Facial nerve canal dehiscence in chronic otitis media without cholesteatoma.

The information on incidence of the facial nerve canal dehiscence in chronic otitis media is important for surgeons. The purpose of this study is to disclose the histopathologic findings of facial nerve canal dehiscence in human temporal bones with chronic otitis media. We divided the human temporal bones into two groups (age 4 years, and under 4 years of age). We evaluated the incidence and the area of the facial nerve canal dehiscence in chronic otitis media under light microscopy. Age-matched normal control temporal bones were also examined. In the age group of 4 years, 68.9 % of temporal bones with chronic otitis media and 71.9 % of controls had the facial nerve canal dehiscence. There was no significant difference between them (P = 0.61). The area of the dehiscence in temporal bones with chronic otitis media was not statistically different from controls (P = 0.53). In the age group under 4 years, 88.2 % of temporal bones with chronic otitis media and 76.5 % of controls had the dehiscence. No significant difference was found between them (P = 0.66). The area of the dehiscence in temporal bones with chronic otitis media was not statistically different from controls in the age group under 4 years (P = 0.43). In chronic otitis media, the incidence of facial nerve canal dehiscence was high and was not statistically different from controls. These results suggest that there is no association between chronic otitis media and the presence of facial nerve canal dehiscence.

Peripheral vestibular system in Down syndrome: quantitative assessment of vestibular histopathology.

OBJECTIVE: To evaluate the maturity of the peripheral vestibular system in Down syndrome by examining the number of Scarpa's ganglion cells and the density of vestibular hair cells. STUDY DESIGN: Case-control study using human temporal bones. SETTING: Tertiary academic center, otopathology laboratory. SUBJECTS AND METHODS: Sixteen temporal bones from 8 patients with Down syndrome and 15 control temporal bones from 8 individuals with no history of otologic disease were selected. Hypoplasia of the lateral semicircular canal (LSC) and vestibule was investigated by measuring the dimensions of the structures. Scarpa's ganglion cells were counted under light microscopy. The vestibular hair cells were counted in the LSC crista and the utricular and saccular maculae under differential interference contrast (Nomarski) microscopy and expressed as density. RESULTS: The patients with Down syndrome were divided into 2 groups: with and without LSC hypoplasia. The number of Scarpa's ganglion cells and the density of vestibular hair cells were significantly smaller in both groups of patients with Down syndrome than in the control group. There was no significant difference in the number of Scarpa's ganglion cells or the density of vestibular hair cells between the groups with and without LSC hypoplasia. CONCLUSION: The peripheral vestibular system, including Scarpa's ganglion cells and vestibular hair cells, is hypoplastic irrespective of the vestibular malformation in Down syndrome.

Histopathological incidence of facial canal dehiscence in otosclerosis.

The objective of this study was to evaluate the histopathological incidence of facial canal dehiscence in otosclerosis cases compared with non-otosclerotic controls. 133 temporal bones from 84 otosclerosis (35 unilateral otosclerosis, 49 bilateral otosclerosis) cases were compared to 102 age-matched normal temporal bones from 70 subjects (38 unilateral normal cases, 32 bilateral normal cases). Temporal bones were serially sectioned in the horizontal plane at a thickness of 20 µm, and were stained with hematoxylin and eosin. We evaluated the location and the invasion of otosclerosis to the facial canal and incidence of facial canal dehiscence under light microscopy. Facial canal was subdivided into four portions: (1) the geniculate ganglion, (2) the tensor tympani muscle, (3) the oval window, and (4) mastoid. The incidence of facial canal dehiscence in otosclerosis [66 temporal bones (49.6%)] was significantly lower than normal controls [67 control temporal bones (65.7%)] in the oval window area (P = 0.019). Temporal bones with otosclerotic invasion to the thin bone of the canal were significantly less likely to have dehiscence [10 temporal bones (31.3%)] compared to the otosclerotic bones without invasion [56 temporal bones (55.5%)] (P = 0.025). There was no significant difference in the incidence of facial canal dehiscence between temporal bones with and without otosclerosis in the entire segment of facial nerve. Our findings in this study suggest that otosclerotic lesions have the potential to close dehiscence of the facial canal in the oval window area.

Posterior semicircular canal dehiscence: a histopathologic human temporal bone study.

BACKGROUND: Posterior semicircular canal dehiscence has been shown to cause ear symptoms. OBJECTIVE: To evaluate the incidence of dehiscence of the posterior semicircular canal, thin bone overlying the posterior semicircular canal, and the normal development of the distance between the posterior semicircular canal and posterior cranial fossa. METHODS: The shortest distance between the posterior semicircular canal and posterior cranial fossa was measured in 1,051 adult human temporal bones (557 cases), and temporal bones with a distance less than 0.1 mm were evaluated. The shortest distance also was measured in 4 fetal temporal bones (2 cases) and 110 temporal bones from children. RESULTS: Of the 1,051 temporal bones, 23 temporal bones (2.2%) had a distance less than 0.1 mm between the posterior semicircular canal and posterior cranial fossa. Two temporal bones (0.2%) had posterior semicircular canal dehiscence, and 2 temporal bones had microfractures in the thin bone; however, related clinical symptoms were not confirmed. In children, the distance between the posterior semicircular canal and the posterior cranial fossa increased with age (rho = 0.68, p < 0.01). CONCLUSION: The histopathologic incidence of posterior semicircular canal dehiscence was lower than the previous radiographic reports. The dehiscence of the posterior semicircular canal may be due to a developmental anomaly. In our study, none of the cases with a distance less than 0.1 mm had apparent symptoms related to canal dehiscence syndrome. Other factors, in addition to thinning of the bone, may be required to cause the clinical manifestations.

Membranous labyrinth volumes in normal ears and Ménière disease: a three-dimensional reconstruction study.

OBJECTIVES: The purpose of this study was to determine the normal volume ranges of cochlear duct, saccule, and utricle, and to assess endolymphatic hydrops in Ménière disease. STUDY DESIGN: Retrospective temporal bone study. METHODS: Three-dimensional (3-D) images of membranous labyrinth were reconstructed from 31 normal temporal bones, six temporal bones from three patients with bilateral Ménière disease, and 16 temporal bones from eight patients with unilateral Ménière disease. Volumes of each part of membranous labyrinth were measured in each temporal bone group after 3-D reconstruction. RESULTS: The mean volumes and upper normal volume limits (over the 95% confidence interval) of the cochlear duct, saccule, and utricle were 7.67 and 9.77 mm(3), 2.42 and 3.68 mm(3), and 10.65 and 16.45 mm(3), respectively. All three patients with bilateral Ménière disease showed endolymphatic hydrops (excess of volume over normal limits) in both ears. Of eight patients with unilateral Ménière disease, five had no symptom in the contralateral ear, whereas three patients had histories of progression from unilateral to bilateral Ménière disease 13-21 years after the initial onset. All of the diseased and three of eight contralateral ears showed endolymphatic hydrops. In contrast, no hydrops was observed in any part of the membranous labyrinth in asymptomatic ears. CONCLUSIONS: Our findings suggest that cochleosaccular hydrops is a sensitive finding in Ménière disease. In addition, the volume data obtained from this study could be useful as a standard value for the assessment of hydrops in diagnostic imaging of the inner ear in Ménière disease.

Vascular findings in the stria vascularis of patients with unilateral or bilateral Ménière's disease: a histopathologic temporal bone study.

HYPOTHESIS: There are pathologic changes of vessels in the stria vascularis in patients with Ménière's disease. BACKGROUND: The cause of Ménière's disease is under debate. METHODS: This study examined 14 temporal bones from 7 patients with bilateral Ménière's disease, 30 temporal bones from 15 patients with unilateral Ménière's disease, and 17 age-matched, normal temporal bones from 12 subjects. The temporal bones were serially sectioned in the horizontal plane at a thickness of 20 mum and stained with hematoxylin and eosin. The midmodiolar section of the cochlea was selected from each subject, and the number of vessels in the stria vascularis in each cochlear turn was counted by light microscopy. The area of the lumen of each vessel in the stria vascularis was also measured. RESULTS: The number of vessels in the stria vascularis in ears with Ménière's disease was smaller than in normal controls in all cochlear turns. The number of vessels in the contralateral stria vascularis in patients with unilateral Ménière's disease was smaller than in normal controls in all cochlear turns. There was no significant difference between the area of the vessel lumen in the stria vascularis in patients with Ménière's disease and that in normal controls. CONCLUSION: The stria vascularis may be ischemic bilaterally both in bilateral and unilateral Ménière's disease. Abnormal findings in the contralateral ears in unilateral Ménière's disease reported in previous studies might be related to poor vascularity of the stria vascularis.

Potential cause of positional vertigo in Ménière's disease.

OBJECTIVES: To compare the incidence of deposits in the semicircular canals between the temporal bones with Ménière's disease and normal controls and to investigate the relationship between the incidence of deposits and the symptoms of positional vertigo, often seen in patients with Ménière's disease. STUDY DESIGN: Retrospective histopathologic human temporal bone study. METHODS: Twenty-two temporal bones from 11 patients with bilateral Ménière's disease, 28 from 14 with unilateral and 50 age-matched normal temporal bones from 30 individuals were histopathologically examined. Medical records were reviewed for clinical history of positional vertigo and duration of disease. RESULTS: Significant differences were found in the incidence of cupular and free-floating deposits in the posterior semicircular canals between temporal bones with and without Ménière's disease. The incidence of free-floating deposits in the lateral semicircular canals was significantly higher in cases with unilateral Ménière's disease compared with controls. The incidence of these deposits was associated with the duration of disease rather than with aging. All 5 patients with positional vertigo (3 of 11 patients of bilateral Ménière's disease and 2 of 14 of unilateral) had free-floating deposits in at least 1 semicircular canal. CONCLUSION: Our findings suggest a possible causative relationship between cupular and free-floating deposits in the semicircular canals and the symptom of positional vertigo in patients with Ménière's disease.

Vascular findings in the facial nerve canal in human temporal bones with diabetes mellitus.

OBJECTIVE: To identify pathological changes to vessels in the facial nerve canal among patients with diabetes mellitus. DESIGN: Histopathologic human temporal bone study. SUBJECT: This study examined 26 temporal bones from 13 patients with type 1 diabetes mellitus and 40 temporal bones from 20 patients with type 2 diabetes mellitus. Temporal bones from patients with type 2 diabetes mellitus were divided into 2 groups according to the method of diabetes management: insulin (n = 11) and oral hypoglycemic agents (n = 9). For the control groups, 16 age-matched normal temporal bones from 11 subjects were recruited for type 1 diabetes mellitus and 11 age-matched normal temporal bones from 8 subjects were recruited for type 2 diabetes mellitus. MAIN OUTCOME MEASURES: Thicknesses of vessel walls in the labyrinthine, tympanic, and mastoid portions of the facial nerve canal were examined under light microscopy. RESULTS: Vessel walls for all portions of the facial nerve canal were significantly thicker in diabetic patients than in normal controls for both types 1 and 2 diabetes. In type 2 diabetic patients, vessel wall thickness was significantly greater in patients treated with insulin therapy than in patients treated via oral hypoglycemic agents. CONCLUSION: The facial nerve in patients with diabetes mellitus is ischemic compared with normal controls. These findings suggest a histologic basis for the high incidence and difficulty in achieving improvement of facial nerve palsy in patients with diabetes mellitus.

Generalized arteriosclerosis and changes of the cochlea in young adults.

HYPOTHESIS: To disclose the histopathologic findings of the cochlea in young adults with generalized arteriosclerosis. BACKGROUND: It is well known that arteriosclerosis begins and progresses during childhood. Although the relationship between arteriosclerosis and auditory function in elderly people was examined in many reports, the histopathologic effect of arteriosclerosis on the cochlea in young adults has not been studied. METHODS: This study involved quantitative analysis, including the number of spiral ganglion cells, the loss of cochlear outer hair cells, and the areas of stria vascularis and spiral ligament. It included 10 temporal bones from 6 subjects with generalized arteriosclerosis and 10 age-matched normal control temporal bones from 7 subjects. RESULTS: The mean number of spiral ganglion cells in the cochlea with generalized arteriosclerosis was significantly lower than that in normal controls in the basal turn. The mean loss of outer hair cells in the cochlea with generalized arteriosclerosis was significantly greater than that of normal controls in the basal and apical turns. The stria vascularis and spiral ligament were severely atrophic, with generalized arteriosclerosis in the basal turn. There was no significant difference in the thickness of the spiral modiolar artery between generalized arteriosclerosis and normal controls. CONCLUSION: Degeneration of the cochlea, especially in the basal turn, was already apparent in young adults with generalized arteriosclerosis.

CRTH2 plays an essential role in the pathophysiology of Cry j 1-induced pollinosis in mice.

PGD(2) is the major prostanoid produced during the acute phase of allergic reactions. Two PGD(2) receptors have been isolated, DP and CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells), but whether they participate in the pathophysiology of allergic diseases remains unclear. We investigated the role of CRTH2 in the initiation of allergic rhinitis in mice. First, we developed a novel murine model of pollinosis, a type of seasonal allergic rhinitis. Additionally, pathophysiological differences in the pollinosis were compared between wild-type and CRTH2 gene-deficient mice. An effect of treatment with ramatroban, a CRTH2/T-prostanoid receptor dual antagonist, was also determined. Repeated intranasal sensitization with Cry j 1, the major allergen of Cryptomeria japonica pollen, in the absence of adjuvants significantly exacerbated nasal hyperresponsive symptoms, Cry j 1-specific IgE and IgG1 production, nasal eosinophilia, and Cry j 1-induced in vitro production of IL-4 and IL-5 by submandibular lymph node cells. Additionally, CRTH2 mRNA in nasal mucosa was significantly elevated in Cry j 1-sensitized mice. Following repeated intranasal sensitization with Cry j 1, CRTH2 gene-deficient mice had significantly weaker Cry j 1-specific IgE/IgG1 production, nasal eosinophilia, and IL-4 production by submandibular lymph node cells than did wild-type mice. Similar results were found in mice treated with ramatroban. These results suggest that the PGD(2)-CRTH2 interaction is elevated following sensitization and plays a proinflammatory role in the pathophysiology of allergic rhinitis, especially pollinosis in mice.