Vertigo With Cochlear Implant

Fig. 16. Tissue seal at cochleostomy. In this 74-year-old man who had undergone implantation of the right ear 12 years before death, the cochlear implant (CIT) can be seen entering the cochlea near the round window. There is a tissue seal at the cochleostomy including both fibrous tissue (F) and new bone (NB).

Fig. 16. Tissue seal at cochleostomy. In this 74-year-old man who had undergone implantation of the right ear 12 years before death, the cochlear implant (CIT) can be seen entering the cochlea near the round window. There is a tissue seal at the cochleostomy including both fibrous tissue (F) and new bone (NB).

However, in a study of 21 specimens from patients who in life had undergone cochlear implantation using a variety of devices, there was a robust tissue response in the form of fibrous and bony tissue in all cases (fig. 16) [48]. A recognizable open communication or potential communication between the middle ear and the inner ear was not identified in this series. In addition, an inflammatory cellular response in the form of mononuclear leukocytes, histiocytes, and foreign body giant cells were present in 12 of the 21 cases (57%) and was most intense near the cochleostomy site (fig. 17). It is therefore possible that delayed meningitis after implantation may be caused by a mechanism other than open communication between the middle and inner ears, namely a delayed hematoge-nous contamination and colonization of the implant similar to the hypothetical mechanism of late infection of cerebrospinal shunt catheters [49, 50].

Histopathology of Vestibular Labyrinth after Cochlear Implantation

The incidence of postoperative dizziness and/or vertigo following cochlear implantation has been reported in the range of 4 [51] to 75% [52] of patients. The vertigo may be immediate or in some cases delayed in onset [53]. In some cases, delayed vertigo following implantation may be similar to attacks of Ménière's syndrome. The histopathology of the vestibular labyrinth in patients who in life had undergone cochlear implantation has been reported [54, 55]. Findings include distortion of the saccular membrane, fibrosis, ossification

Fig. 17. Inflammatory response to cochlear implant. This 70-year-old man underwent a right cochlear implant 11 years before death. The track of the cochlear implant (CIT) is seen. Close by there is an intense cellular inflammatory response (CR) consisting of mononuclear cells and foreign body giant cells.

Fig. 17. Inflammatory response to cochlear implant. This 70-year-old man underwent a right cochlear implant 11 years before death. The track of the cochlear implant (CIT) is seen. Close by there is an intense cellular inflammatory response (CR) consisting of mononuclear cells and foreign body giant cells.

within the vestibule, and cochlear hydrops in 59% of implanted bones. In most cases of cochlear hydrops, the saccule was partially or completely collapsed with or without evidence of collapse of the ductus reuniens (fig. 18). There was no quantifiable effect on residual vestibular neuroepithelial cells or neurons of Scarpa's ganglion.

Histopathologic Correlates of Performance of Cochlear Implants

Basic psychophysical and speech-reception measures made in human implantees vary widely in all published series. The underlying determinants of this variance are poorly understood. Intuitively, differences in residual spiral ganglion cell population or function may play an important role in determining the success of implantation. Furthermore, there is evidence for a correlation between psychophysical parameters and residual spiral ganglion cell counts in animals [56, 57]. Ever since one of the early implantees died in 1986 [41], investigators have searched in vain for reliable and consistent relationships between the degree of spiral ganglion cell survival and measures of human performance [for an overview, see 58]. For instance, in a series of 15 patients who underwent multichannel cochlear implantation during life, the spiral ganglion cell counts in the four segments of Rosenthal's canal and the total spiral ganglion cell count were compared with speech reception scores and no significant correlation was found [39]. Relationships found in one study demonstrating that spiral ganglion

Fig. 18. Cochlear hydrops in a 84-year-old man with a progressive bilateral sensorineural hearing loss who underwent left cochlear implant 10 years prior to death. He had no significant vestibular symptomatology following implantation. There were severe endolymphatic hydrops and collapse of the saccular wall, suggesting dysfunction or obstruction of the ductus reuniens, perhaps secondary to the implantation. Reprinted with permission from Handzel et al. [55].

Fig. 18. Cochlear hydrops in a 84-year-old man with a progressive bilateral sensorineural hearing loss who underwent left cochlear implant 10 years prior to death. He had no significant vestibular symptomatology following implantation. There were severe endolymphatic hydrops and collapse of the saccular wall, suggesting dysfunction or obstruction of the ductus reuniens, perhaps secondary to the implantation. Reprinted with permission from Handzel et al. [55].

cell counts account for a significant percentage of the variance in a psychophysical measure have not proven reliable. For instance, in one population the variance in spiral ganglion cell survival does not account for variance in threshold but does account for 60% of the variance in the stimulus level producing maximum comfortable loudness sensation; but in a different population this variance accounts for 18% of the threshold variance but none of the variance in the stimulus amplitude producing maximum comfortable loudness [58].

It is not surprising that the methods used to date have failed to reveal substantial and consistent relationships between spiral ganglion cell survival and behavioral measures of performance because of the known shortcomings of the methods used to date. For instance, the relative sensitivity of a single electrode contact in eliciting a detectable sound sensation will depend on a number of peripheral factors beside the number of surviving spiral ganglion cells such as: (1) the spatial distribution of current elicited by the electrode which will depend on the electrode configuration (monopolar, bipolar, bipolar + 1...), electrode position (basal/apical, modiolar/lateral wall), the amount of new intracochlear bone and other tissue, and the insertion damage to cochlear structures, and (2) the exact position of the remaining nerve fibers in the elicited current distribution. Because complex, three-dimensional factors like these will determine whether a specific fiber elicits a spike in response to a specific stimulus, new methods that are capable of representing the detailed variance in the peripheral anatomy across subjects will be required before reliable and consistent relationships between these peripheral factors and behavioral performance will be established.

Acknowledgement

This study was supported by NIH grant 5 R01 DC000152-25.

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Joseph B. Nadol Jr, MD

Department of Otolaryngology, Massachusetts Eye and Ear Infirmary

243 Charles St.

Boston, MA 02114 (USA)

Tel. +1 617 573 3652, Fax +1 617 573 3939, E-Mail [email protected]

M0ller AR (ed): Cochlear and Brainstem Implants.

Adv Otorhinolaryngol. Basel, Karger, 2006, vol 64, pp 50-65

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