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Aneurysmal bone cyst (ABC) is an uncommon lesion of the temporal bone (TB), with only 20 cases reported. Facial paralysis is a rare complication (2 cases); however, no cases have been reported with preoperative reversal of paralysis. We report a 60-year-old man with a history of remote head trauma, who presented with serious otitis media and right hemifacial paralysis, which resolved with nonsurgical therapeutic measures. Magnetic resonance imaging and computed tomography showed a destructive and expansile lesion of the TB. The lesion was surgically removed, and ABC was diagnosed histologically. The patient had an uneventful recovery and demonstrated no recurrence at 1 year of follow-up. This report presents an unusual presentation of ABC in the TB, with a review of the clinical, radiological, pathological, and therapeutic features of this entity. [ABSTRACT FROM AUTHOR]

Objectives: Describe quantitatively the number of ganglion cells in the geniculate (G) and meatal (M) segments of the human facial nerve.Study Design: One hundred human temporal bone specimens that were sectioned horizontally and stained with hematoxylin and eosin were selected from a temporal bone collection on the basis of minimal artifact and absence of pathology involving the facial nerve.Methods: Cells with a nucleolus in all sections through the facial nerve were projected on tracing paper with a camera lucida and counted manually. A modified Abercrombie technique was employed to compute total cells in the G and M segments.Results: Ages of patients ranged from 1 month to 92 years; the male-to-female ratio was 56:44. The total number of cells in individual temporal bones ranged from 589 to 4183 (mean, 2162 cells). The range of cells in the G ganglion was from 66 to 4017 (mean, 1713 cells); in the M ganglion the number ranged from 0 to 2764 (mean, 448 cells). There was no correlation of total ganglion cell number to age or sex. The majority of cells were found in the G ganglion in 88% of temporal bones. In 8% temporal bones the majority of cells were in the M ganglion and in 4% the M and G ganglions contained an equal number of cells.Conclusions: The facial nerve sensory ganglion consists of two components: G and M. The G ganglion outnumbers the M component in the majority of temporal bones (88%). The M ganglion was equal to or greater in number than the G ganglion in 12% of temporal bones. [ABSTRACT FROM AUTHOR]

The article focuses on the meatal ganglion in neoplasia and inflammation of the facial nerve. It states that the geniculate ganglion and the meatal ganglion of the facial nerve are derived from different embryologic cell anlages. According to it, the most common cause of idiopathic facial paralysis is now believed to be the reactivation of a latent neurotrophic virus in the sensory neurons of the facial nerve.

Objective: To explain the pathophysiology of the hearing loss in Ménière's disease (MD)., Background: In a previous report, we described a dramatic recovery of hearing in 12/31 patients with MD using antiviral (AV) drugs. The hearing loss in the remaining 19 patients with a longer history of MD remained unchanged or else worsened. Vertigo control was complete in the group with improved hearing but poorer in the group with greater hearing loss (and a longer MD history). Since achieving the recovery of hearing and control of the vertigo using AV drugs in these patients with a shorter history (≤2 years) of MD, we have continued to record dramatic hearing recovery in MD when patients have a shorter history of symptoms. We describe this here in 5 representative MD patients. We feel that the most likely explanation for the outcome is the removal of viral nucleic acids (NA) from the organ of Corti., Summary: A likely explanation for the sensorineural hearing loss in MD is paralysis of the cochlear amplifier function of the outer hair cells due to the toxicity ofNA. These NA are released from neurotropic viruses located in the vestibular nerve ganglion. Key Messages: (1) Viruses (Herpes family) are the cause of the symptoms in MD. (2) Hearing loss is the result of viral NA in the organ of Corti. (3) A short history of MD symptoms (<2 years) favors hearing recovery., (© 2021 S. Karger AG, Basel.)

Objective: Determine the outcome of hearing in Meniere's Disease (MD) after antiviral treatment., Study Design: Prospective study., Setting: University Hospital., Methods: Thirty one new patients with a diagnosis of MD were treated with antiviral drugs during 2012. Acyclovir or valacyclovir was used depending on insurance coverage and cost. A standard dose of 800 mg (acyclovir) or 1g (valacyclovir) 3 times a day for 3 weeks was used. The dose was decreased to twice daily for three weeks, and finally once daily for a year or longer. Hearing test including pure tone average (PTA) and speech discrimination (SD) was performed prior to treatment and 1-2 months, 6 months and 1 year after the initiation of treatment. Effect on dizziness was recorded at each evaluation, hearing was judged to be improved if PTA was lowered by at least 15 db and/or an increase in SD of 20% or greater., Results: Hearing was improved in twelve and not improved in nineteen patients. Complete control of vertigo was achieved in those patients with improved hearing. The nineteen patients with no improvement in hearing were divided into 2 groups based on the level of hearing at diagnosis. Nine patients presenting with a PTA of 50 db and SD of 50% or better experienced good control of vertigo (6 out of 7; 2 with no follow-up). Ten patients with PTA of 60 db or more and SD below 50% exhibited poor control of vertigo with antivirals (3 out of 10). The duration of MD in the group with hearing improvement was shorter (2.4 years) than the group with no improvement (5.5 years)., Conclusion: Significant hearing and balance control in patients with MD can be achieved with orally administered antiviral drugs., (Copyright © 2015 Elsevier Inc. All rights reserved.)

The recurrent nature of the 3 most common vestibulopathies suggests a recurrent cause. Histopathology in temporal bones from patients with these syndromes - vestibular neuronitis (VN, n = 7), Ménière's disease (MD, n = 8) and benign paroxysmal positional vertigo (BPPV, n = 5) - shows focal degeneration of vestibular nerve axons and degenerated nearby facial nerve meatal ganglion cells. Transmission electron microscopic confirmation of intracytoplasmic viral particles in surgically excised vestibular nerves from patients with VN and MD support a viral etiology in these vestibulopathies. Antiviral treatment of these syndromes in a series of 211 patients with a 3- to 8-year follow-up resulted in complete control of vertigo in VN (88%), MD (90%) and BPPV (60%)., (Copyright © 2013 S. Karger AG, Basel.)

Objective: To demonstrate the organization of the spiral ganglion in the mammalian species., Methods: Temporal bone (TB) specimens from man (n = 2), monkey (n = 2), lion (n = 2) and cat (n = 20) were stained, decalcified and dissected according to the Sudan black B method of Rasmussen. These TB specimens were examined under a Zeiss operating microscope and photographed with a Canon 100 camera interfaced with the microscope., Results: Spiral ganglion cells occurred in clusters within Rosenthal's canal in all four species. The location of the clusters was marked by the interface between axon and dendritic bundles as well as groups of ganglion cells. In monkey and man the clusters were more separated than in lion and cat., Conclusions: These observations indicate that the spiral ganglion forms clusters of neurons within Rosenthal's canal at the basal cochlear turn in the mammals investigated here. The formation of clusters may be related to the principles of neurogenesis., (Copyright © 2011 S. Karger AG, Basel.)

Objectives: This study was undertaken to demonstrate changes in the innervation of vestibular and auditory sense organs with the evolutionary ascent of the vertebrate labyrinth., Methods: Dissected labyrinths and their nerve supply prepared by the Sudan black B technique of Rasmussen were examined and photographed with a Canon A100 camera interfaced with a Zeiss operating microscope., Results: In lizards and alligators, the utricular sense organ is represented by 2 small maculae, each with a separate nerve branching off the ampullary nerves to the anterior and lateral canal cristae. These 2 maculae fuse into a bilobed macula with ascent in frogs and pigeons, eventually becoming a single large macula with its nerve supply from the superior vestibular division in guinea pigs, cats, lions, monkeys, and humans. Along with these changes, there is a fusion of the lateral and anterior canal ampullary nerves and of the bifurcating branches of the vertical canal ampullary nerves. The saccular macula is single, but receives a dual innervation from the superior division (anterior ramus) and the inferior division (posterior ramus) of the eighth nerve in alligators, pigeons, guinea pigs, cats, lions, monkeys, and humans. The main innervation is usually from the inferior division; however, saccular innervation is from the inferior division in lizards and from the superior division in frogs. The auditory sense organ is represented by a curved tube with a low-frequency receptor (lagena) at its distal end in lizards, alligators, and pigeons. In mammals, in which there is a coiled cochlea with a variable number of turns, low frequencies are recorded at the apical turn. This configuration may represent fusion of the lagena into the apical end of the auditory sense organ., Conclusions: Fusion of sense organs and of their nerve supply appears to be an evolutionary principle in the vertebrate labyrinth.

Morphological and clinical evidence supports a viral neuropathy in Ménière's disease (MD). Quantitative examination of 11 sectioned temporal bones (TBs) from 8 patients with a history of MD revealed a significant loss of vestibular ganglion cells in both the endolymph hydropic (EH) and non-EH ears. Transmission electron microscopy of vestibular ganglion cells excised from a patient with MD revealed viral particles enclosed in transport vesicles. Antiviral treatment controlled vertigo in 73 of 86 patients with vestibular neuronitis (85%) and 32 of 35 patients with MD (91%)., (Copyright 2009 S. Karger AG, Basel.)

Objective: To provide a road map of the vestibular labyrinth and its innervation leading to a place principle for different forms of vertigo., Method: The literature describing the anatomy and physiology of the vestibular system was reviewed., Results: Different forms of vertigo may be determined by the type of sense organ, type of ganglion cell and location in the vestibular nerve., Conclusion: Partial lesions (viral) of the vestibular ganglion are manifested as various forms of vertigo.

The concept that reactivation of latent neurotropic viruses (i.e. Herpesviridae group) in the vestibular ganglion is responsible for recurrent vestibulopathies is presented. A similar histopathologic degeneration of vestibular ganglion cells in vestibular neuronitis (VN), Ménière's disease and benign paroxysmal positional vertigo is presented to support this concept. The clinical response (relief of vertigo) to the administration of antiviral medication in these syndromes provides practical evidence of a viral neuropathy in patients with recurrent vertigo. Relief of vertigo after this treatment was 90% in VN, Ménière's disease and VN. The relief of positional vertigo (benign paroxysmal positional vertigo) was 66%., ((c) 2008 S. Karger AG, Basel)

Sense organ deposits have been described in temporal bones from patients with vestibular neuronitis, Meniere's disease, and benign paroxysmal positional vertigo that are not found in a comparable series of temporal bones without vestibulopathy. Because the recurrent vestibulopathies are caused by vestibular ganglionitis and the vestibulocochlear anastomosis was degenerated in these temporal bones, the deposits may represent the end buds of regenerating efferent axons injured in passage through the vestibular ganglion. Such neural buds have been described with transmission electron microscopy in animals after vestibular nerve transection and in a human temporal bone with endolymphatic hydrops. The buds may be visible by light microscopy, because their size is comparable to that of hair cell nuclei and they stain blue with hematoxylin because of their nucleic acid content. The variable location and size of these deposits (buds) in the labyrinthine sense organs is described to aid in the recognition of efferent system injury in human temporal bones.

The pathophysiology of benign paroxysmal positional vertigo (BPPV) is not completely understood. Although the concept of degenerated otoconia transforming the posterior canal (PC) crista into a gravity-sensitive sense organ has gained popular support, several temporal bone (TB) series have revealed similar deposits in normal TBs, suggesting they are a normal change in the aging labyrinth. Furthermore, some TBs from patients with BPPV do not contain particles in the posterior canal. Five TBs from patients with BPPV were studied quantitatively and qualitatively. A small PC cupular deposit was found in 1 TB, while none was seen in the other 4 TBs. The major pathological changes were 1) a 50% loss of ganglion cells in the superior vestibular division of all 5 TBs and 2) a 50% loss of neurons in the inferior division of 3 TBs, and a 30% loss in 2 TBs that contained abnormal saccular ganglion cells. These observations support a concept in the pathophysiology of BPPV that includes loss of the inhibitory effect of otolith organs on canal sense organs.

Objective: To determine the effect on hearing and balance symptoms following singular neurectomy (SN) for benign paroxysmal positional vertigo (BPPV) in the ampullary recess of the posterior semicircular canal., Research Design: The charts of 242 patients with chronic disabling BPPV who were treated with SN over a 29-year period (1972-2001) were reviewed. The results on relief of BPPV and hearing function were recorded. A subset of 16 patients where the posterior ampullary recess was entered to expose the SN is described in detail with regard to an effect on hearing and balance., Results: A total of 252 SN were performed in 242 patients. Ten patients underwent bilateral SN sequentially; the remaining 232 patients had unilateral SN. The ages of the patients ranged from 21 to 86 years, with a mean at 57 years. The female:male ratio was 174:68. Complete relief of BPPV was achieved in 244 patients (96.8%), incomplete relief in 3 (1%), and no relief in 5 (2%). Sensorineural hearing loss (SNHL) occurred in 9 patients (3.7%). A subset of 16 patients in whom the ampullary recess was opened during SN ranged in age from 21 to 79 years, with a mean at 56 years. The female:male ratio was 12:4, with right and left sides divided almost equally. Relief of BPPV was achieved in all 16 patients with no loss of hearing function. Five patients complained of a fistula response postoperatively (31%). The fistula response resolved by 6 months postoperatively in all 5 patients., Conclusions: SN is effective in relief of BPPV with little risk of SNHL (3.7%). The risk of SNHL is not increased when the posterior ampullary recess must be entered in order to transect the singular nerve. A positive fistula response may be present temporarily in almost one third of these patients., (Copyright 2002 S. Karger AG, Basel)

We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.

Objective: To present morphologic evidence of viral-induced vestibular nerve pathology in Menière's Disease (MD). MATERIAL STUDIED: Twelve temporal bones (TB) from 8 patients with the clinical symptoms of MD., Results: There was endolymphatic hydrops (EH) and perilymphatic fibrosis in 10 of the 12 TB from MD patients. Of the 10 TB with EH of the pars inferior, 3 also contained outpouchings in the pars superior (utricle and canals), and 3 showed apical spiral ganglion cell loss. Focal vestibular nerve axonal degeneration was observed in all but one TB., Conclusion: Morphologic changes in TB of patients with MD, and clinical observations in patients with recurrent vestibulopathy, support the concept that the pathologic mechanism responsible for auditory and vestibular symptoms in MD may be reactivation of a latent viral vestibular ganglionitis.

Objective: To describe demographic, radiologic, and surgical features in adult patients with spontaneous cerebrospinal fluid otorrhea (SCSFO). STUDIED: Review was made of office and hospital charts of 21 patients with SCSFO and 2 patients with spontaneous CSF rhinorrhea, all of which were repaired successfully from 1989 to 1998., Method: Radiologic examples of the structure responsible for SCSFO and rhinorrhea are used to illustrate the changes essential for diagnosis., Results: The responsible lesion for SCSFO and rhinorrhea in the adult are arachnoid granulations (AG) or villi, which do not reach a venous lumen and are aberrantly distributed in areas of the anterior, middle, and posterior cranial fossae that are in proximity to the middle ear/mastoid space, ethmoid, and sphenoid sinuses. The ages of the 21 patients ranged from 38 to 83 years (mean 63 years) with all but one older than 50 years. The sex ratio was 14 women to 7 men; the CSF leak was right sided in 13 and left sided in 8 patients. Eighteen of the SCSF leaks were located in the middle cranial fossa surface of the temporal bone (TB) while two were on the posterior fossa border of the TB. The middle fossa leaks were managed by craniotomy and repair with fascia, whereas the posterior fossa defects were obliterated by adipose tissue inserted through an intact canal wall mastoidectomy. The most common radiologic finding on computerized tomography (CT) was a soft tissue mass adjacent to a tegmen bone defect. The posterior fossa AG created an erosion of cortical and trabecular bone in the mastoid compartment. Spontaneous CSF rhinorrhea in two patients also radiologically appeared as soft tissue mass adjacent to bone erosion in the sphenoid and ethmoid sinuses. These also represent aberrant AGs, which are responsible for CSF rhinorrhea in later life., Conclusions: The demographic, radiologic, and pathologic findings in this series of 21 TB and 2 paranasal sinus SCSF leaks support the concept that the responsible lesions are AGs that are aberrantly located adjacent to pneumatized parts of the skull. Because these AGs enlarge with age, they may erode through the bony confines of the TB and sinuses and present as SCSFO or rhinorrhea in middle and old age.

Objective: To measure disease of idiopathic nature in the ganglia of the human facial (FN) and vestibular nerves (VN)., Method: One hundred horizontally sectioned human temporal bones (TB) were examined under light microscopy. The TB were sectioned at 20 microm, and every 10th section was stained with hematoxylin and eosin and mounted. The volume fractions (VF) of degenerated cells in the FN ganglion and focal axonal degeneration in the VN were measured with stereologic techniques., Results: Twenty-five TB were excluded because of artifact or poor staining of the FN and VN. Fifty-one TB contained degenerated cells in the FN meatal ganglion (MG) and/or focal axonal degeneration in the VN. Thirty-one FN had degenerated cells in the MG (VF = 1% to 55%) and none in the geniculate ganglion. In 45 TB, focal axonal degeneration was found in the VN (VF = 1% to 50%; the VF was less than 15% in all but one TB). MG and VN degeneration occurred together in 25 TB. None of the cases had a history of FN paralysis, but 20 had a history of vertigo. Twenty-four TB from patients of similar ages with similar otopathologies did not reveal degeneration in the FN or VN., Conclusion: The FN and VN lesions in these 51 TB may be virus-induced and reflect a higher incidence of idiopathic FN and VN neuronitis than previously thought.

Morphometric analysis of the cat's superior vestibulo-ocular neurons (SVON) 8 weeks, and 1 and 2 years following vestibular neurectomy or labyrinthectomy revealed similar changes which indicate that an excitatory mode of input to the denervated SVON is responsible for the behavioral recovery. These changes include an increased proportion of strong asymmetric synapses, somal spines surrounding the SP, increased size of and number of SP at long (> 1 year) survival periods. There is a parallel decrease < 1 year and increase > 1 year of contralateral vestibular nerve SP on SVON which matches in timing and magnitude the number of ipsilateral vestibular nerve SP after surgical ablation. These unexpected SVON are consistent with the hypothesis that neurotrophins regulate symmetry in the adult vestibular system. This hypothesis was tested in a series of 13 heterozygous brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) knockout mice. Following unilateral surgical labyrinthectomy the BDNF and NT4 knockout mice demonstrated no delay in behavioral recovery compared to their normal littermate controls. However, the NT3 knockout mice required twice the time to recover from balance deficits as their littermate controls. These results indicate that NT3 protein is important for normal vestibular function.

On the basis that neurotrophins (NTs) affect neuronal synaptic plasticity, are expressed in various cell types of the vestibular system, and exert a trophic influence on statoacoustic neurons, the authors hypothesized a role for NTs in vestibular compensation. To test this hypothesis, they performed unilateral surgical labyrinthectomy in 11 heterozygous (+/-) neurotrophin 3 (NT3) and brain-derived neurotrophic factor (BDNF) knockout mice and in two neurotrophin 4 (NT4) homozygous (-/-) knockout mice, each with a control (+/+) sibling, for a total of 26 mice. Four BDNF(+/-) and four NT3(+/-) mice with their (+/+) controls each were allowed to recover in a normal lighted room for 3, 7, 14, and 30 days following labyrinthectomy. Two BDNF(+/-) and two NT4(-/-) mice with controls were kept in total darkness for 1- and 16-day survival periods. One NT3(+/-) mouse without a control (which died in surgery) was sacrificed after 16 days in darkness. The behavior of all mice was videorecorded to monitor their recovery. Compared with normal (+/+) littermate controls, NT3(+/-) mice demonstrated a delay in compensation (8 to 10 days) in light surround, whereas NT4(-/-) mice showed only a minor delay in dark surround. Despite a 40% lower vestibular ganglion cell population in BDNF(+/-) mice compared with (+/+) controls, BDNF(+/-) mice did not reveal a detectable delay in recovery following labyrinthectomy. These findings suggest that a 50% loss of NT3 protein significantly affects vestibular recovery in adult mice. Perhaps variations in achieving vestibular compensation in humans may be partly secondary to genetically different NT3 levels in vestibular pathways.

Objective: To describe the anatomic variations of the subarachnoid space (SAS) in the facial nerve canal from human temporal bone specimens., Background: The SAS in the facial canal usually is assumed to terminate in the petrosal segment of the canal. This temporal bone study indicates that in 12% of temporal bones the SAS extends laterally into or beyond the tympanic segment of the facial canal., Methods: Histologic sections through the petrosal and tympanic segments of the facial canal were examined by light microscopy in 1 fetal (30 weeks) and 163 adult human temporal bones. The arachnoidal membrane of the SAS was judged to fall into three types according to its lateral extension in the fallopian canal., Results: One hundred forty-four (88%) of the adult temporal bones contained an SAS limited to the petrosal fallopian canal (type I). Thirteen temporal bones (8%) demonstrated an SAS that extended into the tympanic or geniculate portions of the facial nerve (type II). There were six temporal bones (4%) in which the SAS extended lateral to the tympanic facial nerve or into a separate bony compartment (type III)., Conclusions: Most (88%) temporal bones contain an SAS that is limited to the petrosal fallopian canal. In 12% of temporal bones, however, the SAS may extend laterally in the fallopian canal and present clinically as an asymptomatic enlargement of the canal by computed tomography or as cerebrospinal fluid otorrhea.

The vestibular nerve is composed of fibers with a wide spectrum of diameters. The fibers of largest diameter are known to innervate the type I hair cells of the cristae, while the small-diameter fibers innervate the type II hair cells. Midsized fibers (dimorphic fibers) represent neurons that innervate both type I and type II hair cells. Reports by others have commented on the tendency for clustering of fibers with like diameters. Rigorous statistical proof for or against clustering has not yet been presented. The explanation for this is, in part, the mathematic complexity of analyzing clustering in a system composed of three elements. We report a new method for analysis of fiber clustering and apply this method to large-, medium-, and small-diameter fibers in the feline vestibular nerve. The fiber grouping in the caudal and rostral ends of the vestibular nerves of six normal animals is compared to that in similar areas of the nerves of five animals 12 to 17 months after unilateral labyrinthectomy. No statistically significant clustering of fiber types was found in the rostral portion of either the control or the labyrinthectomized animals. In the caudal portion of the control nerves, clustering of the large fibers was demonstrated (p < .005, chi2 test). This clustering was not demonstrated after labyrinthectomy. An explanation of these findings is discussed. The method used in this study to analyze fiber clustering may be applicable to other nerve systems of greater complexity.

Unilateral ablation of vestibular input causes lasting morphological changes bilaterally in superior vestibulo-ocular neurons (SVON). The present study was performed to see if these changes in SVON are more pronounced after bilateral vestibular neurectomy. Twenty-three SVON from both vestibular nuclei of 2 cats sacrificed 8 weeks after bilateral ablation were examined utilizing morphometric ultrastructural techniques. There was a significantly greater somal atrophy, loss of synaptic profiles, rough endoplasmic reticulum and polyribosomes compared to unilateral neurectomy. These changes indicate a down regulation that is proportional to the level of deafferentation and may account for functional deficits seen in the vestibulo-ocular reflex after peripheral ablation.

Morphological changes in the vestibular nerves and superior vestibulocular neurons (SVON) after unilateral labyrinthectomy in cats revealed a progressive loss of axons in the ipsilateral vestibular nerve (35%) and synaptic profiles (SP) on ipsilateral SVON (60%) up to a 1-year survival period. Although the ipsilateral vestibular nerve showed further degeneration (45%) at 2 years post ablation, the number of SP on ipsilateral SVON increased to 60% of normal (40% loss). These SP likely represent sprouting from crossing commissural or cerebellar pathways. Contralateral vestibular nerves at 1 and 2 years post ablation revealed normal numbers and size spectrum, but the number of SP contacting the contralateral SVON at 8 weeks, 1 and 2 years paralleled the levels of SP found on ipsilateral SVON. The symmetry in adjustment of SP on the SVON of both sides of the brainstem after ablation may be explained by the neurotrophin hypothesis.

Eleven whole organ laryngeal specimens (10 human and 1 dog) with a history of long-standing (6 months to 17 years) paralysis were studied histopathologically for changes in the cricoarytenoid (CA) joints and the intrinsic laryngeal musculature. In 9 cases the paralysis was unilateral and in 2 bilateral. No evidence of CA joint ankylosis (fibrous/osseous obliteration of joint space or degeneration of articular surfaces) was seen in the specimens. The absence of CA joint ankylosis permits the efficacy of thyroplasty medialization procedures.

Ultrastructural changes were measured in 22 contralateral superior vestibulo-ocular neurons (SVONs) from four cats painlessly sacrificed at 8 weeks and 25 contralateral SVONs from four cats sacrificed at 1 year following unilateral labyrinthectomy. The SVONs at 8 weeks showed a 43% decrease in somal size, a 34% loss in rough endoplasmic reticulum (RER), a 48% loss of ribosomes, and a 47% decrease in the number of synaptic profiles (SPs) contacting the soma. At 1 year the SVONs had a 31% decrease in size, a 43% decrease in RER, a 50% loss of ribosomes, and a 71% decrease in SPs. Synaptic vesicles (SVs) in both groups of SVONs showed no change in size or shape compared to control SVs. These findings resemble the contralateral SVON changes that occur following excision of the vestibular ganglion.

One hundred twenty-six patients who were treated with labyrinthectomy (81 patients) or vestibular neurectomy (45) between the years 1979 and 1994 were reviewed. The cause for vertigo in 124 of the 126 patients was Meniere's disease (89 patients), labyrinthitis (15), delayed endolymphatic hydrops (8), vestibular neuritis (7), and failed labyrinthectomy (5). In the remaining 2 patients, a normal labyrinth was sacrificed to fistulize a petrous apex cyst. Both procedures were equally effective in relieving vertigo (labyrinthectomy 98.8%; neurectomy 97.8%), but the length of hospitalization, length of disability before return to work, and cost were twice as great with vestibular neurectomy than with labyrinthectomy. More patients exhibited prolonged ataxia following neurectomy (5 patients) than after labyrinthectomy (2). Vestibular neurectomy was associated with several complications: reversible facial paresis (15 patients), meningitis (1), cerebrospinal fluid leak (1), and epidural hematoma (1). Labyrinthectomy was complicated by postoperative hyponatremia in 1 patient. Selective vestibular neurectomy preserved hearing in 32 (82%) of 39 patients. Criteria for recommending either ablation procedure are discussed. The incidence of sequential involvement of the contralateral ear was 1.5%.

Purpose: This study was performed to determine the contribution of the posterior semicircular canal to the vestibulo-ocular responses (VOR) from caloric stimulation of the labyrinth., Materials and Methods: Seven consecutive patients with disabling benign paroxysmal positional vertigo, which was treated with singular neurectomy, were tested before and after surgery with bithermal stimulation of the operated and nonoperated ears., Results: There was a significant (P = .0156) decrease in the VOR from stimulation of the operated ear following singular neurectomy. The nonoperated ear showed a variety of changes that may have resulted from compensatory mechanisms and/or utricular dysfunction., Conclusions: We conclude that the posterior canal together with the lateral and superior canals are responsible for the VOR following caloric stimulation of the labyrinth.

The ultrastructural changes of the feline superior vestibular commissural neurons (CNs) were quantitatively assessed 8 weeks following ipsilateral vestibular neurectomy. Results indicated a slight degeneration of synaptic profiles (SPs; 25%) representing the primary vestibular afferent input onto CN soma. The synaptic vesicles of the remaining SPs, which likely originate from the cerebellum and the contralateral CNs, were smaller and rounder, suggesting a transition from an inhibitory to an excitatory mode of response. The SP loss had little impact on the CNs' capacity for protein synthesis and structural maintenance, since there was no change in the volume fraction of intracellular organelles. These data suggest that CNs do not degenerate and are likely functional after vestibular compensation. These findings support the role of the commissural pathway in vestibular compensation as proposed by Galiana et al, which is based on the assumption that the intervestibular commissural connections remain intact following vestibular neurectomy.