The temporal bone makes up the inferolateral portion of the skull. It houses the end organs of hearing and balance, the intraosseous segment of the facial nerve, the jugular bulb, and the internal carotid artery. An understanding of the normal anatomy and physiology of the temporal bone and its contents is essential to the diagnosis and management of surgical disease of this area. Traumatic, inflammatory, infectious, and neoplastic disorders can involve the structures in the region. The alterations in structure and function are, in turn, the keys to diagnosis and treatment.

Forming the inferolateral limit of the skull base, the temporal bone is made up of five parts: the tympanic bone, squamous bone, petrous bone, mastoid bone, and zygomatic bone. It is bounded anteriorly by the infratemporal fossa and clivus, posteriorly by the occipital bone, superiorly by the parietal bone, and inferiorly by the cervical spine and soft tissues. Intracranially, the superior surface the temporal bone is formed by the petrous and squamous portions and constitutes the floor of the middle cranial fossa. The medial edge of this petrous ridge is bordered by the superior petrosal sinus. The posterior intracranial aspect of the temporal bone is separated from the middle fossa by the tentorium cerebelli and constitutes the anterior face of the posterior cranial fossa. This posterior fossa face of the temporal bone is the site of the internal auditory meatus and the intradural portion of the sigmoid sinus. The course of the sigmoid sinus continues through the temporal bone down to the jugular bulb within the jugular foramen where the glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves exit the skull. It then descends to the cervical internal jugular vein. The internal carotid artery ascends in the neck to the carotid canal in the inferior aspect of the petrous bone anterior to the jugular foramen, turns anteriorly to the sigmoid portion, and course to exit the anterior petrous apex and enter the cavernous sinus (Fig. 2) 2368.

A large portion of the temporal bone is pneumatized (Fig. 3) 2369. Embryologically, pneumatization extends posteriorly from an initial bud arising in the lateral nasopharynx, up the eustachian tube, through the middle ear, and back through the aditus ad antrum into the mastoid antrum. Pneumatization of the middle ear (hypotympanic, mesotympanic, and epitympanic portions) back to the aditus ad antrum is consistent. There is extreme variability of pneumatization of the mastoid and petrous bones. The volume of the middle ear cleft is estimated at 0.5 to 2.0 ml, and the total pneumatized volume of the temporal bone may exceed 15 ml. All the pneumatized spaces are lined by mucosa. The normal, seromucinous secretion of the glandular components of this mucosa flows anteroinferiorly toward the eustachian tube orifice, where the cilia of the respiratory-type mucosa of this region expels the fluid toward the nasopharynx. Barometric pressure within the temporal bone should be approximately equal to ambient barometric pressure. With each swallow, the eustachian tube opens momentarily to permit pressure equalization. Persistent impairment of eustachian tube opening leads to negative middle ear pressure and retention of mucus.

Housed within the petrous bone is the otic capsule, the densest bone in the body. The otic capsule consists of the coiled cochlea anteriorly and the vestibule and three semicircular canals posteriorly. The eighth (cochleovestibular) cranial nerve enters the medial surface of the temporal bone in the posterior cranial fossa via the internal auditory canal (Fig. 4) 2370. The cochlear division turns anteroinferiorly into the core (modiolus) of the cochlea and the vestibular division bifurcates into superior and inferior divisions which turn posterosuperiorly and posteroinferiorly, respectively, to innervate the five vestibular end organs: the saccule, utricle, and three semicircular canals. Accompanying the cochlear and the two vestibular nerves through the internal auditory canal is the seventh (facial) cranial nerve, which turns anterosuperiorly to course over the superior aspect of the basal turn of the cochlea to the geniculate ganglion where it turns posteriorly (first genu), travels along the medial wall of the middle ear to a point between the oval window inferiorly and the horizontal semicircular canal superiorly, turns inferiorly (second genu), and travels down to exit the medial surface of the mastoid tip at the stylomastoid foramen.

The external ear is a soft tissue and elastic cartilage structure which funnels sound energy into the external auditory canal. The external canal is approximately 2.5 cm long and 5 to 7 mm wide. The lateral half of the canal is cartilagenous and the medial half is bone, formed by the tympanic bone inferiorly and the squamous and mastoid bones superiorly and posteriorly. The canal ends at the tympanic membrane, an elliptical membrane of approximately 11 mm greatest diameter that forms the lateral wall of the middle ear. Embedded within the tympanic membrane is the malleus, the most lateral of the three bones in the ossicular chain. The head of the malleus is within the pneumatized epitympanum and articulates with the body of the incus. The incus long process, in turn, articulates with the capitulum of the stapes. The footplate of the stapes articulates via the annular ligament with the otic capsule at the oval window. Sound entering the external auditory canal sets the tympanic membrane vibrating. These vibrations are conducted through the ossicular chain to the fluid of the cochlea, where the pressure waves stimulate the cochlear hair cells to transmit a signal via the auditory nerve (Fig. 5) 2371. The end organs of balance within the vestibule and semicircular canals similarly transduce a fluid motion to a nerve signal, but these are triggered by motion and gravity rather than by sound vibrations.

Blunt trauma to the auricle can result in formation of a seroma or haematoma between the cartilage and overlying perichondrium. Perichondrium is the sole source of blood supply to the auricular cartilage. Deprivation of this blood supply by a subperichondrial fluid collection leads rapidly to ischaemic necrosis of the cartilage. If left untreated, infection frequently results in destruction of the cartilagenous framework, the so-called ‘cauliflower’ deformity of the ear. Haematomas of the auricle should be incised, drained, and dressed with a pressure dressing to prevent reaccumulation. Fluid for culture should be obtained at the time of drainage, and the patient should be given an antibiotic effective against Staphylococcus aureus.

Human bites of the auricle often result in serious infections which are difficult to treat. Gram-negative bacteria and anaerobes should be expected. Parenteral antibiotics may be required. Bite wounds should be aggressively cleaned and thoroughly debrided of all obviously devitalized tissue, but not primarily closed. Delayed closure 3 to 5 days later or healing by secondary intention are appropriate.

Avulsion injuries of the ear are primarily of cosmetic significance. They are difficult to repair surgically. The auricle has an end-arteriolar blood supply, and avulsed pieces of ear usually require microvascular anastomosis for repair. If the necessary resources to accomplish this type of surgery are not available, the avulsed fragment may be thoroughly cleansed, de-epithialized, and surgically buried in a subcutaneous pocket for later reconstruction.

Perforation of the tympanic membrane may occur as a result of a penetrating injury or a slap on the side of the ear. Such injuries may occur in combination with ossicular injury, and occasionally stapediovestibular subluxation. Most traumatic perforations heal without surgery if the ear is kept strictly dry. Ossicular injuries may require elective repair after the tympanic membrane heals. The presence of vertigo in association with a traumatic perforation should raise the suspicion of a subluxed stapes. The ear should be explored and repaired as soon as possible to avoid permanent sensorineural hearing loss.

Severe blunt trauma to the head may result in basilar skull or temporal bone fracture. The fracture may be parallel to the long axis of the temporal bone (longitudinal), perpendicular to the long axis (transverse), or a mixture of longitudinal and transverse (mixed). Transverse fractures typically pass directly through the otic capsule, leading to total loss of auditory and vestibular function on the affected side. About 50 per cent of patients have associated facial nerve injury. Longitudinal fractures characteristically pass through the middle ear and external auditory canal, causing ossicular disruption with conductive hearing loss and injury to the tympanic membrane. Facial nerve injury is associated with about 5 to 10 per cent of longitudinal fractures. When the fracture is significantly displaced, a CSF leak may result. The presence of blood behind the tympanic membrane or in the external canal after head trauma heralds the presence of a temporal bone fracture, although it may be difficult to demonstrate radiographically. If possible, a CT scan of the head should be obtained to evaluate the fracture and, more importantly to rule out other more serious injuries within the intracranial cavity.

Surgical management of temporal bone fracture is limited to repair of facial nerve injuries and reconstruction of the sound-conducting mechanism of the tympanic membrane and ossicular chain. No surgical intervention is undertaken until the patient is neurologically stable. If facial paralysis is an immediate result of temporal bone fracture and there is radiographic evidence of bony disruption of the fallopian canal, exploration and repair of the nerve is indicated. Delayed facial paralysis can be observed without initial surgical intervention as recovery is usually complete. Delayed exploration or repair of the nerve can be undertaken 6 to 12 months later if spontaneous recovery is poor.

Hearing loss resulting from temporal bone fracture may be sensorineural, conductive, or mixed. Sensorineural hearing loss is not surgically remediable. Conductive hearing loss may be due to blood and oedema within the middle ear. If the loss persists for more than 6 months following injury, the problem is probably related to ossicular injury. Surgical repair by exploratory tympanotomy and ossiculoplasty may be undertaken at any time thereafter.

A cerebrospinal fluid leak through the eustachian tube or through the external canal may occur following severe temporal bone fractures. In most cases, the leak resolves spontaneously within 10 days. Closure may be facilitated by elevating the head of the bed and by lumbar drainage of fluid. If leakage does not cease by 10 days, surgical repair is indicated. Repair frequently requires tympanomastoid obliteration with a resulting permanent conductive hearing loss. Instillation of 0.5 ml of 10 per cent fluorescein solution diluted in 10 ml of cerebrospinal fluid via lumbar puncture prior to surgery facilitates localization of the leak by staining the cerebrospinal fluid.

Otitis externa is an infection of the skin of the external auditory canal. It typically occurs when the ear canal is exposed to chronic moisture, resulting in maceration of the skin and resultant loss of resistance to infection. Minor trauma or chronic dermatitis may also breach the normal protective barrier of the skin. In almost all cases the bacterial species responsible is Pseudomonas aeruginosa. The clinical representation is one of gradual onset of severe otalgia over hours to days. Movement of the pinna produces exquisite discomfort. Examination of the ear discloses erythema, swelling, and purulent exudate lining the canal. Treatment is medical and consists of strict avoidance of water exposure, topical antimicrobial ear drops, preferably with a corticosteroid for reduction of swelling and inflammation, and analgesics. Occasionally, synergistic interactions between Pseudomonas and streptococcal or staphylococcal species may cause simple otitis externa to progress to involve the pinna and face with an erysipeloid spreading cellulitis and/or perichondritis. This is a dangerous situation requiring immediate treatment with parenteral antibiotics.

This variation of otitis externa is found in elderly, diabetic, or other immunocompromised patients. It begins in a similar way to common otitis exerna and is also due to infection with P. aeruginosa. However, a cellulitis with microabscesses develops and spreads rapidly into deep tissue planes along the skull base with resultant osteitis/osteomyelitis. In severe cases there is progressive loss of cranial nerve function from entrapment within the spreading inflammatory phlegmon at the skull base. Examination of the ear canal typically discloses granulation tissue and exposed, devitalized cartilage and bone. A mortality rate of up to 50 per cent is reported when the cranial nerves are affected. Treatment consists of wide debridement of obviously devitalized tissue in conjunction with prolonged parenteral and topical therapy with aminoglycoside antibiotics. Drug therapy is often required for 8 to 12 weeks. Meticulous attention to management of diabetes mellitus throughout treatment is essential.

In the presence of eustachian tube obstruction the middle ear develops a negative pressure, followed shortly by an effusion. Bacterial contamination of the effusion by haematogenous spread results in suppurative infection of the middle ear. Symptoms of progressive hearing loss and pain develop over hours. Examination reveals reduced hearing acuity and a bulging, opaque, erythematous tympanic membrane. Usual causative organisms include Streptococcus pneumoniae, Group A &bgr;-haemolytic S. pyogenes, and Haemophilus influenzae. Oral antibiotic therapy will cure uncomplicated infection in 7 to 10 days, with resolution of residual effusion over the next 2 to 6 weeks. Delays in institution of antibiotic therapy often leads to spontaneous perforation and drainage of purulent or bloody fluid from the ear canal. Paradoxically, perforation produces rapid improvement in symptoms and spontaneous recovery in some patients. Complications may develop, however; these include labyrinthitis with sensorineural hearing loss and vertigo, facial nerve paresis or paralysis, acute mastoiditis, and perforation of the tympanic membrane. Complicated otitis media requires surgical intervention by wide myringotomy for drainage and culture. Suppurative labyrinthitis, in which pus actually fills the inner ear, is a rare complication of centripetal spread of sepsis from the middle ear and mastoid to the inner ear. It is more often seen as centrifugal spread from bacterial meningitis. Suppurative labyrinthitis secondary to middle ear infection, as well as acute mastoiditis, are surgical emergencies requiring prompt intervention to open and drain the mastoid.

Usually seen as a complication of acute otitis media, this suppurative complication presents with toxicity, fever, pain, fluctuant, erythematous swelling of the postauricular area, with lateral and anteroinferior displacement of the pinna and erythematous ‘sagging’ of the posterosuperior wall of the external auditory canal. In uncomplicated acute otitis media the pneumatized spaces of the temporal bone are filled with pus; the mucosa is inflamed but intact with normal bone beneath. In contrast, acute mastoiditis is characterized by ‘coalescence’ of pneumatized spaces due to demineralization and destruction of bony trabeculae in the mastoid. This finding on mastoid radiographs is an ominous sign and warrants immediate surgical intervention in addition to medical treatment with high dose parenteral antibiotics. Wide postauricular incision and drainage in conjunction with curettage and drilling to remove the entire lateral wall of the mastoid bone and its contents down to the otic capsule, facial nerve canal, and posterior and middle fossa dural plates is necessary. Actual exposure and exploration of the dural surfaces is recommended to prevent overlooking an epidural abscess. The post-auricular incision is closed loosely over a drain, which is left in place for several days until the infection is clearly under control. Parenteral antibiotics and then oral antibiotics are continued until complete resolution is obtained, generally 2 to 6 weeks.

Chronic otitis media is defined as a middle ear chronically open due to persistent tympanic membrane perforation; it may be either active or inactive. Inactive chronic otitis media requires no treatment except avoidance of water exposure that will carry bacteria into the middle ear and cause suppurative infection. The perforation may be repaired electively (tympanoplasty) to eliminate the need for water precautions and/or to improve hearing in patients where enough tympanic membrane is absent (usually more than 30 per cent) to cause an associated conductive hearing loss. Active chronic otitis media is characterized by purulent otorrhoea. Typically the middle ear mucosa visible through the perforation is erythematous and granular. Granulation tissue often surrounds the perforation and extends on to the canal wall. The condition is seen both with and without associated cholesteatoma, a collection of keratin debris entrapped within the middle ear and/or mastoid. Cholesteatoma develops slowly as a traction diverticulum of the tympanic membrane in response to chronic negative middle ear pressure that occurs with inadequate eustachian tube function. It may also be due to migration of squamous epithelium from the ear canal or outer surface of the tympanic membrane through a perforation. Eventually, the accumulated keratin debris exerts pressure on surrounding structures. The combination of pressure, infection, and inflammation at the interface between the cholesteatoma sac wall and underlying bones results in bone destruction. Ossicular erosion with conductive hearing loss, exposure and injury of the facial nerve, invasion of the otic capsule with sensorineural hearing loss and/or vertigo, and epidural or intracranial extension follow. Presence of cholesteatoma is marked by cheesy white material visible through a perforation (Fig. 8) 2374. Surgical management is by tympanomastoidectomy. Mastoid cortex and bony trabeculae are removed using a high speed drill and operating microscope to expose the posterior and middle fossa dural plates, the otic capsule of the semicircular canals, and the bone overlying the facial nerve canal. The damaged portion of the tympanic membrane is resected and the bone lateral to the epitympanum (the scutum) is removed. The entire bony external auditory canal wall can be removed if this is necessary to gain adequate surgical exposure. Temporalis muscle fascia or tragal perichondrium is used to create a new tympanic membrane. Split-thickness skin grafts are often used to resurface the tympanic membrane graft laterally. Ossicular reconstruction to improve hearing may be undertaken simultaneously or as a second stage operation 6 to 12 months later. Where complete extirpation of cholesteatoma is in doubt, a repeat operation to look for persistent or recurrent disease is planned after 6 to 12 months. Sutures are removed from the postauricular incision 1 week postoperatively. Packing remains in the ear canal for 10 to 14 days to stabilize the reconstruction during the early stages of healing. Final hearing results are expected after 3 to 4 months of healing.

Active chronic otitis media, with or without cholesteatoma, can be associated with the same complications as acute mastoiditis, including labyrinthitis, facial nerve paresis or paralysis, epidural abscess, meningitis, brain abscess, sigmoid sinus thrombosis, or otitic hydrocephalus. Labyrinthitis, facial paralysis, and epidural abscess are treated by tympanomastoidectomy. Meningitis requires the additional administration of appropriate parenteral antibiotics which are able to cross the blood–brain barrier. Suspected brain abscess requires neurosurgical consultation. Brain abscess is often treated medically, but may require surgical drainage. Otitic hydrocephalus is increased intracranial pressure in association with mastoiditis; its cause is not known. Although it often occurs in association with sigmoid sinus thrombosis this is not always the case; most cases of sigmoid sinus thrombosis do not result in elevated intracranial pressure. Clinically, patients usually present with headache, vomiting, visual blurring, and diplopia in association with other signs of acute mastoid infection. Examination reveals papilloedema, mental status changes, and occasionally sixth nerve paralysis. Lumbar puncture demonstrates elevated cerebrospinal fluid pressures with normal composition. It is critical that other causes of elevated intracranial pressure should be ruled out, especially the presence of a brain abscess. Once the diagnosis of increased intracranial pressure is made, and the existence of space-occupying lesions has been ruled out, the patency of the sigmoid sinus should be assessed with either rapid contrast infusion CT, venous subtraction angiography, or MRI. Patients with suspected sigmoid sinus thrombosis should undergo surgical exploration as soon as possible (Fig. 9) 2375. The sinus should be uncovered from the sinodural angle to the jugular bulb to identify and remove any nidus of pus or granulation tissue. Once this has been accomplished, the sinus should be aspirated. If free flow is encountered, the sinus need not be entered. If sluggish flow is encountered, the aspirate should be sent for culture and the sinus not opened. If no flow is obtained, then the sinus should be entered. A clot should be sent for culture to ascertain whether the thrombus is septic or sterile. If empyema is encountered, the sinus should be opened, the pus evacuated, and the thrombosed sinus drained into the mastoid. If, upon evacuation of pus or thrombus, bleeding is encountered, the sinus can be packed extraluminally at the region of the jugular bulb and the superior petrosal sinus with an absorbable topical thrombotic agent such as Surgicel. Ligation of the internal jugular vein should be reserved for patients with evidence of jugular empyema on aspiration and in patients with septic pulmonary emboli. Treatment of otitic hydrocephalus involves management of the underlying otological disease and prevention of complications from increased intracranial pressure. Mastoidectomy with exploration of the lateral sinus from the sinodural angle to the jugular bulb should be accomplished as soon as the patient is medically stable. Treatment of the increased intracranial pressure usually requires steroids, acetazolamide, hyperosmolar agents, and occasionally drainage of cerebrospinal fluid. Patients usually have a prolonged clinical course ranging from weeks to months, even after resolution of the mastoid infection.

These lesions of the auricle include sebaceous cysts, seborrhoeic keratosis, senile keratosis, and chondrodermatitis nodularis chronicis helicis. Because they are often difficult to differentiate from malignant tumours, biopsy should be performed to establish the diagnosis.

The most common benign tumours of the external canal are exotoses and osteomas (Fig. 10) 2376. These are bony, hard, rarely of pathological significance, and may be observed without biopsy or removal.

Paragangliomas, or glomus tumours, may occur within the middle ear and in the region of the jugular bulb and foramen. When these tumours are confined to the middle ear space, they are referred to as glomus tympanicum tumours. Tumours arising from the jugular bulb are referred to as glomus jugulare tumours. These tumours are highly vascular and frequently present with pulsatile tinnitus. Glomus jugulare tumours may result in paralysis of cranial nerves IX, X, and XI. Examination usually reveals a pulsatile vascular mass behind the tympanic membrane. Evaluation of these tumours should always include CT scanning to determine location, extent, and other possible paragangliomas in the head and neck, which affect 10 per cent of patients. Four per cent of these tumours secrete catecholamines.

Glomus tympanicum tumours should be removed surgically through a postauricular or endaural hypotympanotomy. The tumour is usually supplied by the inferior tympanic artery, which can be cauterized to reduce the bleeding. Removal of glomus jugulare tumours is best accomplished through a lateral infratemporal fossa approach with mobilization and rerouting of the facial nerve. This usually results in temporary weakness of the face as well as permanent or temporary paralysis of cranial nerves IX, X, and XI, with difficulty in swallowing. Larger glomus jugulare tumours and those showing intracranial extension may be treated with low dose radiation therapy. Radiation effectively arrests tumour growth for extended periods. If growth continues, surgical intervention is not precluded.

Acoustic neurinomas are amongst the common intracranial neoplasms and typically present with symptoms of hearing loss and tinnitus. These tumours originate on the vestibular division of the cochleovestibular nerve and may also result in symptoms of vertigo or dysequilibrium. When the tumour arises within the internal auditory canal, compression of the cochlear nerve occurs early and symptoms begin while the tumour is small. Tumours which originate in the subarachnoid space of the cerebellopontine angle outside the internal auditory canal may become quite large before symptoms develop. Large tumours may result in fifth (trigeminal) cranial nerve compression with numbness of the ipsilateral side of the face. Although the facial nerve is intimately involved with these tumours, facial nerve symptoms are unusual. Audiometry usually demonstrates an asymmetric sensorineural hearing loss with reduced discrimination. Auditory evoked response testing when available demonstrates a retrocochlear pattern. Diagnosis is confirmed best by MRI with gadolinium.

Surgical removal of acoustic neurinomas is accomplished by a suboccipital, translabyrinthine, or middle fossa approach, depending upon the location and size of the tumour and level of residual hearing. The use of intraoperative facial nerve monitoring has improved facial nerve preservation. In recent times there has been a focus on hearing preservation in patients who have small tumours.

Squamous cell and basal cell carcinomas are the most common malignant tumours of the auricle. Local excision with adequate margins is necessary for cure. Malignant melanoma is fortunately much less common and, once diagnosed by biopsy, requires wide local excision. When deep invasion has occurred, local lymph node dissection should be performed in conjunction with wide excision.

When basal cell or squamous cell carcinoma occur within 1 cm of the inside of the external auditory canal, adequate excision requires lateral temporal bone resection. Postoperative radiation therapy is indicated for larger squamous cancers.

Squamous cell carcinoma of the external canal or middle ear occurs most frequently in patients with long-standing chronic otitis media. In this setting, tumour extends medial to the tympanic membrane and is no longer encompassable by lateral temporal bone resection. Although subtotal and total temporal bone resection have been advocated in such circumstances, they are associated with high operative mortality. Wide field tympanomastoidectomy with fat obliteration and postoperative radiation therapy is usually curative when tumour is confined to the temporal bone. Patients with squamous cell cancers of the temporal bone should undergo CT and MRI scanning prior to surgical removal to determine whether or not there is intracranial extension. In general, intracranial extension carries a poor prognosis, and if extensive may contraindicate surgical intervention. In such cases, radiation may be helpful for palliation.

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