Letter to the Editor Regarding Oyewumi M, Wolter NE, Heon E, Gordon KA, Papsin BC, Cushing SL. “Using Balance Function to Screen for Vestibular Impairment in Children with Sensorineural Hearing Loss and Cochlear Implants”
The authors state that more than 50% of children with profound sensorineural hearing loss (SNHL) have an associated vestibular deficit, but do not mention that one of the greatest concerns of CI surgeons is vestibular deficit caused by cochlear implantation. However, there is mounting evidence that vestibular lesions can result from CI surgery (3,4–10).
There are single reports of improved vestibular function after CI activation (11,12), and single reports showing no statistically significant influence of CI on vestibular function (13). However, it is well established that CI can significantly impair vestibular system function (3,5–8,10), via direct injury and inflammation. Damage can be related to improper placement of electrodes in scala vestibuli, disturbance of the endolymph flow causing endolymphatic hydrops, foreign body reaction with labyrinthitis, intravestibular fibrosis, and electrical stimulation of the vestibular organ. Histopathologic studies of temporal bones have confirmed these changes following CI (4,7,9). In addition, intracochlear trauma may also be documented by fluoroscopy at the time of implantation (14).
Wienner Vacher et al. (10) reported postoperative vestibular modifications in approximately half of their patients, and ipsilateral vestibular areflexia in 10% of patients. The author reported that simultaneous bilateral CI was associated with a 2% risk of TBVL. In addition, the author described one case of a 3-year-old with normal speech and hearing who exhibited severe walking and standing impairments due to bilateral vestibular areflexia, with no associated disorders. Moreover, another child was reported to exhibit sudden and complete vestibular loss due to meningitis before the age of independent walking, indicating that posturomotor control was significantly delayed. This led to long-lasting posturomotor instability in the absence of any neurological impairment (10,15).
Unilateral vestibular areflexia with normal contralateral vestibular function or even hypofunction resulting from unilaterally implanted CI would not be expected to have a major impact on a child's life, due to compensatory processes. However, complete bilateral absence of vestibular function at a very young age is likely to cause severely delayed posturomotor development, causing impairments in stabilizing the head, sitting, and walking independently (5,16,17).
The age at which TBVL occurs has a substantial influence on the severity of symptoms and disability later in life, and later-occurring TBVL is associated with less severe symptoms. Devroede et al. (3) reported an 8-year-old patient with normal preoperative psychomotor function who developed TBVL after a second CI. After 1 month of persistent symptoms of vomiting and dizziness, the patient became asymptomatic and was able to resume sporting activity. In contrast, children suffering from TBVL at an earlier age experience substantially more difficulty, particularly if the condition develops before the ability to walk. Devroede et al. (3) concluded that the presence of hyporeflexia in the yet-to-be implanted ear is a particularly important risk factor.