Inner Ear Anatomy and Cochlear Implantation: Morphological Observations Relevant to Implant Trauma
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Our work has focused on use of temporal bone microdissection for evaluation of cochlear implant electrode arrays and for anatomical study of those parts of the cochlea that are vulnerable to trauma during electrode insertion (1–4). The microdissection technique is an effective approach for study of human cochlear and vestibular anatomy and is well suited for evaluation of the insertional properties of cochlear implant electrodes (1, 5, 6). The microdissection method was in fact used in the earliest postmortem studies of temporal bones from cochlear implant recipients (7) and continues to be employed in studies on electrode arrays and inner ear trauma associated with electrode insertion (2–4). Details of the dissection procedure have been described in previous publications (1, 8). In brief, tissues of the membranous labyrinth are stained with osmium after which the otic capsule bone is drilled to a thin shell and then opened in a manner that permits direct observation of the three-dimensional anatomy of the cochlea as illustrated in Figures 1, 2, 3, 4, 5, 6, 7.
Either before or after the dissection procedure, implant electrode arrays may be inserted into the cochlea using surgical approaches that approximate those employed in living patients. As shown in Figures 8, 9, 10, 11, these preparations permit evaluation of the positioning of electrode arrays in scala tympani and documentation of any trauma that may have occurred during the insertion process.
Conservation of residual hearing has become an important goal in cochlear implant surgery, particularly for patients who may be candidates for combined electrical and acoustic stimulation (9, 10). In spite of advancements in surgical technique and electrode design, residual hearing is lost in 10-20 percent of cochlear implant patients (11, 12). It seems likely that a variety of factors may contribute to hearing loss associated with implant surgery, however, mechanical trauma to various intracochlear structures probably plays an important role. Structures that are particularly susceptible to implant-related injury include the modiolus, basilar membrane, soft tissues of the lateral cochlear wall, and blood vessels associated with scala tympani.
In recent years various “perimodiolar” electrode arrays have come into clinical use. These arrays are designed to place their contacts in close proximity to the modiolus so as to provide more focused stimulation of spiral ganglion cells. Although they offer the prospect of efficient electrical stimulation, perimodiolar arrays also pose a risk for injury to the spiral ganglion and associated nerve fibers. These neural structures are protected only by the very delicate bone of the modiolar wall and osseous spiral lamina, as illustrated in Figures 12 and 13. Blood vessels near the modiolar surface are also at risk of injury, since they too are poorly protected from mechanical trauma occurring during cochlear implant placement (Fig. 14).
A different perspective on the structure of the modiolar wall is offered by scanning electron microscopy which shows that the surface of the modiolus is covered by a highly porous meshwork of connective tissue and thin bone (Figs. 15, 16, 17) which provides a route for fluid exchange between the interior of the modiolus and the perilymphatic compartment of the cochlea (13).
Although it has received relatively little attention in previous studies, vascular injury occurring during cochlear implant surgery may compromise inner ear function and thereby contribute to loss of residual hearing. Vascular trauma is of concern given the significant exposure of scala tympani vessels to the perilymphatic space.
The superficially located vessels of scala tympani are primarily of the venous type. They include the venules found on the lateral wall and floor of scala tympani, the anterior and posterior spiral veins associated with the modiolus and the spiral vessel beneath the basilar membrane.
The venules of the lateral wall drain the stria vascularis and spiral ligament and they converge to form the small veins crossing the floor of scala tympani which empty into the posterior spiral vein (Figs. 18, 19, 20, 21, 22, 23). The posterior spiral vein also collects blood from the spiral ganglion and receives connecting vessels from the anterior spiral vein which drains the osseous lamina and scala vestibuli. In the lower basal cochlear turn the two spiral veins join to form the common modiolar vein, which after uniting with the vestibulocochlear vein, becomes the vein of the cochlear aqueduct (14) (Fig. 24).
As the images shown here illustrate, many of the venous vessels in scala tympani have little or no bony covering, leaving them essentially exposed to the perilymphatic space. They are therefore vulnerable to compression or mechanical injury associated with insertion of electrode arrays.
Previous work has demonstrated that implant electrodes sometimes tear or compress the delicate tissues of the spiral ligament immediately below the area of attachment of the basilar membrane (2, 15). Scanning electron microscopic study shows that portion of the spiral ligament to be composed of an open connective tissue meshwork which appears susceptible to mechanical disruption by electrode arrays (Figs. 25, 26, 27). Such injuries will inevitably traumatize the venules coursing through the spiral ligament (Figs. 18, 25, and 27). These small vessels drain the stria vascularis and the portion of the spiral ligament that lies adjacent to the lateral wall of scala media. Interruption of the venous outflow in the lateral wall would compromise oxygen delivery and thereby impair spiral ligament and strial function, which is essential for maintenance of the ionic composition of the cochlear fluids and the endolymphatic potential of the cochlear duct (16).
Recent temporal bone studies have demonstrated that electrode arrays are often positioned so that they make firm contact with the lateral wall of scala tympani over part (or sometimes all) of their length as illustrated in Figure 28. Subsequent study of dissected preparations following careful removal of the arrays has provided evidence that compression of the spiral ligament venules can occur and may be severe enough to compromise circulation in lateral wall tissues (Figs. 29, 30). It is of interest to note that Sutton et al. have in fact described pathological changes in the stria vascularis in animal studies after insertion of electrodes positioned in contact with the spiral ligament. In at least one case they found strial changes without evidence of basilar membrane penetration, suggesting that the strial pathology may have been due to vascular compromise rather than to intermixing of cochlear fluids (17).
As noted above, the bone of the modiolar wall is very fragile and shows numerous gaps and open spaces in its structure. Because of that, the posterior spiral vein and its tributaries are in some areas uncovered by bone. Thus, perimodiolar electrode arrays positioned in close contact with the modiolus have the potential to injure these vessels. Such injury may occur if the tip of an electrode strikes the modiolar wall during insertion or if the body of the array is pushed into contact with the modiolus by a positioner device (18). Modiolar trauma may also occur if explanation becomes necessary because of the tendency for a perimodiolar array to be pulled into tighter contact with the modiolus as it is withdrawn from the cochlea.
In addition to the possibility of vascular injury produced by electrode arrays, the veins in the lower basal turn of scala tympani are vulnerable to trauma during surgical drilling associated with cochleostomy placement. Such injuries may occur during drilling of a standard promontory cochleostomy or in the course of a round window insertion involving drilling of the anterior-inferior margin of the round window near the so-called crista fenestrae (4). Observations from the authors laboratory have confirmed that the cochlear aqueduct may lie within one-half millimeter of the inferior margin of the round window membrane (4). Caution is therefore necessary when drilling in this area to avoid injury of the common modiolar vein which enters the bony channel immediately adjacent to the aqueduct to become the vein of the cochlear aqueduct. Injury or occlusion of this vessel would be particularly significant since it is widely believed to provide virtually the entire venous drainage of the cochlea (14,19). As illustrated in Figure 24, the common modiolar vein also receives the vestibulocochlear vein which carries blood from the vestibular sensory organs and the basal end of the cochlea (14). There is therefore the potential for circulatory compromise of the vestibular apparatus as a result of vascular injury in the lower basal portion of scala tympani.
As mentioned above, the vein of the cochlear aqueduct is believed to provide virtually 100% of the venous outflow of the cochlea in most individuals. The possibility of collateral venous circulation does, however, exist. In the older literature a central auditory vein which follows the course of the auditory nerve is described (20, 21) (Fig. 31). This vessel is now thought to be inconsistently present (14). In cases where such a vessel does exist there may be connections between it and the posterior spiral vessel and/or the common modiolar vein, providing the potential for collateral circulation (21). Another possible route for collateral drainage may be via connections between the cochlear veins and the vessels of the mucoperiosteum of the middle ear (22). It might therefore be expected that injury of the common modiolar vein or vein of the cochlear aqueduct during implant surgery could result in variable damage to inner ear tissues depending on the degree to which collateral vessels are present in a particular patient.
Various types of basilar membrane damage have been reported in association with placement of electrode arrays in scala tympani. Electrodes may occasionally penetrate the basilar membrane and enter scala media or, if they remain within scala tympani, they may directly contact the underside of the basilar membrane and elevate the cochlear partition and/or fracture the osseous spiral lamina (2,15,23,24). In either case, the spiral vessel and associated arterioles found on the lower surface of the basilar membrane and osseous lamina may be damaged or occluded. As shown in figures 32 and 33, these vessels lie in an unprotected position where they could easily be subject to electrode trauma. Since the spiral vessel is believed to be important for oxygen delivery to the organ of Corti (14,25), its injury could be a factor in loss of residual hearing in patients who have viable organ of Corti remaining on the basilar membrane.
In addition to circulatory compromise produced by vascular occlusion, bleeding due to implant-related injury of cochlear vessels may have detrimental effects on inner ear function. As has been known for sometime, significant intracochlear bleeding due to hemorrhage can produce sudden hearing loss, a fact which has been confirmed by recent imaging studies (26,27). However, Radeloff et al. (28) have demonstrated that even a few microliters of blood introduced into scala tympani in laboratory animals cause significant permanent shifts in hearing thresholds. These findings raise the possibility that relatively small amounts of bleeding, such as might occur during cochlear implantation, might negatively impact auditory function and thereby contribute to post-implantation hearing loss.
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