Fallopian canal dehiscences: a survey of clinical and anatomical findings.

This survey investigates fallopian canal dehiscences in order to assess the risk of encountering an unprotected facial nerve during routine ear surgery. In a prospective non-randomized study, the intraoperative appearance of the facial canal in 357 routine ear operations was compared with 300 temporal bone specimens from 150 autopsies. Intraoperatively, a dehiscence was detected in 6.4% (23/357) of the operations, most frequently at the oval niche region (16/23 cases). The incidence increased with the number of operations (P<0.0002). Cholesteatoma surgery had the highest relative risk (RR 4.6) of exposing an unprotected facial nerve. Postoperatively, no persistent facial paralysis was observed. In four of five cases with a transient facial palsy due to local anesthetics, a bony dehiscence could be found. The anatomical study revealed fallopian canal dehiscences in 29.3% (44/150) of the autopsies. One-third (15/44) of the individuals affected displayed bilateral findings, thus resulting in 19.7% (59/300) of temporal bones affected. A total of 17/59 bones showed microdehiscences, and most (55/59) were located at the oval niche. The actual prevalence of fallopian canal dehiscences is significantly higher than intraoperative findings suggest. The oval niche is the most affected region. High-resolution computed tomography is of diagnostic value only in selected cases. Facial paralysis following local anesthesia is the most significant clinical sign. Vigilance in acute facial palsy after local anesthetics and in cholesteatoma surgery and adequate intraoperative exposure help to prevent iatrogenic injury of the uncovered nerve. In unclear cases, nerve monitoring can facilitate a safe outcome.

The vestibular nerve: its course to the anterior and lateral ampullae.

The course of the ampullary nerve to the anterior and lateral ampullae was studied using 25 human temporal bones. Sudan Black B staining was applied to decalcified temporal bones in order to stain nerve fibers. After removing the external and middle ear, each temporal bone was divided into four blocks by three parallel planes, making an angle of 45 degrees to the long axis of the stapes footplate or a line along the stapedial tendon. Two planes were in contact with the anterior and posterior margin of the oval window, respectively. The third plane passed through the capitulum of the stapes. Distances from the upper margin of the oval window, to the distal and proximal part of the ampullary nerve, to the facial nerve, and to the utricular macula were measured in the third plane. The thickness of the thinnest part of the wall of the facial canal facing the stapes was also measured. A new surgical approach to the ampullary nerve is discussed.

Transposition of the facial nerve in congenital aural atresia.

It is generally recognized that surgery for congenital aural atresia is difficult. The success or failure of the operation is often directly related to the degree of development of the middle ear. In poorly developed middle ears, the facial nerve may overhang and conceal the oval window niche, making this area inaccessible to inspection, let alone manipulation. The criteria for transposing the facial nerve are; (1) the atresia must be bilateral, (2) there must be preoperative imaging evidence of a stapes and/or patent oval window, (3) there must be no large blood vessels feeding or draining the facial nerve, and (4) facial nerve monitoring must be available. Over the past 2 years, 6 of 94 patients undergoing surgery for atresia were operated with an intent to transpose the facial nerve in order to access the oval window. In all patients, it was impossible to see the oval window niche due to a displaced nerve. In four of six cases, the facial nerve was transposed. The ossicular chain was reconstructed with a total ossicular replacement prosthesis. In no case was there a postoperative facial paralysis or paresis. Facial nerve transposition allows a final chance of achieving serviceable hearing through surgery. The lack of facial nerve injury and the potential for hearing restoration make this procedure feasible in otherwise marginal or poor surgical candidates.

Posterior canal-activated excitatory vestibuloocular relay neurons participate in the vestibulocortical pathways in cats.

We have previously reported that axon collaterals of posterior canal-activated excitatory vestibular (PC) neurons project to the contralateral oculomotor nucleus, and rostrally to the thalamus. To elucidate the vestibulothalamocortical pathways we investigated the synaptic connections of the PC neurons with the thalamic neurons by post-spike averaging of compound potentials triggered by spikes of the PC neuron in anesthetized cats. The averaged field potential evoked in the ventrobasal complex (VBC) revealed a spike followed by a negative wave. Latencies of the wave ranged from 0.8 to 1.5 ms. Next, we examined the location and axonal projection of 36 thalamic neurons which were activated by nose-up head rotation and by contralateral labyrinth stimulation. Most of them were located in the VBC and some in the medial geniculate body. Thirteen of the 36 neurons were antidromically activated from the anterior suprasylvian sulcus or postcruciate dimple of the cortex. These results suggest that the PC neurons participate, at least in part, in the vestibulocortical pathways contributing to spatial orientation.