Hironao Otake

Endolymphatic hydrops revealed by intravenous gadolinium injection in patients with Ménière's disease

CONCLUSION Visualization of endolymphatic hydrops became possible after intravenous gadolinium (Gd) injection in patients with Ménières disease. OBJECTIVE To visualize endolymphatic hydrops after intravenous Gd injection. METHODS Gd (gadoteridol; 0.2 mmol/kg) was injected intravenously in three patients with unilateral Ménières disease. We performed three-dimensional fluid attenuated inversion recovery (3D-FLAIR) and three-dimensional real inversion recovery (3D-real IR) magnetic resonance imaging (MRI) 4 h after the injection using a 3-Tesla MRI unit. We used a 32-channel array coil to obtain a high signal-to-noise ratio. RESULTS Endolymphatic hydrops was observed in the ears of patients with Ménières disease. However, Gd concentration in the perilymph was lower compared with that obtained after intratympanic Gd injection.

Endolymphatic hydrops and blood-labyrinth barrier in Ménière's disease.

Abstract Conclusions: The blood–labyrinth barrier is impaired in association with the hydrops grade in Ménières disease. Objectives: To investigate the relationship between endolymphatic hydrops and the clinical characteristics of patients with Ménières disease revealed by 3 T magnetic resonance imaging (MRI). Methods: A double dose of gadoteridol (Gd; 0.2 mmol/kg) was injected intravenously in 12 patients with Ménières disease. We performed three-dimensional fluid attenuated inversion recovery MRI and three-dimensional real inversion recovery MRI 4 h later using a 3 T MRI unit. Ten patients had unilateral and two had bilateral Ménières disease. Results: Fourteen ears with Ménières disease showed intense Gd contrast on MRI compared with that in the 10 asymptomatic contralateral ears of patients with unilateral Ménières disease (1.12 ± 0.36 vs 0.82 ± 0.15). The hydrops grade was correlated significantly with the contrast effect. The 14 ears with Ménières disease had endolymphatic hydrops. Of the 10 contralateral ears of patients with unilateral Ménières disease, 2 had endolymphatic hydrops in the cochlea and 6 had endolymphatic hydrops in the vestibule.

Relationship between the Degree of Endolymphatic Hydrops and Electrocochleography

The purpose of this study was to evaluate the relationship between the endolymphatic space image obtained using magnetic resonance imaging (MRI) and the results of electrocochleography. Electrocochleography recordings were obtained from 25 ears of 24 patients, who underwent MRI 1 day after the intratympanic injection of gadolinium diethylenetriamine pentaacetic acid bismethylamide. The average summating potential to action potential (SP/AP) ratio in patients with significant endolymphatic hydrops in the cochlea was 54 ± 17%. However, in some patients who had significant endolymphatic hydrops in the cochlea, the SP/AP ratio was not enlarged. This may imply that elevation of the SP/AP ratio is related to not only the degree of endolymphatic hydrops but also to the persistence of hydrops.

3 Tesla magnetic resonance imaging obtained 4 hours after intravenous gadolinium injection in patients with sudden deafness

Conclusion: 3 Tesla (3T) magnetic resonance imaging (MRI) performed 4 h after intravenous gadolinium (Gd) injection provides sufficient anatomic resolution of the inner ear fluid spaces in sudden deafness. The signal intensity ratio (SIR) between the cochlea and cerebellum may be a good indicator of disruption of the blood–labyrinthine barrier. Objectives: We evaluated the inner ear 4 h after intravenous Gd injection to determine whether 3T MRI enables the acquisition of images of the affected inner ear in sudden deafness. Methods: Ten patients underwent 3T MRI scanning 4 h after intravenous Gd injection. Three-dimensional fluid-attenuated inversion recovery (3D-FLAIR) MRI was performed. Results: The SIR varied from 0.45 to 2.17 in 11 affected ears and from 0.43 to 1.48 in 9 unaffected ears. The difference of contrast (affected ear vs unaffected ear) could be detected in five of the nine patients with unilateral sudden deafness. The Gd distribution was recognized in the vestibule of 10 affected ears and in the cochlea of 5 affected ears, in which no significant hydrops was observed. In the remaining vestibules and cochleas of affected ears, the Gd enhancement was too faint to evaluate the endolymphatic hydrops.

Endolymphatic Hydrops Revealed by Magnetic Resonance Imaging in Patients With Acute Low-Tone Sensorineural Hearing Loss

Objective Acute low-tone sensorineural hearing loss (ALHL) has been reported to be associated with endolymphatic hydrops (EHs). However, evaluation of the size of the endolymphatic space has not been reported. We attempted to visualize EH in ALHL using magnetic resonance imaging (MRI). Study Design Prospective diagnostic study. Setting University hospital. Methods We evaluated 25 ears of 25 unilateral ALHL patients. Three-tesla MRI was obtained 24 hours after intratympanic injection of gadolinium (Gd) (n = 5) or 4 hours after intravenous injection of Gd (n = 20). A radiologist blinded to the patients’ clinical data classified the degree of EH in the vestibule and cochlea into 3 groups: none, mild, and significant. Results On the affected sides, cochlear EH was recognized in 23 ears (92%) and was classified as significant EH (n = 15) or mild EH (n = 8); vestibular EH was detected in 22 ears (88%), classified as significant EH (n = 16) or mild EH (n = 6). Cochlear EH was more frequently observed in the affected ear than in the contralateral ear (90% versus 40%, p < 0.05). Conclusion In ALHL, EH was observed not only in the cochlea but also in the vestibule as in Ménière’s disease.

Endolymphatic hydrops revealed by magnetic resonance imaging in patients with atypical Meniere's disease

Abstract Conclusion: Our study showed that patients with atypical Menieres disease had endolymphatic hydrops (EH) in both the cochlea and the vestibule. Using an imaging method, we provide evidence that atypical Menieres disease is a true variant of classic Menieres disease. Objectives: The aim of present study was to investigate images of the endolymphatic space in patients with atypical Menieres disease (cochlear and vestibular Menieres disease). Methods: Sixty-four patients divided into two groups were enrolled in this study. The first group included 36 patients who had fluctuating hearing loss without vertigo, as candidates for cochlear Menieres disease (CMD). The second group included 28 patients who had recurrent vertigo without hearing loss, as candidates for vestibular Menieres disease (VMD). The patients underwent 3 T magnetic resonance imaging (MRI) after injection of gadolinium enhancement medium intratympanically or intravenously. We evaluated EH using MRI. Results: Of 56 ears (36 patients) with CMD, 38 showed EH in the cochlea and 44 showed EH in the vestibule. Of 56 ears (28 patients) with VMD, 29 showed EH in the cochlea and 47 showed EH in the vestibule. The VMD group had a significant vestibular predominance in EH distribution whereas the CMD group showed no significant regional predominance of EH.

Association of interleukin‐1 gene polymorphisms with sudden sensorineural hearing loss and Ménière’s disease

Sudden sensorineural hearing loss (SSNHL) and Ménière’s disease are the most common inner ear diseases in which the causes are unknown. As recent magnetic resonance imaging has demonstrated disruption of the blood–labyrinth barrier in these inner ear diseases, inflammatory reaction associated with increased permeability of the blood vessels may be involved. The genotypes of interleukin 1A (IL1A) (−889C/T; rs1800587) and interleukin 1B (IL1B) (−511C/T; rs16944) were determined using an allele‐specific primer–polymerase chain reaction method in 72 patients with SSNHL, 68 patients with Ménière’s disease, and 2202 control subjects living almost in the same area as the patients. A significantly higher prevalence of the IL1A−889T allele was observed in SSNHL and Ménière’s disease compared with controls, although no significant difference in distribution of IL1B−511C/T genotypes was observed between the patients and controls. Adjusted odd ratios for SSNHL and Ménière’s disease risks in the −889TT genotypes were 25.89 (95% confidence interval (CI) 12.19–54.98) and 18.20 (95% CI 7.80–42.46), respectively, after age and gender were taken as moderator variables. Our results suggested that IL1A is closely associated with susceptibility of SSNHL and Ménière’s disease.

Polymorphisms in Genes Involved in Inflammatory Pathways in Patients with Sudden Sensorineural Hearing Loss

Abstract: Although the etiology of idiopathic sudden sensorineural hearing loss (SSNHL) remains unclear, the pathologically increased permeability of blood vessels, elucidated by gadolinium-enhanced magnetic resonance imaging (MRI), suggests the involvement of inflammation. Because SSNHL is considered a multifactorial disease, possibly caused by interactions between genetic factors and environmental factors, the authors investigated the associations of polymorphisms of inflammatory mediator genes with susceptibility to SSNHL. The authors compared 72 patients affected by SSNHL and 2010 adults (1010 men and 1000 women; mean age 59.2 years; range 40–79) who participated in the National Institute for Longevity Sciences Longitudinal Study of Aging. Multiple logistic regression was used to obtain odds ratios (ORs) for SSNHL in subjects with polymorphisms in the genes IL-6 C − 572G, IL-4R G1902A, IL-10 A − 592C, TNFα C − 863A, TNFRSF1B G593A, VEGF C936T, VEGF C − 2578A, and VEGF G − 1154A, with adjustment for age, gender, and any history of hypertension, diabetes, or dyslipidemia. The per-allele OR for the risk of SSNHL in subjects bearing IL-6 C − 572G was 1.480 (95% confidence interval [CI], 1.037–2.111) in model 1 (no adjustment), 1.463 (CI, 1.022–2.094) in model 2 (adjusted for age and gender), and 1.460 (CI, 1.016–2.097) in model 3 (adjusted for age, gender, and a history of hypertension, diabetes, or dyslipidemia). Under the dominant model of inheritance, the ORs were 1.734 (CI, 1.080–2.783) in model 1, 1.690 (CI, 1.050–2.721) in model 2, and 1.669 (CI, 1.035–2.692) in model 3. The remaining seven polymorphisms failed to show any associations with the risk of SSNHL. These data need to be confirmed on larger series of patients. In conclusion, the IL-6 C − 572G polymorphism is associated with a risk of SSNHL. Because permeability of blood vessels in the inner ear is frequently increased in patients with SSNHL, inflammation of the inner ear might be involved.

Relationship between adenoid size and severity of obstructive sleep apnea in preschool children

OBJECTIVE To investigate the contributions of adenoid and tonsil sizes to obstructive sleep apnea syndrome (OSAS) in normal-weight children in two age categories: preschool and schoolchildren. METHODS Fifty-eight normal-weight (body mass index z-score<2) symptomatic children with OSAS (apnea-hypopnea index ≥ 2) were evaluated. The patients were divided into two age categories: preschool (age<6; n=33) and schoolchildren (age ≥ 6; n=25). Polysomnographic findings and adenoid and tonsil sizes were compared. The relative contributions of body mass index and adenoid and tonsil sizes were also investigated with a regression analysis. RESULTS Adenoid grade and apnea index correlated significantly in preschool children (r=0.45, p<0.01). On regression analysis, adenoid grade was a significant predictor of the apnea index in preschool children. The influence of adenoid hypertrophy decreased from preschool to schoolchildren. Tonsil size had little influence on the apnea index in either group. CONCLUSION Adenoid hypertrophy was a major contributor to OSAS in normal-weight preschool children. The upper airway morphology of younger children with OSAS differed from that of older children with OSAS.

Children with severe or moderate obstructive sleep apnoea syndrome show a high incidence of persistence after adenotonsillectomy

Abstract Conclusion: Persistent obstructive sleep apnoea syndrome (OSAS) occurs in approximately 20% of normal-weight children after adenotonsillectomy (T&A) and, in nearly 70% of them, it is caused by adenoid regrowth. Patients with severe or moderate OSAS showed a high incidence of persistent disease even after T&A. Allergic disease, severity and large adenoid size are associated with adenoid regrowth and persistent disease. Objectives: To investigate factors contributing to persistent OSAS and adenoid regrowth after T&A in normal-weight children. Methods: This was a prospective, observational study at a single institute and involved 49 normal-weight children with severe or moderate OSAS (apnoea–hypopnoea index, AHI, ≥ 5) who underwent T&A. Background information, nasal endoscopic data and pre- and postoperative polysomnographic data were collected. A third polysomnography (PSG) was performed 1.5 year postoperatively in children who subsequently developed symptoms of sleep disturbance. Results: Thirteen children (27%, 13/49) were symptomatic 1.5 years after T&A. Allergic rhinitis (38.5% vs 11.1%, p = 0.03) and allergic disease (69.2% vs 30.6%, p = 0.02) were seen more frequently in these children. A third PSG confirmed persistent disease (AHI ≥ 5) in nine children (18.4%, 9/49). Six children (12.2%, 6/49) were diagnosed as having adenoid regrowth and three (6.1%, 3/49) underwent revision adenoidectomy.