DOI: 10.1148/rg.235025046
(Radiographics. 2003;23:1185-1200.)
© RSNA, 2003
Pediatric and Adult Cochlear Implantation1
Robert J. Witte, MD,
John I. Lane, MD,
Colin L. W. Driscoll, MD,
Larry B. Lundy, MD,
Matt A. Bernstein, PhD,
Amy L. Kotsenas, MD and
Armen Kocharian, PhD
1 From the Departments of Radiology (R.J.W., J.I.L., M.A.B., A.K.) and Otolaryngology (C.L.W.D.), Mayo Clinic, 200 First Street SW, Rochester, MN 55905; and the Departments of Otolaryngology (L.B.L.) and Radiology (A.L.K.), Mayo Clinic, Jacksonville, Fla. Recipient of a Certificate of Merit award for an education exhibit at the 2001 RSNA scientific assembly. Received March 5, 2002; revision requested April 24; final revision received February 13, 2003; accepted February 19. Address correspondence to R.J.W. (e-mail: witte.robert@mayo.edu).
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Abstract
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The frequency of cochlear implantation has increased tremendously over the past decade. Cochlear implantation is often performed as an outpatient procedure and is considered an acceptable treatment for severe to profound sensorineural hearing loss in patients who are refractory to conventional hearing augmentation. Imaging plays an important part in the work-up of cochlear implant candidates, and an understanding of imaging evaluation procedures is essential. The radiologist must be familiar with imaging findings that contraindicate implantation (absence of the cochlea or cochlear nerve) and with those that could significantly alter surgery (facial nerve dehiscence, cochlear ossification). It is also imperative to be familiar with the growing number of imaging options (particularly magnetic resonance [MR] imaging pulse sequences) to optimize evaluation of cochlear implant candidates. Imaging choices will be substantially influenced by the manufacturer of the computed tomographic scanner or MR imager. Radiologists will assume an expanding role in evaluating affected patients as the frequency of cochlear implantation continues to increase.
© RSNA, 2003
Index Terms: Ear, CT, 21.1211 • Ear, inflammation and infection, 21.26, 2133.872 • Ear, MR, 21.1214 • Ear, prostheses, 2133.456 • Hearing loss Surgery, complications, 21.458
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Describe the components and unique function of a cochlear implant.
- Discuss the various MR imaging options that are available for cochlear implant candidates.
- Identify the radiologic findings that contraindicate cochlear implantation and those that will likely alter surgery.
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Introduction
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More than 28 million Americans had some degree of hearing impairment in 1993 (1). Cochlear implantation has become an accepted treatment for severe to profound deafness in patients who derive only minimal benefit from conventional amplification. As the number of centers performing cochlear implantation grows, an increasing number of radiologists will encounter imaging requests as part of a cochlear implant evaluation. It is important to be familiar with the various available imaging options and with findings that could significantly impact or even preclude implantation.
In this article, we discuss and illustrate various hearing augmentation devices, surgical technique and complications in cochlear implantation, contraindications for cochlear implantation, clinical and imaging evaluation of cochlear implant candidates, and important radiologic findings in these patients.
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Hearing Augmentation Devices
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There are three devices available for hearing augmentation: a hearing aid, a cochlear implant, and an auditory brainstem implant (ABI). A hearing aid functions as an amplifier by magnifying received acoustic signals. Once magnified, the acoustic signal travels along the auditory pathway normally (Fig 1). If potential augmentable hearing is present, a conventional hearing aid is the initial device of choice. The greatest limitation of a hearing aid is not technologic; rather, it relates to the number of surviving functional cochlear hair cells. If only a small percentage of the cochlear hair cells are viable, their stimulation by amplification of the sound signal cannot completely compensate for the hearing loss caused by the nonfunctional hair cells.
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Figure 1. Drawing illustrates hearing aid function. Sound waves are amplified by the hearing aid (1). The tympanic membrane and ossicles convert the sound waves into mechanical energy (2). Pressure waves generated in the perilymphatic fluid pass from the scala vestibuli to the scala tympani (3). The hair cells in the organ of Corti convert this mechanical-pressure energy into an electrical impulse (4). The impulse travels through the spiral ganglia to the ventral and dorsal cochlear nuclei, located in the lateral brainstem adjacent to the foramen of Luschka (5). Crossed and uncrossed fibers carry the impulse through the lateral lemniscus, inferior colliculus, and medial geniculate body, and finally to the auditory cortex of the Heschl transverse temporal gyri (6).
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A cochlear implant differs from a hearing aid in that the auditory signal–sound wave received by the device is processed (not just amplified) and converted into an electrical impulse (2). Cochlear implants are intended for patients with severe to profound sensorineural hearing loss. Sound and speech are captured by a microphone worn behind the ear and sent to a speech processor, which may be incorporated with the microphone behind the ear or worn remotely. The speech processor digitally encodes the speech with use of various encoding strategies, depending on the manufacturer and model of the implant. It then sends the encoded signal to a transmitter. The transmitter is located behind the ear and overlies the implanted stimulator, being held in place by a magnet attached to the implanted stimulator. The transmitter then sends the signal transcutaneously to the implanted stimulator, which in turn directly stimulates the spiral ganglion cells and axons of the cochlea by means of an electrode array implanted in the basal turn. This process bypasses the severely degenerated hair cells in the organ of Corti. The impulse then travels normally along the remainder of the auditory pathway (Figs 2, 3).
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Figure 2. Drawings illustrate cochlear implant function. The microphone receives the sound (1). The sound is sent to the speech processor, which analyzes and digitizes the sound into coded signals (2). The coded signals are sent to the transmitter, which sends the code across the skin to the internal implant (3). The implant converts the code into electrical signals (4). The signals are sent to the electrodes to stimulate the nondegenerated cochlear nerve spiral ganglia-axons (5). The electrical impulse travels normally along the remaining auditory pathway (6).
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Figure 3. Drawing illustrates a cochlear implant. E = stimulator electrode array, G = ground electrode, M = magnet (which "binds" transcutaneously to the transmitter), R = receiver-stimulator. A U.S. quarter is shown for size comparison.
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An ABI is similar to a cochlear implant in the way it receives and processes sound. It differs from a cochlear implant in that an electrical impulse is sent directly to the cochlear nuclei in the brainstem, bypassing the organ of Corti and the cochlear nerve. The flat rectangular shape of the stimulating array facilitates placement in the foramen of Luschka. The impulse then travels normally along the remainder of the auditory pathway (Fig 4). An ABI is currently indicated for neurofibromatosis type 2 patients with deafness following removal of bilateral vestibular schwannomas.
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Figure 4. Drawings illustrate ABI function. The microphone receives the sound (1). The sound is sent to the speech processor, which analyzes and digitizes the sound into coded signals (2). The coded signals are sent to the transmitter, which sends the code across the skin to the internal implant (3). The implant converts the code into electrical signals (4). The signals are sent to electrodes to stimulate the cochlear nuclei in the brainstem (5). The electrical impulse travels normally along the remaining auditory pathway (6).
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Surgical Technique
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The U.S. Food and Drug Administration has approved cochlear implants for children as young as 12 months old. Implants have also been successfully placed in adults in their 90s. Cochlear implantation usually takes about 2 hours and is often performed on an outpatient basis, although an overnight stay is occasionally required. The risks and recovery are similar to those associated with other common otologic procedures performed for cholesteatoma or chronic otitis media. Because of its proximity, the facial nerve is monitored intraoperatively by most surgeons.
Most clinicians currently favor placing the implant in the better hearing ear. Experience has yielded improved results, likely reflecting more surviving neural elements available for implant stimulation. There are always exceptions, particularly in patients who are extremely anxious about "saving" their better hearing ear.
The compact size of the implant allows it to fit nicely behind the ear. A skin flap incision is made behind the ear (Fig 5a). After an intact canal wall mastoidectomy is performed, a recess is created in the skull posterior and superior to the mastoidectomy for placement of the internal receiver-stimulator. The facial recess is opened, and a cochleostomy is created by drilling anteriorly from the round window into the basal turn of the cochlea (Fig 5b). An introducer is used to implant the electrode array in the cochlea (Fig 5c).
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Figure 5. Drawings illustrate surgical technique. In A, a skin flap incision is made behind the ear. In B, after an intact canal wall mastoidectomy is performed, the facial recess is opened. A cochleostomy is then created by drilling anteriorly (arrow) from the round window into the basal turn of the cochlea. A = antrum, C = chorda tympani, F = facial nerve, HSC = horizontal semicircular canal, I = incus, R = round window, S = stapes. In C, an electrode array is placed (arrow) in the cochlea with an introducer.
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Contraindications for Cochlear Implantation
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The absolute requirements for cochlear implantation are the presence of a cochlea (either normal or malformed) and of a cochlear nerve. Cochlear aplasia is readily apparent at computed tomography (CT) or MR imaging (Fig 6).
Absence of the cochlear nerve is best seen on oblique sagittal MR images obtained through the internal auditory canal (IAC) (Figs 7, 8). The embryologic development of the inner ear is complex (3,4). The independent development of the organ of Corti and cochlear nerve explains how a normal-appearing (or nearly so) cochlea does not ensure the presence of a normal cochlear nerve (Fig 9).
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Figure 7. Sequential 3D oblique sagittal constructive interference in the steady state (CISS) images of the lateral (top left) to middle (bottom right) IAC show the cochlear nerve (C) in the anteroinferior canal to be similar in size to the facial nerve (F). The closely approximated superior and inferior vestibular nerves (VN) are seen in the posterior canal.
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Figure 8a. Absence of the cochlear nerve. (a) On a sagittal two-dimensional (2D) fast spin-echo MR image of the right IAC, the cochlear nerve is absent. Arrow indicates its expected location. (b) Coronal CT scan demonstrates a severely dysplastic cochlea (arrow).
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Figure 8b. Absence of the cochlear nerve. (a) On a sagittal two-dimensional (2D) fast spin-echo MR image of the right IAC, the cochlear nerve is absent. Arrow indicates its expected location. (b) Coronal CT scan demonstrates a severely dysplastic cochlea (arrow).
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Figure 9a. Absent and hypoplastic cochlear nerves. (a) Axial 3D CISS image shows a severely atretic right IAC with only a sliver of signal intensity (arrow). The cochlear nerve cannot be identified. B = adjacent basal cochlear turn. (b) Adjacent image shows the middle cochlear turn (M). (c) On a maximum-intensity-projection (MIP) image of the left inner ear, the left IAC (I) is narrowed. The cochlea (C) is unremarkable. (d) Sagittal 3D CISS image depicts a hypoplastic left cochlear nerve (C).
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Figure 9b. Absent and hypoplastic cochlear nerves. (a) Axial 3D CISS image shows a severely atretic right IAC with only a sliver of signal intensity (arrow). The cochlear nerve cannot be identified. B = adjacent basal cochlear turn. (b) Adjacent image shows the middle cochlear turn (M). (c) On a maximum-intensity-projection (MIP) image of the left inner ear, the left IAC (I) is narrowed. The cochlea (C) is unremarkable. (d) Sagittal 3D CISS image depicts a hypoplastic left cochlear nerve (C).
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Figure 9c. Absent and hypoplastic cochlear nerves. (a) Axial 3D CISS image shows a severely atretic right IAC with only a sliver of signal intensity (arrow). The cochlear nerve cannot be identified. B = adjacent basal cochlear turn. (b) Adjacent image shows the middle cochlear turn (M). (c) On a maximum-intensity-projection (MIP) image of the left inner ear, the left IAC (I) is narrowed. The cochlea (C) is unremarkable. (d) Sagittal 3D CISS image depicts a hypoplastic left cochlear nerve (C).
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Figure 9d. Absent and hypoplastic cochlear nerves. (a) Axial 3D CISS image shows a severely atretic right IAC with only a sliver of signal intensity (arrow). The cochlear nerve cannot be identified. B = adjacent basal cochlear turn. (b) Adjacent image shows the middle cochlear turn (M). (c) On a maximum-intensity-projection (MIP) image of the left inner ear, the left IAC (I) is narrowed. The cochlea (C) is unremarkable. (d) Sagittal 3D CISS image depicts a hypoplastic left cochlear nerve (C).
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Cochlear Dysplasia
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Cochlear dysplasias (ie, Mondini dysplasias) do not contraindicate cochlear implantation (Fig 10). Although no correlative studies have been performed, cochlear implantation is expected to provide some clinical benefit regardless of the degree of dysplasia.
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Figure 10a. Cochlear dysplasia. (a) Axial CT scan of the left temporal bone shows incomplete partition (Mondini dysplasia) of the middle and apical cochlear turns (arrow). (b) Axial CT scan of the right temporal bone shows more severe cochlear dysplasia (black arrow) with associated vestibular and semicircular canal anomalies (white arrow). (c) Axial CT scan demonstrates a cochlea with a normal middle and apical turn (arrow) for comparison.
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Figure 10b. Cochlear dysplasia. (a) Axial CT scan of the left temporal bone shows incomplete partition (Mondini dysplasia) of the middle and apical cochlear turns (arrow). (b) Axial CT scan of the right temporal bone shows more severe cochlear dysplasia (black arrow) with associated vestibular and semicircular canal anomalies (white arrow). (c) Axial CT scan demonstrates a cochlea with a normal middle and apical turn (arrow) for comparison.
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Figure 10c. Cochlear dysplasia. (a) Axial CT scan of the left temporal bone shows incomplete partition (Mondini dysplasia) of the middle and apical cochlear turns (arrow). (b) Axial CT scan of the right temporal bone shows more severe cochlear dysplasia (black arrow) with associated vestibular and semicircular canal anomalies (white arrow). (c) Axial CT scan demonstrates a cochlea with a normal middle and apical turn (arrow) for comparison.
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Surgical Complications
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Complications from implantation of newer model cochlear implants occur in less than 1% of adults and children (5). Many such complications are related to the scalp flap (infection, necrosis, thickening). Tinnitus and vertigo may occur but usually resolve spontaneously. Facial nerve stimulation can rarely occur following an aggressive cochleostomy and electrode extrusion through the cochlear wall (Fig 11). Migration of the electrode array is very uncommon but can lead to mechanical malfunction. Comparison of follow-up radiographs with prior postoperative studies can allow detection of retraction or of change in the position of the electrode. Figure 12 demonstrates the normal position of the electrode array.
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Figure 11. Electrode extrusion through the cochlear wall. Slightly off-axis axial reformatted CT scan of an extruded electrode array shows the stimulator electrode (E) protruding through the basal cochlear turn (B).
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Clinical Evaluation
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A complete review of hearing history is the first step in evaluating a cochlear implant candidate. When did hearing loss begin? Has hearing loss been gradual, or have there been sudden drops or fluctuations? Did both ears progress together? When did the patient begin wearing hearing aids? Is there a family history of hearing loss? Has there been excessive noise exposure or ototoxic medication?
Patients then undergo a series of hearing tests and must demonstrate certain levels of hearing loss to qualify for a cochlear implant. Because of improvements in hearing augmentation devices, these levels continue to increase. A complete neurotologic and head and neck examination is also performed. Particular attention is paid to evidence of subtle otologic malformations and syndromic features. Most commonly, the examination findings are normal. Laboratory testing varies considerably depending on the clinical picture. A patient with rapidly progressive bilateral fluctuating hearing loss will undergo a battery of tests to assess for autoimmune or inflammatory disorders. An elderly patient with an extensive history of noise exposure doesn’t necessarily need to undergo any tests other than imaging. Most patients who receive implants have hearing loss due to genetic factors (familial hearing loss, syndromic and nonsyndromic deafness), noise exposure, or infectious and inflammatory diseases.
The goal of clinical and imaging evaluation is to select those patients who will benefit the most from implantation. The expected degree of success will depend on the clinical situation. Most cognitively healthy children can be expected to be "mainstreamed" into elementary school (without special classes or interpreters) if they receive an implant by 2–3 years of age. This disposition is also dependent on optimal speech and language therapy and on supportive, motivated parents or caregivers. After age 5 years, it is much more difficult for implantation to allow pure, fluent oral communication. However, significant benefit is still gained, such as the ability to hear alarms or sirens. These differences likely result from auditory deprivation, resulting in auditory neuronal atrophy. Adults who lose normal hearing do very well following implantation because they have a lifetime of auditory memory to call upon when the auditory system is stimulated. They can expect to use a standard telephone and pure hearing, with no lip reading.
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Imaging Evaluation
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Computed Tomography
CT has been the predominant imaging modality for evaluation of the temporal bone and has previously been the primary modality for evaluation of cochlear implant candidates. However, with the emergence of high-resolution MR imaging of the temporal bone, the role of CT in work-up is continually being reevaluated (6). Nevertheless, useful and unique information can still be obtained with CT, particularly in pediatric implant candidates (7,8).
CT technique generally consists of thin-collimation (
1 mm) scanning performed contiguously or with a 0.5–1-mm overlap. Raw data can be retrospectively processed with a sharp bone algorithm. Scanning time is substantially reduced in helical CT, offering an advantage in nonsedated pediatric patients. Image reformation allows coronal imaging in adult patients who are unable to attain adequate neck hyperextension for direct coronal imaging. Helical CT can be performed at submillimeter (0.5-mm) increments with a 0.5-mm overlap (9).
MR Imaging
Recent advances in MR imaging technology have added to the importance of this modality in the evaluation of cochlear implant candidates. Although these advances are welcome, the imaging choices have become more complicated. There are a number of coil and pulse sequence options available for imaging of the temporal bone. Each option has advantages and disadvantages, depending on the manufacturer of the imaging system.
A standard birdcage head coil is the standard multipurpose coil used for head imaging. It is very versatile, providing an acceptable signal-to-noise (S/N) ratio and homogeneity throughout the superficial and deep imaging volume. With its "sweet spot," a surface coil provides a considerably better S/N ratio than does a birdcage coil. The depth of penetration of a surface coil depends on the diameter of the coil, and deeper structures are not as well seen as with the birdcage coil. The temporomandibular joint coil is an example of a surface coil that is commonly used for temporal bone imaging. The recent development of hybrid phased-array coils and integrated phased-array imaging systems has allowed simultaneous data acquisition with custom-designed surface coils and the vendor head coil (10). The improved superficial S/N ratio of the surface coils (although it can be slightly less than that attainable with surface-coil-only imaging) allows higher-resolution cochlear imaging while maintaining the improved S/N ratio of the head coil for deeper structures.
Imaging of the temporal bone for potential cochlear implantation is best performed with T2-weighted sequences, which provide optimal contrast between nerves and cerebrospinal fluid (CSF) and between the membranous and bony labyrinth. Two-dimensional rapid acquisition with refocused echoes sequences (2D fast spin-echo imaging) or 2D turbo spin-echo imaging provides the desired contrast, but resolution is limited to approximately 1–2 mm per section. The intrinsic contiguous-section feature and superior S/N ratio of three-dimensional (3D) sequences permit improved resolution with an achievable section thickness of 1 mm or less, resulting in better visualization and evaluation of the IAC and inner ear.
The 3D fast-recovery fast spin-echo pulse sequence (11,12) makes use of a negative 90° pulse at the end of the echo train, so that bright fluid signal intensity can be achieved with a repetition time of 2 seconds or less. Drawbacks include blurring from T2 decay during the echo train and generally lower S/N unit acquisition time compared with gradient-echo methods. CISS (13) is a 3D gradient-echo pulse sequence that allows reduced sensitivity to susceptibility changes and flow while retaining the bright fluid signal intensity achievable with true fast imaging with steady-state precession (FISP). (As implemented on our General Electric (Milwaukee, Wisc) scanner, CISS is called "fast imaging employing steady-state acquisition with phase cycling," or FIESTA-C.) The CISS pulse sequences can be used to acquire two complete steady-state free precession data sets with differing phase cycling schemes. Care must be taken to ensure that the patient does not move, or misregistration can occur when the sets are recombined. Three-dimensional true-FISP (14) is a gradient-echo pulse sequence in which the net gradient areas are zero during any repetition time interval. Consequently, the S+ (FID-like) and S- (echo-like) steady-state signals refocus at the same time. Advantages of true-FISP include excellent S/N efficiency. Drawbacks include banding artifacts in the presence of susceptibility changes. Reducing the repetition time can minimize these artifacts, as does using the phase cycling of CISS. The implementation of 3D true-FISP on our General Electric scanner is called 3D FIESTA.
No matter which pulse sequence is chosen, the thinner sections of a 3D data set allow optimal multiplanar reformatting (Fig 13). Better image resolution of the nerves can be achieved with oblique sagittal imaging perpendicular to the plane of the IAC (Fig 7). The cochlea can be further evaluated by generating MIP images. The process is the same as that used in MR angiography, except the inner ear is targeted in the reformatting process (Fig 14).
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Figure 14. On an MIP image of the left inner ear generated from a 3D CISS data set, the cochlear turns and scalar chambers are readily discerned. A = apical turn, B = basal turn, M = middle turn, S = semicircular canal, V = vestibule.
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Important Imaging Findings
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In addition to cochlea–cochlear nerve aplasia and dysplasia (discussed earlier), other imaging findings can also impact surgery.
Otomastoiditis
Acute otitis media is treated prior to implantation to avoid potential labyrinthitis or meningitis. Treatment may involve placement of tympanostomy tubes. Isolated mastoid air cell opacification from chronic mastoiditis may not require treatment prior to implantation. If signs and symptoms of inflammation are present (Fig 15a), an intact canal wall mastoidectomy may be performed prior to implantation. Dense mastoid sclerosis (Fig 15b) can potentially complicate the creation of the implant well-reservoir and limit exposure to the middle ear. If the changes are asymmetric, the aerated side may be chosen for implantation.
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Figure 15a. Otomastoiditis. (a) Axial CT scan demonstrates increased attenuation of the mastoid process (black arrows) and middle ear (white arrow). (b) Axial CT scan demonstrates dense mastoid sclerosis (arrows).
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Figure 15b. Otomastoiditis. (a) Axial CT scan demonstrates increased attenuation of the mastoid process (black arrows) and middle ear (white arrow). (b) Axial CT scan demonstrates dense mastoid sclerosis (arrows).
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Labyrinthitis
Sensorineural hearing loss can result from meningitis, with subsequent labyrinthine fibrosis and eventual ossification (Figs 16, 17). Cochlear ossification with luminal obstruction is not a contraindication for implantation but is important to identify preoperatively. Cochlear ossification makes the cochleostomy more challenging and often results in choosing an implant with a shorter electrode array. MR imaging is superior to CT in assessing the presence or absence of fibrosis within the cochlea.
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Figure 16a. Labyrinthitis. (a) Axial 3D fast-recovery fast spin-echo image demonstrates replacement of the normally bright endolymphatic signal intensity of the basal turn of the cochlea (arrow). (b) On an axial contrast material-enhanced T1-weighted MR image, the basal turn of the cochlea demonstrates enhancement (arrow).
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Figure 16b. Labyrinthitis. (a) Axial 3D fast-recovery fast spin-echo image demonstrates replacement of the normally bright endolymphatic signal intensity of the basal turn of the cochlea (arrow). (b) On an axial contrast material-enhanced T1-weighted MR image, the basal turn of the cochlea demonstrates enhancement (arrow).
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Facial Nerve Dehiscence and Otosclerosis
Facial nerve compromise or paralysis resulting from cochlear implantation is rare. Recognizing facial nerve dehiscence or an atypical course preoperatively can help prevent this complication. Facial nerve dehiscence is readily apparent at CT (Fig 18).
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Figure 18. Facial nerve dehiscence. Coronal CT scan demonstrates a dehiscent left facial nerve (arrow), which is at risk for injury during cochleostomy performed prior to electrode array implantation.
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Retrofenestral otosclerosis is not a contraindication for cochlear implantation. However, facial nerve stimulation following transplantation is more common in patients with otosclerosis and is likely related to conduction of current through otospongiotic bone (Fig 19) (15). This problem is usually corrected by programming out the electrodes causing the stimulation.
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Figure 19. Bilateral retrofenestral otosclerosis in a 60-year-old patient. Axial CT scan of the right temporal bone demonstrates the typical osteopenic appearance of the bony labyrinth in retrofenestral otosclerosis (arrows). Such a finding does not preclude implantation.
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Sagittal T2-weighted MR images are essential in evaluating toddlers or older pediatric patients with hearing loss and facial nerve paralysis. Although rare, an absent facial nerve (Fig 20) can be differentiated from an absent cochlear nerve (Fig 8) and would not prevent implantation on the affected side.
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Figure 20a. Absent right facial nerve in a 3-year-old cochlear implant candidate with bilateral sensorineural hearing loss and right facial paralysis. (a) On a sagittal 3D fast spin-echo MR image of the right IAC, the right facial nerve is absent (F). Although sensorineural hearing loss was most severe on the right side, the cochlear nerve (C), albeit small, is present. VN = vestibular nerve. (b) Sagittal 3D fast spin-echo MR image demonstrates a normal left IAC. C = cochlear nerve, F = left facial nerve, VN = vestibular nerve.
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Figure 20b. Absent right facial nerve in a 3-year-old cochlear implant candidate with bilateral sensorineural hearing loss and right facial paralysis. (a) On a sagittal 3D fast spin-echo MR image of the right IAC, the right facial nerve is absent (F). Although sensorineural hearing loss was most severe on the right side, the cochlear nerve (C), albeit small, is present. VN = vestibular nerve. (b) Sagittal 3D fast spin-echo MR image demonstrates a normal left IAC. C = cochlear nerve, F = left facial nerve, VN = vestibular nerve.
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Enlarged Endolymphatic Duct and Sac
Meningitis following implantation is very rare and is likely caused by a CSF leak. Preoperative imaging can be used to identify patients in whom a potential intraoperative CSF leak ("gusher") may be encountered. For example, in sensorineural hearing loss associated with an enlarged endolymphatic duct and sac, the dilated sac is seen at MR imaging (Fig 21), whereas CT readily depicts the enlarged vestibular aqueduct (Fig 22). The relationship of an enlarged cochlear duct to the CSF-perilymph gusher phenomenon is less certain (16). The risk of a CSF gusher is also significantly increased in the presence of a bulbous, dilated distal IAC, often associated with absence of the bone partition that separates the distal canal and the base of the cochlea (17–19). The potential for a gusher to occur during cochleostomy does not preclude implantation. It is important to identify the anomaly preoperatively because the leak is readily treated with packing of the fascia and soft tissue around the electrode array at cochleostomy.
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Figure 21a. Enlarged endolymphatic sac. (a) Axial 3D fast-recovery fast spin-echo MR image shows an enlarged left endolymphatic sac (arrow). (b) Surface-rendered reformatted image generated from the same data set also shows the enlarged sac (arrows).
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Figure 21b. Enlarged endolymphatic sac. (a) Axial 3D fast-recovery fast spin-echo MR image shows an enlarged left endolymphatic sac (arrow). (b) Surface-rendered reformatted image generated from the same data set also shows the enlarged sac (arrows).
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Figure 22a. (a) Dilated vestibular aqueduct in a patient with bilateral sensorineural hearing loss (worse on the right side). Axial CT scan of the right temporal bone shows a dilated vestibular aqueduct (white arrow). The diameter of the duct is greater than that of the adjacent posterior semicircular canal (black arrow). (b) Axial CT scan obtained in a different patient demonstrates a normal-sized vestibular aqueduct (white arrow). The posterior semicircular canal (black arrow) is shown for comparison.
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Figure 22b. (a) Dilated vestibular aqueduct in a patient with bilateral sensorineural hearing loss (worse on the right side). Axial CT scan of the right temporal bone shows a dilated vestibular aqueduct (white arrow). The diameter of the duct is greater than that of the adjacent posterior semicircular canal (black arrow). (b) Axial CT scan obtained in a different patient demonstrates a normal-sized vestibular aqueduct (white arrow). The posterior semicircular canal (black arrow) is shown for comparison.
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Vascular Conditions
Abnormal middle ear vascular anatomy could potentially complicate mastoidectomy and cochleostomy. Anomalies such as a high-riding jugular bulb and an aberrant carotid artery are often apparent clinically and are easily confirmed with MR imaging or CT (Fig 23).
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Figure 23. Aberrant carotid artery. On a coronal CT scan of the right temporal bone, the right internal carotid artery (arrow) has an aberrant course and overlies the cochlear promontory.
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Other Imaging Findings
Various unusual and unsuspected causes of sensorineural loss may be encountered during imag-ing evaluation. Implantation should not be performed on the ipsilateral side in a patient with a brainstem infarct involving the cochlear nuclei that leads to unilateral sensorineural hearing loss (Fig 24). Hemosiderosis from previous subarachnoid hemorrhage can cause cranial neuropathies including sensorineural hearing loss (Fig 25). Although such hemosiderosis is not a contraindication for cochlear implantation, the degree of hearing recovery in this setting is not known.
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Figure 24a. Brainstem infarct resulting in profound sensorineural hearing loss. (a) Axial T2-weighted MR image shows an unsuspected infarct of the left pons and brachium pontis (arrow). (b) More inferior axial T2-weighted MR image shows atrophy of the left medulla at the level of the eighth nerve nuclei (arrow).
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Figure 24b. Brainstem infarct resulting in profound sensorineural hearing loss. (a) Axial T2-weighted MR image shows an unsuspected infarct of the left pons and brachium pontis (arrow). (b) More inferior axial T2-weighted MR image shows atrophy of the left medulla at the level of the eighth nerve nuclei (arrow).
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Figure 25. Hemosiderosis in a patient whose primary presenting symptom was bilateral sensorineural hearing loss, although other cranial neuropathies were also present. Axial gradient-echo MR image accentuates dark hemosiderin deposits that line the brainstem and adjacent cisterns (arrows).
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MR Imaging Safety in Cochlear Implantation
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Until recently, patients with cochlear implants were unable to undergo MR imaging at field strengths of 1.5 T or higher. Ferromagnetic materials in the implant, and the magnet used to "anchor" the transmitter transcutaneously to the implanted receiver-stimulator, were both incompatible with the MR imaging environment. Companies have begun to manufacture MR imaging–compatible implants without ferromagnetic materials and with magnets that can be surgically removed prior to imaging. The microphone, speech processor, and transmitter are also removed before the patient is p
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Abstract
LEARNING OBJECTIVES
