mastoid, a transmastoid/supralabyrinthine approach for exploration and management of the facial nerve is recommended. If this approach is still not adequate for good exposure of the nerve, the alternative is a combined transmastoid/middle cranial fossa approach.[31]

Unusual complications of temporal bone fractures

Paralysis of cranial nerves IX (glossopharyngeal), X (vagus) and XI (spinal accessory)

These cranial nerves can be affected at the jugular foramen in petrous apex fractures. The treatment is conservative

Paralysis of cranial nerve VI (abducens)

This condition usually occurs in the area of the Meckel cave and the Dorello canal. Recovery within 6 months is usual. Alternate eye patching may be the only treatment necessary.

Paralysis of cranial nerve V (trigeminal)

This condition usually occurs in the area of Meckel cave. Treatment is conservative. Mastication muscles may be involved.

Intratemporal carotid artery injury[30, 41]

This type of injury is rare; however, it can be severe and even life threatening. If a fracture of the carotid canal is noted using CT scanning, a carotid artery injury is a possibility, and a stable patient will require CT angiography or MR angiography to assess the possibility of vascular complications.  If a patient has significant bleeding, the carotid artery into the skull base is involved. Significant or massive bleeding can be seen from the external auditory canal, nose, and oral cavity and is associated with rapid deterioration of neurologic status. In such cases, bleeding can be partially controlled by applying pressure on the ear canal, nose, or both. Immediate IV fluid resuscitation is necessary in these patients, as well as preparation for control of the airway with possible intubation. Once the carotid artery injury is inspected and the patient is adequately stabilized, the patient should be taken for angiography, balloon occlusion, or carotid ligation. Balloon occlusion appears to be more effective than ligation in resolving the massive bleeding than ligation.[31]

Carotid cavernous fistula

This is a delayed vascular complication of temporal bone fracture. It is suspected by a pulsatile or nonpulsatile exophthalmus, chemosis, and a bruit detected in the affected area.[30, 42]

Sigmoid sinus thrombosis

This condition occurs but is rare. Sigmoid sinus thrombosis is usually aseptic and nonsymptomatic. It may cause elevated CSF pressure and septicemia if infection is present. Diagnosis is made by means of MRI, magnetic resonance angiography, magnetic resonance venography, or angiography. The Griesinger sign (mastoid emissary vein thrombosis due to thrombus extension) may be noted. Treatment may require exploration of the sinus and ligation of the jugular veins in the neck.

Posttraumatic cholesteatoma

This is a late complication of temporal bone fracture and is caused by skin entrapment in the cranial vault or temporal bone. It can grow undetected for years and become extremely invasive, owing to its size. Treatment is surgical.

Classic Eagle syndrome

This condition may follow tonsillectomy. It consists of pain in the throat with foreign body sensation associated with difficult and painful swallowing. Referred otalgia is common. Traumatic fracture of an ossified styloid and stylohyoid ligament can cause pressure on the external or internal carotid artery and pain may be referred to the cheek or eye, producing atypical pain. Diagnosis is somewhat difficult after trauma and is made by means of palpation and CT scanning. Relief of symptoms by intraoral anesthetic injection may help the diagnosis. Treatment is surgical.

Sympathetic cochleolabyrinthitis

This is a rare complication of temporal bone fracture. The condition is clinically significant because of the potential for hearing loss in the sole ear with hearing. Etiology may be related to the initiation of autoimmune inner ear damage with development of autoantibodies directed against inner ear proteins, as seen in polyarteritis nodosa. Cochlear fracture may release inner ear antibodies and cause host sensitization. Diagnosis is difficult and requires a high index of clinical suspicion. Results of Western blot assays for anticochlear antibodies may or may not be positive. Treatment includes immunosuppression.