Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Temporal Bone Fractures Treatment & Management

  • Author: Antonio Riera March, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
 
Updated: Nov 23, 2015
 

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.

Next

Complications

Common complications of temporal bone fractures include hearing loss, CSF fistula, facial nerve paralysis, external auditory canal stenosis, cholesteatoma formation, and vascular injuries.

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:[13, 22]

  • 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.[23]

Also see the Medscape Reference article Ossiculoplasty.

Sensorineural hearing loss

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.

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.

Vertigo/nystagmus

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. 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%).[13, 24] 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. Pneumatoceles and brain herniations are rare. Pneumatoceles may resolve but 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.[25] Rathmore found no difference in the rate of meningitis with or without prophylactic antibiotics.[26] Demetriades and colleagues found that the incidence of meningitis and other co-infections was higher in the group that did not receive prophylaxis.[27] 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.[28] 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. HRCT 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, CT cisternography rarely depicts the site of leakage. Intrathecal fluorescein can be used when other tests have failed to detect the site of leakage.[23] If the fistula is inactive at the time the localizing technique is used, the CSF leak is not detected.

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.

Meningitis

The risk of meningitis is low (5-11%) in patients with leaks that last less than 7 days.[13, 29] 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.[24] 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.

The controversies regarding facial nerve paralysis involve the decision to operate, the timing of the operation, and the preferred surgical approach to the injured segment.[30] 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%.[31] Maiman and associates treated 21 patients with complete traumatic facial paralysis and reported full recovery in 52% and partial recovery in 43%.[32] 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.

The decision to operate is made with the assistance of the electrodiagnostic studies. Generally, surgery should be performed in the case of "nerve degeneration," whether the paralysis is immediate or delayed. The electrodiagnostic studies help the clinician to differentiate degeneration and percentage of degeneration on the traumatized side as compared with the normal side.

The most common electrical tests are the maximum stimulation test (MST), the nerve excitability test (NET), electroneuronography (ENOG), and electromyography (EMG).

Unusual complications of temporal bone fractures

See the list below:

  • 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: [23, 33] 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. Significant or massive bleeding can be seen from the external auditory canal, nose, and oral cavity associated with a rapid deterioration of the neurological status. In such cases, bleeding can be partially controlled by applying pressure on 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 in resolving the massive bleeding than ligation.
  • Carotid cavernous fistula is a delayed vascular complication of temporal bone fracture. This is suspected by a pulsatile or nonpulsatile exophthalmus, chemosis, and a bruit detected in the affected area. [23, 34]
  • 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.
Previous
 
Contributor Information and Disclosures
Author

Antonio Riera March, MD, FACS Professor, Department of Otolaryngology-Head and Neck Surgery, University of Puerto Rico School of Medicine

Antonio Riera March, MD, FACS is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, Society for Ear, Nose and Throat Advances in Children, American Cleft Palate-Craniofacial Association, American College of Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Peter C Belafsky, MD, MPH, PhD Assistant Professor, Department of Otolaryngology, University of California at Davis

Peter C Belafsky, MD, MPH, PhD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: Nothing to disclose.

Sarah Connell, MD Fellow, Department of Otolaryngology, Head and Neck Surgery, University of Miami, Jackson Memorial Hospital

Sarah Connell, MD is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Cleft Palate-Craniofacial Association, Triological Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Peter S Roland, MD Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director, Clinical Center for Auditory, Vestibular, and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Chief of Pediatric Otology, Children’s Medical Center of Dallas; President of Medical Staff, Parkland Memorial Hospital; Adjunct Professor of Communicative Disorders, School of Behavioral and Brain Sciences, Chief of Medical Service, Callier Center for Communicative Disorders, University of Texas School of Human Development

Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Auditory Society, The Triological Society, North American Skull Base Society, Society of University Otolaryngologists-Head and Neck Surgeons, American Neurotology Society, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, American Otological Society

Disclosure: Received honoraria from Alcon Labs for consulting; Received honoraria from Advanced Bionics for board membership; Received honoraria from Cochlear Corp for board membership; Received travel grants from Med El Corp for consulting.

Chief Editor

Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and Neck Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250 from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received consulting fee from Covidien for consulting.

Additional Contributors

Jack A Shohet, MD President, Shohet Ear Associates Medical Group, Inc; Associate Clinical Professor, Department of Otolaryngology-Head and Neck Surgery, University of California, Irvine, School of Medicine

Jack A Shohet, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Neurotology Society, American Medical Association, California Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Envoy Medical <br/>Received consulting fee from Envoy Medical for medical advisory board member. for: Envoy Medical .

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Mark L Belafsky, MD, FACS, to the development and writing of this article.

The author wishes to acknowledge Joan Flaherty, RN, for her editorial assistance.

References
  1. Sun GH, Shoman NM, Samy RN, Cornelius RS, Koch BL, Pensak ML. Do contemporary temporal bone fracture classification systems reflect concurrent intracranial and cervical spine injuries?. Laryngoscope. 2011 May. 121(5):929-32. [Medline].

  2. Johnson F., Semaan M. T., Megerian C. A. Temporal Bone Fracture: Evaluation and Management in the Modern Era. Otolaryngol. Clin. N. Am. 2008. 41:597-618.

  3. Alvi A, Bereliani A. Acute intracranial complications of temporal bone trauma. Otolaryngol Head Neck Surg. Dec 1998. 119(6:609-613.

  4. Darrouzet V, Duclos JY, Liguoro D, Truilhe Y, De Bonfils C, Bebear JP. Management of facial paralysis resulting from temporal bone fractures: Our experience in 115 cases. Otolaryngol Head Neck Surg. Jul 2001. 125(1):77-84.

  5. Lee D, Honrado C, Har-El G, Goldsmith A. Pediatric temporal bone fractures. Laryngoscope. Jun 1998. 108(6):816-821.

  6. Lee D, Honrado C, Har-El G, Goldsmith A. Pediatric temporal bone fractures. Laryngoscope. 1998 Jun. 108(6):816-21. [Medline].

  7. Dunklebarger J, Branstetter B 4th, Lincoln A, Sippey M, Cohen M, Gaines B, et al. Pediatric temporal bone fractures: Current trends and comparison of classification schemes. Laryngoscope. 2013 Dec 17. [Medline].

  8. Ulrich K. Verletzungen des Gehorlorgans bel Schadelbasisfrakturen(Ein Histologisch und Klinissche Studie). Acta Otolaryngol Suppl. 1926. 6:1-150.

  9. Ghorayeb BY, Yeakley JW. Temporal bone fractures: longitudinal or oblique? The case for oblique temporal bone fractures. Laryngoscope. 1992 Feb. 102(2):129-34. [Medline].

  10. Kerr AG, Smyth GDL. Ear Trauma. Maran AGD, Stell PM. Clinical Otolaryngology. Blackwell Scientific Publications; 1979. 113-114.

  11. Olsson JE, Shagets FW, MC, USAF. Blunt Trauma of the Temporal Bone. Second Edition 1986.

  12. Choi HG, Lee HJ, Lee JS, et al. The Rates and Clinical Characteristics of Pneumolabyrinth in Temporal Bone Fracture. Otol Neurotol. 2015 Jul. 36 (6):1048-53. [Medline].

  13. Diaz R, Brodie HA. Middle Ear and Temporal Bone Trauma. Cummings CW, Haughey BH, Thomas JR, Harker LA, Flint PW. Otolaryngology-Head and Neck Surgery. Fourth edition. Elsevier Mosby; 2005. 4: 2057-2079/139.

  14. Ghorayeb BY, Yeakley JW, Hall JW 3d, Jones BE. Unusual complications of temporal bone fractures. Arch Otolaryngol Head Neck Surg. 1987 Jul. 113(7):749-53. [Medline].

  15. Woodcock R. Temporal Bone, Fractures. Medscape Reference. [Full Text].

  16. Ghorayeb BY, Yeakley JW, Hall JW 3rd, Jones BE. Unusual complications of temporal bone fractures. Arch Otolaryngol Head Neck Surg. 1987 Jul. 113(7):749-53. [Medline].

  17. Montava M, Mancini J, Masson C, Collin M, Chaumoitre K, Lavieille JP. Temporal bone fractures: sequelae and their impact on quality of life. Am J Otolaryngol. 2015 May-Jun. 36 (3):364-70. [Medline].

  18. Schell A, Kitsko D. Audiometric Outcomes in Pediatric Temporal Bone Trauma. Otolaryngol Head Neck Surg. 2015 Oct 6. [Medline].

  19. Jones RM, Rothman MI, Gray WC, Zoarski GH, Mattox DE. Temporal lobe injury in temporal bone fractures. Arch Otolaryngol Head Neck Surg. 2000. 126 (2):131-135.

  20. Schuknecht B, Graetz K. Radiologic assessment of maxillofacial, mandibular, and skull base trauma. Eur Radiol. 2005 Mar. 15(3):560-8. [Medline].

  21. Fisch U. Facial paralysis in fractures of the petrous bone. Laryngoscope. 1974 Dec. 84(12):2141-54. [Medline].

  22. Hough JV, Stuart WD. Middle ear injuries in skull trauma. Laryngoscope. 1968 Jun. 78(6):899-937. [Medline].

  23. Brodie HA. Management of Temporal Bone Trauma. Cummings/ Otolaryngology-Head and Neck Surgery, 3-Volume Set. 5th ed. Mosby Elsevier; 2010. 2036-47.

  24. Brodie HA, Thompson TC. Management of complications from 820 temporal bone fractures. Am J Otol. 1997 Mar. 18(2):188-97. [Medline].

  25. MacGee EE, Cauthen JC, Brackett CE. Meningitis following acute traumatic cerebrospinal fluid fistula. J Neurosurg. 1970 Sep. 33(3):312-6. [Medline].

  26. Rathmore MH. Do prophylactic antibiotics prevent meningitis after basilar skull fracture?. Ped Inf Dis J. 1991 Feb. 10(2):87-88. [Medline].

  27. Demetriades D, Charalambides D, Lakhoo M, Pantanowitz D. Role of prophylactic antibiotics in open and basilar fractures of the skull: a randomized study. Injury. 1992. 23(6):377-80. [Medline].

  28. Villalobos T, Arango C, Kubilis P, Rathore M. Antibiotic prophylaxis after basilar skull fractures: a meta-analysis. ALYSIS. 1998 Aug. 27(2):364-9. [Medline].

  29. Leech PJ, Paterson A. Conservative and operative management for cerebrospinal-fluid leakage after closed head injury. Lancet. 1973 May 12. 1(7811):1013-6. [Medline].

  30. Kumar A, Patni A. Facial paralysis caused by temporal bone fractures, chapter XII in Update on Facial Nerve Disorders (Shelton C. MD, editor). 2001.

  31. Turner JWA. Facial paralysis in closed head injuries. Lancet. 1944. 246:756-57.

  32. Maiman DJ, Cusick JF, Anderson AJ, Larson SJ. Nonoperative management of traumatic facial nerve palsy. J Trauma. 1985 Jul. 25(7):644-8. [Medline].

  33. Diaz RC, Kamal SM, Brodie HA. Middle Ear and Temporal Bone Trauma. Johnson JT, Rosen CA, eds. Bailey's Head & Neck Surgery Otolaryngology. 5th. Walters Kluwer/Lippincott Williams & Wilkins; 2014. 2410-2432.

  34. Korkmazer B, Kocak B, Tureci E, Islak C, Kocer N, Kizilkilic O. Endovascular treatment of carotid cavernous sinus fistula: A systematic review. World J Radiol. 2013 Apr 28. 5(4):143-55. [Medline]. [Full Text].

  35. Arriaga Moises A. Traumatic Facial Paralysis. Gates George A. Current Therapy in Otolaryngology-Head and Neck Surgery. Sixth Edition. Mosby; 1998. 121-125.

  36. Barber HO. Head injury audiological and vestibular findings. Ann Otol Rhinol Laryngol. 1969 Apr. 78(2):239-52. [Medline].

  37. Bobad MS. Eagle syndrome caused by traumatic fracture of a mineralized stylohyoid ligament: literature review and case report. Journ Craniomand Pract. 1995. 13(3):189-92.

  38. Brodie HA. Management of Temporal Bone Trauma. Bailey Byron J. & Johnson Jonas T. Head & Neck Surgery-Otolaryngology. 4th edition. Lippincott Williams & Wilkins; 2006. Vol. 2: 125/2848-2866.

  39. Cannon CR, Jahrsdoerfer RA. Temporal bone fractures. Review of 90 cases. Arch Otolaryngol. 1983 May. 109(5):285-8. [Medline].

  40. Chang CY, Cass SP. Management of facial nerve injury due to temporal bone trauma. Am J Otol. 1999 Jan. 20(1):96-114. [Medline].

  41. Clark JM, Shockley WW. Management and Reanimation of the Paralyzed Face. Papel Ira D. Facial Plastic and Reconstructive Surgery. Second Edition. Thieme; 2002. 660-685/53.

  42. Darrouzet V, Duclos JY, Liguoro D, Truilhe Y, De Bonfils C, Bebear JP. Management of facial paralysis resulting from temporal bone fractures: Our experience in 115 cases. Otolaryngol Head Neck Surg. 2001 Jul. 125(1):77-84. [Medline].

  43. DiBiase P, Arriaga MA. Post-traumatic hydrops. Otolaryngol Clin North Am. 1997 Dec. 30(6):1117-22. [Medline].

  44. Eagle WW. Elongated styloid process: report of two cases. Arch Otolaryn Head Neck Surg. 1937. 25:584-87.

  45. Felix H, Eby TL, Fisch U. New aspects of facial nerve pathology in temporal bone fractures. Acta Otolaryngol. 1991. 111(2):332-6. [Medline].

  46. Fisch U. Current surgical treatment of intratemporal facial palsy. Clin Plast Surg. 1979 Jul. 6(3):377-88. [Medline].

  47. Gianoli GJ, Amedee RG. Temporal bone fractures. J La State Med Soc. 1989 Oct. 141(10):11-3. [Medline].

  48. Girdjian ES, Lissnerl IR. Deformation of the skull in head injury studied by the "Stesscoat" technique, quantitative determinations. Surg Gynecol Obstret. 1946. 83:219-233.

  49. Goodwin WJ Jr. Temporal bone fractures. Otolaryngol Clin North Am. 1983 Aug. 16(3):651-9. [Medline].

  50. Grahne B. Traumatic cranionasal fistulas persistent cerebrospinal fluid rhinorrhoea and their repair with frontal sinus osteoplasty. Acta Otolaryngol. 1970 Nov-Dec. 70(5):392-400. [Medline].

  51. Griffin JE, Altenau MM, Schaefer SD. Bilateral longitudinal temporal bone fractures: a retrospective review of seventeen cases. Laryngoscope. 1979 Sep. 89(9 Pt 1):1432-5. [Medline].

  52. Hagan WE, Tabb HG, Cox RH, Travis LW. Gunshot injury to the temporal bone: an analysis of thirty-five cases. Laryngoscope. 1979 Aug. 89(8):1258-72. [Medline].

  53. Kahn JB, Stewart MG, Diaz-Marchan PJ. Acute temporal bone trauma: utility of high-resolution computed tomography. Am J Otol. 2000 Sep. 21(5):743-52. [Medline].

  54. Lambert PR, Brackmann DE. Facial paralysis in longitudinal temporal bone fractures: a review of 26 cases. Laryngoscope. 1984 Aug. 94(8):1022-6. [Medline].

  55. Lyos AT, Marsh MA, Jenkins HA, Coker NJ. Progressive hearing loss after transverse temporal bone fracture. Arch Otolaryngol Head Neck Surg. 1995 Jul. 121(7):795-9. [Medline].

  56. McKennan KX, Chole RA. Facial paralysis in temporal bone trauma. Am J Otol. 1992 Mar. 13(2):167-72. [Medline].

  57. McKennan KX, Chole RA. Post-traumatic cholesteatoma. Laryngoscope. 1989 Aug. 99(8 Pt 1):779-82. [Medline].

  58. Meriot P, Veillon F, Garcia JF, Nonent M, Jezequel J, Bourjat P, et al. CT appearances of ossicular injuries. Radiographics. 1997 Nov-Dec. 17(6):1445-54. [Medline].

  59. Morgan WE, Coker NJ, Jenkins HA. Histopathology of temporal bone fractures: implications for cochlear implantation. Laryngoscope. 1994 Apr. 104(4):426-32. [Medline].

  60. Nelson EL, Melton LJ 3rd, Annegers JF, Laws ER, Offord KP. Incidence of skull fractures in Olmsted County, Minnesota. Neurosurgery. 1984 Sep. 15(3):318-24. [Medline].

  61. Nosan DK, Benecke JE Jr, Murr AH. Current perspective on temporal bone trauma. Otolaryngol Head Neck Surg. 1997 Jul. 117(1):67-71. [Medline].

  62. Ort S, Beus K. Pediatric temporal bone fractures in a rural population. Otolaryngology Head Neck Surgery. 2004. 131:433-437.

  63. Quaranta A, Campobasso G, Piazza F, Quaranta N, Salonna I. Facial nerve paralysis in temporal bone fractures: outcomes after late decompression surgery. Acta Otolaryngol. 2001 Jul. 121(5):652-5. [Medline].

  64. Resnick DK, Subach BR, Marion DW. The significance of carotid canal involvement in basilar cranial fracture. Neurosurgery. 1997 Jun. 40(6):1177-81. [Medline].

  65. Ryall RG, Peacock MK, Simpson DA. Usefulness of beta 2-transferrin assay in the detection of cerebrospinal fluid leaks following head injury. J Neurosurg. 1992 Nov. 77(5):737-9. [Medline].

  66. Schindler JS, Niparko JK. Imaging quiz case 1. Transverse temporal bone fractures (left) with subsequent progressive SNHL, consistent with sympathetic cochleolabyrinthitis. Arch Otolaryngol Head Neck Surg. 1998 Jul. 124(7):814-818. [Medline].

  67. Schuknecht HF. A clinical study of auditory damage following blows to the head. Ann Otol Rhinol Laryngol. 1950 Jun. 59(2):331-58. [Medline].

  68. Shindo ML, Fetterman BL, Shih L, Maceri DR, Rice DH. Gunshot wounds of the temporal bone: a rational approach to evaluation and management. Otolaryngol Head Neck Surg. 1995 Apr. 112(4):533-9. [Medline].

  69. Spetzler RF, Wilson CB. Management of recurrent CSF rhinorrhea of the middle and posterior fossa. J Neurosurg. 1998. 49:393-97. [Medline].

  70. Stone JA, Castillo M, Neelon B, Mukherji SK. Evaluation of CSF leaks: high-resolution CT compared with contrast-enhanced CT and radionuclide cisternography. Am J Neuroradiol. 1999 Apr. 20(4):706-12. [Medline].

  71. Travis LW, Stalnaker RL, Melvin JW. Impact trauma of the human temporal bone. J Trauma. 1977 Oct. 17(10):761-6. [Medline].

  72. Tuohimaa P. Vestibular disturbances after acute mild head injury. Acta Ololaryngol (Suppl). 1978. 359:1-67. [Medline].

  73. Weissman JL, Curtin HD. Pneumolabyrinth: a computed tomographic sign of temporal bone fracture. Am J Otolaryngol. 1992 Mar-Apr. 13(2):113-4. [Medline].

  74. Wennmo C, Spandow O. Fractures of the temporal bone--chain incongruencies. Am J Otolaryngol. 1993 Jan-Feb. 14(1):38-42. [Medline].

  75. Wennmo C, Svensson C. Temporal bone fractures. Vestibular and other related ear sequele. Acta Otolaryngol Suppl. 1989. 468:379-83. [Medline].

  76. Yanagihara N, Murakami S, Nishihara S. Temporal bone fractures inducing facial nerve paralysis: a new classification and its clinical significance. Ear Nose Throat J. 1997 Feb. 76(2):79-80, 83-6. [Medline].

  77. Yeakley JW. Temporal bone fractures. Curr Probl Diagn Radiol. 1999 May-Jun. 28(3):65-98. [Medline].

  78. Ylikoski J, Palva T, Sanna M. Dizziness after head trauma: clinical and morphologic findings. Am J Otol. 1982 Apr. 3(4):343-52. [Medline].

 
Previous
Next
 
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 (C), condyle (CO), foramen magnum (FM), jugular foramen (J), foramen lacerum (L), foramen ovale (O), pterygoid plates (P), styloid foramen (S), foramen spinosum (SP).
Internal aspect of the skull base that represents, in black and blue colors, the pathway of the longitudinal temporal bone fracture lines.
Internal aspect of the skull base that represents, in black and red colors, the pathways of the transverse temporal bone fracture lines.
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.
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.
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).
Left temporal bone fracture line crossing the mastoid process and into Henle's spine and the external auditory canal (surgeon's view).
Table 1. Longitudinal and Transverse Fractures
Feature Longitudinal Fractures Transverse Fractures
Incidence Approximately 80% Approximately 20%
Mechanism Temporal or parietal trauma Frontal or occipital trauma
CSF otorrhea Common Occasional
Tympanic membrane perforation Common Rare
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)
Hemotympanum Common (associated with otorrhagia) Possible (not associated with otorrhagia)
Nystagmus 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)
Otorrhagia Common Rare
Vertigo 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
Feature Otic Capsule Sparing Otic Capsule Disrupting
Incidence Approximately 95% Approximately 5%
Mechanism Temporal or parietal trauma Occipital trauma
Line of fracture Anterolateral to the otic capsule Through the otic capsule
Pathway
  • 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 Common Rare
Hearing loss Conductive or mixed Sensorineural
Facial paralysis Less common Common
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.