(Radiology. 2000;216:342-349.)
© RSNA, 2000
Imaging of Tinnitus: A Review1
Jane L. Weissman, MD and
Barry E. Hirsch, MD
1 From the Department of Radiology and Otolaryngology, Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd, Mail Code CR-135, Portland, OR 97201-3098 (J.L.W.), and the Department of Otolaryngology, University of Pittsburgh Medical Center, Pa (B.E.H.). Received June 8, 1999; revision requested August 5; revision received August 31; accepted September 9. Address correspondence to J.L.W. (e-mail: weissmaj@ohsu.edu).
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ABSTRACT
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Tinnitus, a buzzing or ringing in the ear, may be pulsatile or continuous (nonpulsatile). The distinction, with a detailed clinical evaluation, determines the most appropriate imaging study. Pulsatile tinnitus suggests a vascular neoplasm, vascular anomaly, or vascular malformation. Most of the neoplasms are glomus tympanicum and glomus jugulare tumors. Vascular anomalies may cause pulsatile tinnitus, but the mechanism is unknown, and another (treatable) cause should be sought. Most neoplasms and anomalies are best seen on bone algorithm computed tomographic (CT) studies. Dural vascular malformations are often elusive on all cross-sectional imaging studies; conventional angiography may be necessary to make this diagnosis. Flow-sensitive magnetic resonance (MR) images show vascular loops compressing the eighth cranial nerve. Carotid dissections, aneurysms, atherosclerosis, and fibromuscular dysplasia can be identified on both MR imaging or MR angiographic studies and CT or CT angiographic studies. Otosclerosis and Paget disease are CT diagnoses. Benign intracranial hypertension often has no abnormal imaging findings. For patients with nonpulsatile tinnitus, MR imaging is the study of choice to exclude a vestibular schwannoma or other neoplasm of the cerebellopontine angle cistern. Multiple sclerosis and a Chiari I malformation are rare causes of pulsatile tinnitus, also best seen on MR studies. Many patients with tinnitus have no abnormal imaging findings.
Index terms: Arteriovenous malformations, craniofacial, 10.75 • Arteriovenous malformations, dural, 10.75, 379.75 • Cerebral blood vessels, abnormalities, 17.75 • Ear, abnormalities • Paraganglioma 154.3641
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INTRODUCTION
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Tinnitus is a "sound in one ear or both ears, such as buzzing, ringing, or whistling, occurring without an external stimulus" (1). As many as 40 million people in the United States have tinnitus (2). The reported prevalence ranges from 7% to 32% (3–6). The number of people who complain of some form of tinnitus varies with how tinnitus is defined, what population is sampled, and how the subjects are questioned (4). It is important to make a distinction between the presence of tinnitus, which may be universal (and normal), and the complaint of tinnitus, which suggests abnormality (7,8). The severity of tinnitus varies from scarcely noticeable (by the patient) to an unbearable roar that drives some to suicide (7,9).
The evaluation of a patient with tinnitus requires a detailed history to determine if the patient also has hearing loss, vertigo, or headaches; a complete medical examination including a neurotologic physical examination (with otoscopy to look for a middle ear mass and auscultation to search for a bruit); a comprehensive audiologic evaluation with hearing thresholds, word understanding (discrimination), and assessment of hyperacusis (2); and, often, imaging studies. A full clinical evaluation should precede the radiologic studies. The knowledge of whether the tinnitus is pulsatile or nonpulsatile, combined with a detailed clinical assessment, helps determine the most appropriate imaging study.
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CLASSIFICATION OF TINNITUS
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Many classification schemes have been developed to facilitate the diagnosis and treatment of tinnitus. Tinnitus has been divided according to the characteristics of the sound and based on the location of the cause. The sound may be pulsatile (coinciding with the patient’s heartbeat) or continuous (nonpulsatile), and subjective (perceived only by the patient) or objective (also perceptible to another person) (7,10,11). More people have nonpulsatile tinnitus than pulsatile; subjective is more frequent than objective. Pulsatile tinnitus may be subjective or both subjective and objective. With rare exceptions (12), nonpulsatile tinnitus is subjective only.
Some investigators evaluate the pitch, composition, and loudness of the noise; how annoying the noise is; and how well the patient copes with it (10). Other investigators divide tinnitus by etiology into sources within the auditory system (cochlear) and sources outside the auditory system (extracochlear) (9,10,13). The patient may perceive the tinnitus as unilateral or bilateral, and as coming from the ear (tinnitus aurium) or from the head (tinnitus cerebri) (10,13).
This review considers tinnitus from the perspective of imaging strategies and divides tinnitus into pulsatile and nonpulsatile forms. This division helps direct the radiologic work-up.
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IMAGING STRATEGIES IN PULSATILE TINNITUS
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Pulsatile tinnitus raises the considerations of a vascular tumor, a vascular malformation, and other congenital or acquired vascular abnormality (13–15). In patients with objective pulsatile tinnitus, the work-up often discloses an abnormality (16). However, in our experience, many patients have no imaging abnormalities to explain their symptom. In addition, one study of patients with subjective pulsatile tinnitus and a normal otoscopic examination found no magnetic resonance (MR) imaging abnormalities to explain the tinnitus (14).
Our evaluation of the patient with pulsatile tinnitus starts with a contrast material–enhanced computed tomographic (CT) examination. The scanning protocol covers the temporal bones and skull base (transverse sections, 1-mm collimation, with no intersection gap) and the brain, calvaria, and overlying soft tissues (3–5-mm collimation). We obtain all of the images with use of intravenous contrast material, and view all of the images at bone and soft-tissue algorithms.
Neoplasms
Glomus tumors (chemodectomas, paragangliomas) are vascular neoplasms that arise from the paraganglia. Paraganglia are normal structures that accompany cranial nerves. The most accurate name for these tumors is therefore paragangliomas (17). The paragangliomas most likely to present with pulsatile tinnitus are the glomus tympanicum tumor, the glomus jugulare tumor, and the glomus jugulotympanicum tumor.
Glomus tympanicum tumors range at presentation from millimeters in diameter to a mass that fills the middle ear. The tumor is usually visible otoscopically as a reddish, pulsatile mass behind an intact tympanic membrane. Small tumors are best seen on a thin-section (1-mm) bone algorithm CT scan (Fig 1a). The diagnosis is made on the bone algorithm scans, and it is usually not possible to appreciate enhancement of a small tumor confined to the middle ear on a CT study. As with glomus jugulare tumors, MR imaging shows the tumor enhancement better than CT (11) (Fig 1b), but CT delineates the anatomic extent of the tumor much more clearly (Fig 1a). Most glomus tympanicum tumors arise on the promontory, which is a convexity on the medial wall of the middle ear overlying the basal turn of the cochlea (Fig 1). However, glomus tympanicum tumors can occur anywhere along the Jacobson nerve, which runs across the medial wall of the middle ear (17). It is therefore important to examine the entire middle ear closely when imaging a patient with pulsatile tinnitus. A gadolinium-enhanced MR study can show the small, intensely enhancing mass, but the precise anatomic location may be difficult to determine (Fig 1b).
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Figure 1a. Glomus tympanicum tumors. (a) Transverse thin-section CT scan (bone algorithm) shows a mass (white arrow) on the promontory, the bone over the basal turn of the cochlea (black arrow). (Reprinted from reference 24.) (b) Transverse T1-weighted gadolinium-enhanced MR image (500/25 [repetition time msec/echo time msec], one signal acquired) shows an intensely enhancing glomus tympanicum tumor (curved arrow) filling the middle ear. The promontory is a convex signal void (straight arrow), but other landmarks are more easily seen on the CT scan in a.
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Figure 1b. Glomus tympanicum tumors. (a) Transverse thin-section CT scan (bone algorithm) shows a mass (white arrow) on the promontory, the bone over the basal turn of the cochlea (black arrow). (Reprinted from reference 24.) (b) Transverse T1-weighted gadolinium-enhanced MR image (500/25 [repetition time msec/echo time msec], one signal acquired) shows an intensely enhancing glomus tympanicum tumor (curved arrow) filling the middle ear. The promontory is a convex signal void (straight arrow), but other landmarks are more easily seen on the CT scan in a.
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Glomus jugulare tumors arise from paraganglia in the adventitia of the jugular bulb, which is where the sigmoid sinus becomes the internal jugular vein. When a glomus jugulare tumor is confined to the jugular fossa, the otoscopic examination is normal. A glomus jugulare tumor that extends superiorly into the middle ear is called a glomus jugulotympanicum tumor, and the middle ear component is visible at otoscopy.
Perhaps the earliest abnormality detectable on cross-sectional images of a glomus jugulare tumor is erosion of the lateral and anterior walls of the osseous jugular fossa on a thin-section bone algorithm CT scan (Fig 2a). Occasionally, an enlarged inferior tympanic canaliculus can be seen (Fig 2a), which is evidence of hypertrophy of the inferior tympanic artery that supplies this vascular tumor (18).
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Figure 2a. Glomus jugulare tumors (and mimic). (a) Transverse thin-section CT scan (bone algorithm) shows erosion of the anterior and lateral cortex (open arrow) of the jugular fossa. The tumor (solid white arrow) extends into the middle ear, making this a glomus jugulotympanicum. The inferior tympanic canaliculus is markedly enlarged (arrowhead), which is indirect evidence of hypertrophy of the inferior tympanic artery, which supplies the tumor. (Reprinted from reference 24.) (b) Transverse T1-weighted MR image (500/11, one signal acquired) of a glomus jugulare tumor shows the intensely enhancing tumor (arrow) in the right jugular fossa. Punctate signal voids of tumor vessels create the "salt and pepper" pattern. (c) Transverse T2-weighted MR image (3,000/90, two signals acquired) in a patient with no complaints of pulsatile tinnitus shows high signal intensity in the left jugular fossa (curved arrow) and sigmoid sinus (straight arrows). No cause for this slow flow was found.
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Figure 2b. Glomus jugulare tumors (and mimic). (a) Transverse thin-section CT scan (bone algorithm) shows erosion of the anterior and lateral cortex (open arrow) of the jugular fossa. The tumor (solid white arrow) extends into the middle ear, making this a glomus jugulotympanicum. The inferior tympanic canaliculus is markedly enlarged (arrowhead), which is indirect evidence of hypertrophy of the inferior tympanic artery, which supplies the tumor. (Reprinted from reference 24.) (b) Transverse T1-weighted MR image (500/11, one signal acquired) of a glomus jugulare tumor shows the intensely enhancing tumor (arrow) in the right jugular fossa. Punctate signal voids of tumor vessels create the "salt and pepper" pattern. (c) Transverse T2-weighted MR image (3,000/90, two signals acquired) in a patient with no complaints of pulsatile tinnitus shows high signal intensity in the left jugular fossa (curved arrow) and sigmoid sinus (straight arrows). No cause for this slow flow was found.
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Figure 2c. Glomus jugulare tumors (and mimic). (a) Transverse thin-section CT scan (bone algorithm) shows erosion of the anterior and lateral cortex (open arrow) of the jugular fossa. The tumor (solid white arrow) extends into the middle ear, making this a glomus jugulotympanicum. The inferior tympanic canaliculus is markedly enlarged (arrowhead), which is indirect evidence of hypertrophy of the inferior tympanic artery, which supplies the tumor. (Reprinted from reference 24.) (b) Transverse T1-weighted MR image (500/11, one signal acquired) of a glomus jugulare tumor shows the intensely enhancing tumor (arrow) in the right jugular fossa. Punctate signal voids of tumor vessels create the "salt and pepper" pattern. (c) Transverse T2-weighted MR image (3,000/90, two signals acquired) in a patient with no complaints of pulsatile tinnitus shows high signal intensity in the left jugular fossa (curved arrow) and sigmoid sinus (straight arrows). No cause for this slow flow was found.
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Because these tumors enhance intensely, it may not be possible on a contrast-enhanced CT study to differentiate the normal opacified internal jugular vein from tumor. On gadolinium-enhanced MR images, the tumor also enhances intensely. The characteristic MR pattern is "salt and pepper": The salt is the enhancing tumor stroma (on T1-weighted images after contrast material enhancement and on T2-weighted images), and the pepper is the signal voids of tumor vessels (19) (Fig 2b). However, not all glomus tumors demonstrate this distinctive pattern. Both glomus jugulare and jugulotympanicum tumors may grow into the neck within the lumen of the internal jugular vein, and so obstruct the vein partially (causing slow flow) or completely. High signal intensity and enhancement in the sigmoid sinus suggest slow or absent flow on spin-echo MR images. On time-of-flight or phase-contrast MR images, absent signal (ie, absence of the high signal intensity seen in a normal patent vessel) suggests occlusion or very slow flow. However, on spin-echo images, a normal jugular vein may have any level of signal intensity and may enhance, even in the absence of tumor (Fig 2c). MR imaging can therefore sometimes be confusing or misleading in the diagnosis of a glomus jugulare tumor.
Facial nerve hemangiomas are rare tumors. The two most frequent locations are the geniculate ganglion and within the internal auditory canal (IAC) (20). The clinical presentation depends on the location: Geniculate tumors cause facial nerve weakness; IAC tumors cause sensorineural hearing loss. The otoscopic examination is usually normal. In either location, this vascular tumor rarely may cause tinnitus. Gadolinium-enhanced MR imaging is the best study to demonstrate facial nerve hemangiomas in the IAC (20) and the intensely enhancing geniculate tumor (Fig 3a). However, a bone algorithm CT scan provides more specific information, as the geniculate tumors often have a distinctive appearance of punctate bone opacities giving the tumor a stippled appearance (21) (Fig 3b).
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Figure 3a. Ossifying hemangioma of the facial nerve. (a) Transverse T1-weighted MR image (566/25, one signal acquired) shows the enhancing mass (arrow) in the right geniculate fossa. (b) Transverse CT scan (bone algorithm) shows enlargement of the geniculate fossa (arrow). Stippled bone, characteristic of an ossifying hemangioma, is seen best at the anterior aspect of the tumor.
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Figure 3b. Ossifying hemangioma of the facial nerve. (a) Transverse T1-weighted MR image (566/25, one signal acquired) shows the enhancing mass (arrow) in the right geniculate fossa. (b) Transverse CT scan (bone algorithm) shows enlargement of the geniculate fossa (arrow). Stippled bone, characteristic of an ossifying hemangioma, is seen best at the anterior aspect of the tumor.
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A cavernous hemangioma is a rare middle ear neoplasm (15) that may resemble a glomus tympanicum tumor at otoscopy and on imaging studies. Sometimes, a more lateral location of the hemangioma helps differentiate this tumor from the glomus tumor. The clinician usually makes the diagnosis at surgery. Tinnitus is a rare manifestation of this vascular tumor.
Most acoustic neuromas cause nonpulsatile tinnitus (these are discussed in the section Imaging Strategies in Nonpulsatile Tinnitus). Very rarely, a patient with an acoustic neuroma or meningioma presents with pulsatile tinnitus (15). The mechanism is not understood.
Vascular Causes
Both intracranial and extracranial vascular abnormalities may cause pulsatile tinnitus that is objective as well as subjective. In addition, the patient may have an audible bruit or a palpable thrill (15).
Vascular malformations.—Abnormal communications between the arterial and venous systems may be congenital or acquired (15). Most extracranial arteriovenous malformations (AVMs) are apparent clinically, although imaging studies are helpful in delineating the extent of the abnormality. Brain parenchymal AVMs may be more obscure clinically, but are usually quite readily identified on contrast-enhanced CT and MR studies. Conventional angiography identifies arterial supply and venous drainage. CT angiography may also prove useful. Time-of-flight MR angiography complements spin-echo sequences. A full discussion of the imaging of AVMs is beyond the scope of this review.
A dural AVM or arteriovenous fistula (AVF) is a well-known cause of headache and hemorrhagic infarction (22). However, dural AVM or AVF is also the most frequent cause of objective pulsatile tinnitus in the patient with a normal otoscopic examination (23). The transverse, sigmoid, and cavernous sinuses are the most frequent locations of dural AVMs and AVFs (22); transverse and sigmoid sinus involvement causes pulsatile tinnitus (23). Branches of the external carotid artery supply these dural AVMs; venous drainage may be extracranial, intracranial, or both (11).
CT or MR studies may demonstrate a dilated dural venous sinus, unusually large or numerous cortical veins, or abnormal vessels in the soft tissues beneath the skull base (14,22,23) (Fig 4a). However, dural AVMs or AVFs are often invisible on CT and MR studies (11,18,22). A normal contrast-enhanced CT or MR study therefore does not exclude a dural AVM or AVF. Conventional angiography may be the only modality that shows the abnormality (18,22) (Fig 4b). When a patient has convincing history and physical findings and normal cross-sectional imaging studies, conventional angiography is an important diagnostic option.
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Figure 4a. Posterior fossa dural AVMs. (a) Transverse T1-weighted MR image (520/20, one signal acquired) in a patient with an angiographically proved posterior fossa dural AVM shows only a cluster of small vessels (arrows) in the left occipital subcutaneous soft tissues. This may be the only CT or MR finding of a dural AVM. (b) Lateral view of a common carotid arteriogram in another patient shows a dural AVM. Branches of the occipital artery (arrows) provide most of the blood supply.
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Figure 4b. Posterior fossa dural AVMs. (a) Transverse T1-weighted MR image (520/20, one signal acquired) in a patient with an angiographically proved posterior fossa dural AVM shows only a cluster of small vessels (arrows) in the left occipital subcutaneous soft tissues. This may be the only CT or MR finding of a dural AVM. (b) Lateral view of a common carotid arteriogram in another patient shows a dural AVM. Branches of the occipital artery (arrows) provide most of the blood supply.
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Congenital vascular anomalies.—An "aberrant" carotid artery is a congenital anomaly in which the cervical internal carotid artery never develops. Instead, the inferior tympanic artery (a branch of the ascending pharyngeal artery) enlarges, anastomoses with the caroticotympanic artery in the middle ear, and resumes the usual course of the internal carotid artery in the horizontal portion of the petrous carotid canal (24,25). Normally, the inferior tympanic artery passes through the skull base in its own minuscule canal, the inferior tympanic canaliculus, between the carotid canal and the jugular fossa (Fig 2a). The so-called aberrant carotid artery is, in fact, the markedly hypertrophied inferior tympanic artery. The inferior tympanic canaliculus, which enlarges to accommodate the artery, resembles the carotid canal in both size and location. The aberrant carotid artery may be dehiscent and visible to the clinician through the tympanic membrane, or may be covered by cortical bone so that the otoscopic examination is normal. An internal carotid artery that follows an otherwise normal course may also be dehiscent (25,26). The dehiscence allows the artery to herniate into the middle ear, where the otoscopist sees a pulsatile reddish mass in the anterior middle ear (26,27). A thin-section bone algorithm CT scan of the temporal bones and skull base shows the lateral course of an aberrant, dehiscent carotid artery through the middle ear (Fig 5). MR angiography and conventional angiography show the lateral course of the artery in both of these anomalies best on frontal and base views.
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Figure 5. Transverse thin-section CT scan (bone algorithm) shows an aberrant and dehiscent left internal carotid artery ( ). The artery swings laterally (arrow) into the middle ear, where it was visible with an otoscope through the normal tympanic membrane.
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Rarely, a persistent stapedial artery arises from an aberrant or even a normal internal carotid artery (25). The stapedial artery is a normal fetal artery that ordinarily regresses before birth. The persistent stapedial artery runs through the obturator foramen (the space between the crura of the stapes) and across the promontory in the middle ear, then leaves the middle ear to run along the tympanic portion of the facial nerve canal near the geniculate fossa, finally exiting the facial nerve canal to supply the territory of the middle meningeal artery (27,28). When the stapedial artery persists, the middle meningeal artery never develops, and neither does its opening in the skull base, the foramen spinosum (28). A frontal view of the arterial phase of conventional angiography shows the persistent stapedial artery. The artery may be too small to be resolved by current MR angiographic techniques. However, thin-section bone algorithm transverse CT scans show the soft tissue (artery) in the middle ear on the promontory, as well as the enlarged facial nerve canal. These CT scans also show absence of the foramen spinosum. When the identity of a middle ear mass is in question, absence of the foramen spinosum strongly suggests that the "mass" is a persistent stapedial artery.
A sigmoid sinus that swings farther laterally or anteriorly than normal is considered aberrant (27). The lateral course takes the sinus into the mastoid air cells. With medial displacement, which is more frequent, the sinus runs close to the posterior semicircular canal and endolymphatic sac (27). CT bone algorithms show this anatomy well. Phase-contrast MR venography in the sagittal and transverse planes also delineates the course of the sigmoid sinus, though not the relationship to the inner ear structures.
A dehiscent jugular vein lacks a complete cortical covering. As a result, the vein bulges into the middle ear from below (Fig 6). Otoscopy shows a bluish, pulsatile mass.
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Figure 6. Coronal CT scan (bone algorithm) shows a dehiscent jugular vein (white arrow) bulging into the middle ear through a discontinuity (black arrows) in the cortex of the jugular fossa.
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The jugular bulb is a normal structure; it is the dilated portion of the upper jugular vein, at the junction between the sigmoid sinus and the jugular vein (29). A jugular bulb is considered "high" or "high-riding" if it extends into the middle ear, above the level of the floor of the IAC (27) or tympanic annulus (15). A dehiscent high jugular bulb is visible at otoscopy as a smooth, convex, bluish mass, different from the pulsating reddish mass of a glomus tumor (27). It is sometimes impossible to differentiate venous anomalies clinically, so identifying the osseous anatomy on thin-section bone algorithm CT scans helps to make the diagnosis. On spin-echo MR images, the signal void of the internal jugular vein may be identical to the signal void of cortical bone and air in the mastoid air cells and middle ear. For these reasons, spin-echo MR is not our imaging study of choice and may even miss the anomaly altogether (30). MR angiograms will show most of these vascular anomalies, but thin-section bone algorithm CT scans demonstrate the anatomy most clearly.
A jugular diverticulum is a protrusion of the jugular bulb superior and medial to the jugular fossa (31). Although the diverticulum may be associated with tinnitus, it does not extend into the middle ear and cannot be seen at otoscopy.
The internal jugular veins may be very asymmetric; the right is usually the larger. Similar asymmetry of the transverse sinus is sometimes called "stenosis;" other authors use the term to refer to a focal narrowing of the transverse sinus (14), although the cause and importance of this finding on MR angiograms or conventional angiograms are not elucidated.
It is unclear why any of these structures cause pulsatile tinnitus, especially tinnitus of sudden onset (15). A vascular anomaly or asymmetry may, in fact, be an incidental observation identified in patients with other causes of pulsatile tinnitus (15), or in patients with no complaints of pulsatile tinnitus who undergo CT or MR imaging for other reasons. When one of these vascular anomalies is identified in a patient with pulsatile tinnitus, it is best to continue the search for another (treatable) cause of the patient’s symptom.
Other vascular abnormalities.—An aneurysm is a rare cause of pulsatile tinnitus (15,18,32). Intracranial aneurysms are far more frequent than a petrous carotid aneurysm. Atherosclerotic carotid artery disease (Fig 7) causes objective pulsatile tinnitus; the tinnitus is sometimes the first manifestation of atherosclerosis (32,33). Fibromuscular dysplasia of the internal carotid artery most frequently manifests with intracranial ischemia, but tinnitus is the next most frequent manifestation, and many patients have both (15,32). Contrast-enhanced CT or CT angiography shows atherosclerotic plaque. MR imaging or MR angiography shows narrowing of the vessel lumen depending on the size of the aneurysm, both contrast-enhanced CT or CT angiography and MR imaging or MR angiography are useful.
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Figure 7. Transverse contrast-enhanced CT scan shows calcified (solid arrow) atherosclerotic plaque at the bifurcation of the left common carotid artery, and noncalcified plaque (open arrow) that severely narrows the lumen of the right external carotid artery just above the bifurcation.
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Spontaneous dissection of the internal carotid artery most frequently causes pain, cerebral ischemia, Horner syndrome, or intracranial hemorrhage (34). Rarely, a dissection manifests with pulsatile tinnitus (32,34). This is one diagnosis that is difficult or impossible to make on conventional thin-section transverse contrast-enhanced CT scans of the skull base and temporal bones. If there is any concern that a carotid dissection is present, additional imaging studies are essential. Transverse T1-weighted MR images show the hyperintense methemoglobin in the false lumen surrounding the narrowed true lumen of the artery (Fig 8). Fat suppression makes the methemoglobin more conspicuous. MR angiography and CT angiography both demonstrate the narrowed true lumen of the artery. Conventional angiography is not necessary to make the diagnosis.
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Figure 8. Transverse T1-weighted MR image (525/25, one signal acquired) of a dissection of the left internal carotid artery shows hyperintense methemoglobin (black arrow) narrowing the patent lumen of the artery (white arrow). Compare the left internal carotid artery lumen to the lumen of the normal right internal carotid artery (c).
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Some investigators believe that a vessel that compresses the cochlear nerve in the IAC or the eighth cranial nerve at the brainstem root entry zone causes pulsatile tinnitus (13,35,36). These authors implicate "redundant arterial loops" (35), often the anterior inferior cerebellar artery (37) and veins (although usually the offending vessels are unnamed), and describe resolution or improvement of the tinnitus after microvascular decompression or even ligation of the eighth nerve (35,36). Other investigators believe the MR finding of a blood vessel in contact with the eighth cranial nerve is not necessarily pathologic (38). We have seen a vein or artery in close contact with the eighth cranial nerve in patients who are undergoing scanning for other reasons and have no complaints of tinnitus. Spin-echo pulse sequences can show vessels around the nerve in the cerebellopontine angle cistern (Fig 9a); gradient-echo sequences (Fig 9b) provide better detail of these small vessels.
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Figure 9a. Vascular loops adjacent to the eighth cranial nerve. (a) Transverse thin-section T2-weighted spin-echo MR image (4,000/90, four signals acquired) shows the anterior inferior cerebellar artery (open arrows) looping out into the IAC and displacing the nerves, which are seen faintly at the fundus (solid arrow) of the IAC. (b) Coronal reformattion spoiled gradient-recalled acquisition in the steady state, or SPGR, (50/2.4, 30° flip angle) gadolinium-enhanced MR image through the brainstem shows several blood vessels (short arrows) adjacent to the cisternal portions (long arrow) of the left seventh and eighth cranial nerves. It is not possible to determine which vessels these represent.
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Figure 9b. Vascular loops adjacent to the eighth cranial nerve. (a) Transverse thin-section T2-weighted spin-echo MR image (4,000/90, four signals acquired) shows the anterior inferior cerebellar artery (open arrows) looping out into the IAC and displacing the nerves, which are seen faintly at the fundus (solid arrow) of the IAC. (b) Coronal reformattion spoiled gradient-recalled acquisition in the steady state, or SPGR, (50/2.4, 30° flip angle) gadolinium-enhanced MR image through the brainstem shows several blood vessels (short arrows) adjacent to the cisternal portions (long arrow) of the left seventh and eighth cranial nerves. It is not possible to determine which vessels these represent.
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A venous hum is normally heard over both sides of the lower neck in infants and children (15), in approximately half the asymptomatic adult population (39), and in adults with a "hyperdynamic" state (such as the increased cardiac output of anemia and thyrotoxicosis) (15). Unilateral venous hum tinnitus ("cephalic bruit") is both subjective and objective pulsatile tinnitus that may result from turbulent flow in the internal jugular vein (39). Occasionally, an obstruction of the vein is identified as the cause. When a detailed CT or MR study of the temporal bone fails to disclose a cause of pulsatile tinnitus, it may be useful to image the neck and the superior mediastinum, to search for a mass compressing the internal jugular vein anywhere along its course. We have not found neck compression helpful in determining which study to order, or helpful during the course of the CT or MR examination. Most of the time, no radiologic cause for venous hum tinnitus is found (Fig 2c).
Otosclerosis is an osseous dysplasia of the inner ear that causes both sensorineural and conductive hearing loss, and sometimes also causes tinnitus (9,13). Abnormal foci of vascular haversian bone replace the normal endochondral layer of the otic capsule (40). Anastomoses between normal vessels, vessels in the otosclerotic bone, and mucosal vessels may contribute to the tinnitus (27). Inflammation may also be present (40). The hyperemic mucosa overlying the otosclerotic bone has a reddish color that can be seen at otoscopy (the Schwartze sign) (27).
A thin-section CT study (bone algorithm, 1-mm collimation, without administration of intravenous contrast material) best demonstrates otosclerosis. Overgrowth of abnormally hypoattenuating or sclerotic bone in the region of the fissula ante fenestram is the imaging manifestation of fenestral otosclerosis (Fig 10a), which causes conductive hearing loss by impeding normal movement of the stapes footplate in the oval window (24). Cochlear (retrofenestral) otosclerosis appears on a CT study as a hypoattenuating halo around the cochlea (Fig 10a). Less often, otosclerotic foci are radiopaque (sclerotic). T2-weighted MR studies can show a faint hyperintense focus near the fissula ante fenestram (40), but the abnormality is far more apparent on a CT study. Patients with Paget disease of the temporal bone also have pulsatile tinnitus (15,33). As in otosclerosis, intraosseous arteriovenous shunts may be responsible (15).
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Figure 10a. Osseous dysplasias. (a) Transverse CT scan (bone algorithm) in a patient with otosclerosis shows a hypoattenuating halo (black arrow) surrounding the cochlea (cochlear otosclerosis) and overgrowth of abnormal hypoattenuating bone at the fissula ante fenestram (white arrow) (fenestral otosclerosis). (b) Transverse CT scan (bone algorithm) in a different patient who had Paget disease of the skull base shows abnormal hypoattenuating bone (white arrows) encroaching on the normally sclerotic bone (black arrow) of the otic capsule.
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Figure 10b. Osseous dysplasias. (a) Transverse CT scan (bone algorithm) in a patient with otosclerosis shows a hypoattenuating halo (black arrow) surrounding the cochlea (cochlear otosclerosis) and overgrowth of abnormal hypoattenuating bone at the fissula ante fenestram (white arrow) (fenestral otosclerosis). (b) Transverse CT scan (bone algorithm) in a different patient who had Paget disease of the skull base shows abnormal hypoattenuating bone (white arrows) encroaching on the normally sclerotic bone (black arrow) of the otic capsule.
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Patients with benign intracranial hypertension (idiopathic intracranial hypertension) often present with headaches or visual disturbances (33,41). However, benign intracranial hypertension has been reported to be the most frequent diagnosis in patients with pulsatile tinnitus (33,42). An elevated opening pressure at lumbar puncture confirms the diagnosis. Imaging studies are usually normal and are useful to exclude other causes of increased intracranial pressure. Rarely, CT or MR imaging shows small (compressed) ventricles or an empty sella. Other causes of elevated intracranial pressure (aqueductal stenosis) may also be associated with pulsatile tinnitus (33). The precise cause of the tinnitus remains obscure.
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IMAGING STRATEGIES IN NONPULSATILE TINNITUS
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Nonpulsatile tinnitus is almost always subjective. The most important pathologic condition to consider in patients with nonpulsatile tinnitus is a tumor of the cerebellopontine angle cistern. Most of these are acoustic neuromas (more accurately, vestibular schwannomas) (24). Interestingly, tinnitus may persist and even worsen after successful removal of a vestibular schwannoma (13). This is presumed to reflect nerve damage during surgery and has also been reported after microvascular decompression surgery for trigeminal neuralgia and hemifacial spasm (13,36). The pathophysiology of the tinnitus in patients with vestibular schwannomas is not well understood. Compression of the cochlear nerve or of its arterial supply is known to cause sensorineural hearing loss and is presumably the cause of the tinnitus as well.
A gadolinium-enhanced MR study is the study of choice to identify (or exclude) a vestibular schwannoma or other neoplasm of the IAC or cerebellopontine angle cistern (Fig 11a). Thin-section T2-weighted images of the temporal bones and IACs may prove to be an acceptable screening test (43) (Fig 11b). A thin-section contrast-enhanced CT scan is a useful alternative in a patient who cannot or will not undergo an MR study (Fig 11c).
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Figure 11a. Vestibular schwannomas. (a) Transverse T1-weighted gadolinium-enhanced MR image (783/23, one signal acquired) shows a large tumor extending from the left IAC (arrow) into the cerebellopontine angle cistern. (Reprinted from reference 24.) (b) Transverse thin-section T2-weighted MR image (4,000/108, one signal acquired) shows a small, hypointense tumor (arrow) in the fundus of the left IAC. (c) Transverse thin-section contrast-enhanced CT scan (soft-tissue algorithm) shows an enhancing intracanalicular tumor (arrow) filling the left IAC . Compare this to the low attenuation of the normal contents of the right IAC.
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Figure 11b. Vestibular schwannomas. (a) Transverse T1-weighted gadolinium-enhanced MR image (783/23, one signal acquired) shows a large tumor extending from the left IAC (arrow) into the cerebellopontine angle cistern. (Reprinted from reference 24.) (b) Transverse thin-section T2-weighted MR image (4,000/108, one signal acquired) shows a small, hypointense tumor (arrow) in the fundus of the left IAC. (c) Transverse thin-section contrast-enhanced CT scan (soft-tissue algorithm) shows an enhancing intracanalicular tumor (arrow) filling the left IAC . Compare this to the low attenuation of the normal contents of the right IAC.
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Figure 11c. Vestibular schwannomas. (a) Transverse T1-weighted gadolinium-enhanced MR image (783/23, one signal acquired) shows a large tumor extending from the left IAC (arrow) into the cerebellopontine angle cistern. (Reprinted from reference 24.) (b) Transverse thin-section T2-weighted MR image (4,000/108, one signal acquired) shows a small, hypointense tumor (arrow) in the fundus of the left IAC. (c) Transverse thin-section contrast-enhanced CT scan (soft-tissue algorithm) shows an enhancing intracanalicular tumor (arrow) filling the left IAC . Compare this to the low attenuation of the normal contents of the right IAC.
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Muscular tinnitus (middle ear myoclonus and palatal myoclonus) produces clicking or snapping sounds that may vary with movement of the muscle. Muscular tinnitus is sometimes objective as well as subjective (8). Middle ear myoclonus is rapid, rhythmic contractions of the stapedius and tensor tympani muscles. We are unaware of any imaging findings. Palatal myoclonus is myoclonus of the tensor and levator veli palatini muscles, the tensor tympani, salpingopharyngeus, and the superior constrictor muscles. Cerebellar and brainstem diseases (multiple sclerosis, infarcts) cause palatal myoclonus (9), so an MR evaluation should include close inspection of these structures. Palatal myoclonus also occurs as an isolated abnormality that does not progress (8).
Patients with disorders of the temporomandibular joint complain of tinnitus more often than comparable subjects without temporomandibular joint problems (44,45). A satisfactory explanation has yet to be offered for this. Imaging studies may show internal derangement of the temporomandibular joint, but we are unaware of imaging demonstration of an objective explanation for the tinnitus in these patients. Jaw clenching may augment tinnitus (44). The tension in the pterygoid muscles may increase tension in the tensor tympani, possibly mediated by their common innervation, the mandibular division of the trigeminal nerve (44).
Multiple sclerosis may present with fluctuating sensorineural hearing loss, vertigo, and tinnitus (46). Rarely, an Arnold-Chiari malformation causes tinnitus, which some believe is the effect of "stretching" of the eighth nerve complex (24,46,47). Sagittal MR images readily show the low-lying cerebellar tonsils.
We are unaware of CT or MR abnormalities that would explain most of the other causes of nonpulsatile tinnitus. Tinnitus is a known complication of aspirin, other nonsteroidal antiinflammatory drugs (including ibuprofen and indomethacin), the aminoglycoside antibiotics, and loop diuretics, among others (7,13,44). Noise-induced hearing loss is often accompanied by tinnitus (7,13). Presbycusis, the hearing loss of aging, is sometimes less debilitating than the accompanying tinnitus (7,9). Tinnitus may develop after head or temporal bone trauma. Temporal bone surgery, particularly stapedectomy, has also been reported to cause tinnitus (7). Patients with Ménière disease experience vertigo, hearing loss, and tinnitus (13,46). An MR or CT study of the temporal bones and brain is often useful in these patients, to exclude another process, such as a vestibular schwannoma, that would be amenable to surgery or other therapy.
Finally, other conditions are reported to present with tinnitus, but the type is not specified. These include spontaneous intracranial hypotension (48) and endolymphatic sac tumors (49).
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RECOMMENDATIONS AND SUMMARY
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Pulsatile tinnitus suggests the presence of a vascular abnormality (a tumor, a congenital anomaly, a malformation, or an acquired vasculopathy). For patients with objective pulsatile tinnitus, our preferred imaging study is contrast-enhanced CT of the temporal bone (1-mm collimation with no intersection gap) and of the brain and scalp (transverse images 3–5 mm thick) (Fig 12). Often, the CT study is normal. Clinical concern can then determine further work-up (if any). Occasionally, contrast-enhanced CT scans of the neck and superior mediastinum disclose an abnormality that explains the symptom. If there is the serious consideration of a dural vascular malformation, conventional angiography may be indicated, as this is often the only study to demonstrate a dural AVM. If a dissecting carotid aneurysm is a possibility, transverse T1-weighted MR images of the neck or CT angiography or MR angiography is essential. For patients with subjective pulsatile tinnitus, we obtain the same contrast-enhanced CT scan of the temporal bones and brain as we do for objective tinnitus (Fig 12). Patients with only subjective pulsatile tinnitus usually have no imaging abnormalities. Patients with life-threatening allergies to contrast material or other contraindications to contrast-enhanced CT can undergo contrast-enhanced MR imaging instead (Fig 12). Nonpulsatile tinnitus suggests the presence of a cerebellopontine angle tumor, most often a vestibular schwannoma. Gadolinium-enhanced MR imaging (with thin transverse and coronal T1- and T2-weighted images through the temporal bones, and transverse images through the entire brain) is the study of choice. Thin-section contrast-enhanced CT of the temporal bones and brain is an acceptable alternative for patients unable or unwilling to undergo MR imaging (Fig 12).
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Figure 12. Decision tree for the imaging of tinnitus. CT(1) = Technique: Contrast-enhanced, bone and soft-tissue algorithms for all images; 1-mm transverse sections (with or without coronal sections) through the temporal bones and skull base; 3-5-mm transverse sections through the brain, calvaria, and overlying soft tissues. Interpretation: special attention to middle ear (mass), jugular fossa (erosion), petrous carotid canal (course), foramen spinosum (absent), posterior fossa and scalp (abnormal blood vessels). MR(1) = Technique: contiguous (0.7 mm) or overlapping (up to 3 mm), thin-section T2-weighted transverse images and gadolinium-enhanced T1-weighted transverse and coronal images through the temporal bones and skull base; transverse images through the brain. Interpretation: special attention to the IACs (mass, enhancement), cerebellopontine angle cisterns (mass), brainstem. CT(1) is an acceptable alternative study. CT(2) = Technique: contrast-enhanced, 3-5-mm transverse sections through the neck and superior mediastinum. Interpretation: special attention to the course of the internal jugular veins and superior vena cava (compressing mass) and internal carotid arteries (narrowing, dissection, aneurysm).
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ACKNOWLEDGMENTS
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We are grateful to Sabrina Jennings, who skillfully and patiently prepared the manuscript, and to Jonathan Lang for technical assistance with Figure 12.
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FOOTNOTES
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Abbreviations: AVF = arteriovenous fistula,
AVM = arteriovenous malformation,
IAC = internal auditory canal
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ABSTRACT
INTRODUCTION
