Background: Lindsay-Hemenway syndrome was first described as an acute unilateral peripheral vestibulopathy followed by positional vertigo. A vascular etiology was proposed. An association between cardiovascular risk factors and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy has been described with contradictory evidence. The study aimed to evaluate the prevalence of cardiovascular risk factors in patients with benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy and analyze differences in prior history of benign paroxysmal positional vertigo, affected semicircular canals, and response to repositioning maneuvers between patients with idiopathic benign paroxysmal positional vertigo and secondary to acute unilateral peripheral vestibulopathy.
Methods: We performed a retrospective, descriptive study of all cases of benign paroxysmal positional vertigo between January/2017 and June/2020, with or without a history of acute unilateral peripheral vestibulopathy within the previous year. Cases secondary to trauma or otoneurological causes and acute unilateral peripheral vestibulopathy without confirmatory tests and cases with auditory symptoms were excluded.
Results: In total, 242 cases were obtained; 158 idiopathic benign paroxysmal positional vertigo and 84 secondary to acute unilateral peripheral vestibulopathy. No statistically significant differences were found in relation to age: 61.2 ± 14.6 versus 62.4 ± 16.2 years (P=.55), sex: female 78.5% versus 73.8% (P=.41), presence of cardiovascular risk factors: 52.5% versus 54.8% (P=.67), prior history of benign paroxysmal positional vertigo: 22.2% versus 27.7% (P=.43), affected semicircular canals (P=.16) or number of repositioning maneuvers (P=.57).
Conclusion: Associations between age, cardiovascular risk factors, and benign paroxysmal positional vertigo secondary to acute unilateral peripheral vestibulopathy have been described with conflicting evidence. This is the first study to evaluate cardiovascular risk factors specifically for Lindsay-Hemenway syndrome, and we did not observe any differences between idiopathic benign paroxysmal positional vertigo cases and those secondary to acute unilateral peripheral vestibulopathy.
Background: Vestibular schwannoma is a benign intracranial tumor of the vestibulocochlear nerve. Although it is a well-known pathology, growth factors and cytokine changes in vestibular schwannoma patients have not been totally elucidated. The objective of our study was to evaluate the concentration changes of transforming growth factor beta1, vascular endothelial growth factor, immunoglobulins A, M, and carcinoembryonic antigen in vestibular schwannoma patients.
Methods: In our study, we performed an immunological analysis of 35 patients with vestibular schwannoma of different stages. According to the evolution of vestibular schwannoma, 20 patients did not show tumor growth, but 15 patients had a growing tumor.
Results: The level of vascular endothelial growth factor in the blood serum of study groups exceeded the control values by 8 times and transforming growth factor beta1 by 1.65. Increased values of immunoglobulin A and immunoglobulin M were observed in patients with intracanal, second, and third stages of tumor, compared with the control group. Carcinoembryonic antigen was found to be of increased values in patients with intracanal and third-stage vestibular schwannoma, in comparison to the control group.
Conclusion: Growth factors such as vascular endothelial growth factor and transforming growth factor beta1 can play a significant role in the genesis of vestibular schwannoma. In vestibular schwannoma patients, their investigation is appropriate both in the process of monitoring and in the assessment of treatment effectiveness. Immunoglobulins M and A can be used as additional markers of vestibular schwannoma, especially in tumor growth. Carcinogenic embryonic antigen has high values only in the late stages of vestibular schwannoma development.
Background: Stress could be a contributing cause of sudden hearing loss. This study intended to develop an animal model of stress-induced sudden hearing loss and to evaluate the effects of dexamethasone.
Methods: Two stress models (I and II) for rats were designed using various stressors and modified by adjusting the stress protocol to increase the threshold significantly. For the stress model with a significant increase in threshold after stress exposure, changes in cortisol levels according to stress exposure were measured. The threshold shift and the change in the cellular structure associated with stress exposure and dexamethasone administration were analyzed.
Results: While hearing thresholds increased only at 16 kHz in rats of stress model I (n=10), the thresholds increased at 16 and 32 kHz in rats of stress model II (n=16). Cortisol level increased after stress exposure (P = .015) in stress model II. Among stress model II rats (stress only and stress+dexamethasone groups), the threshold shift at 16 kHz significantly decreased 1 day after dexamethasone injection in the stress+dexamethasone group (n=8). Histologically, the cochlear cellularity of the stress+dexamethasone group was more compact than that of the stressonly group (n=8).
Conclusion: Our preliminary study presented the development of an animal model of stress-induced sudden hearing loss and the positive results of steroids in terms of hearing recovery.
Background: Surgical rehearsal - patient-specific preoperative surgical practice - can be provided by virtual reality simulation. This study investigated the effect of surgical rehearsal on cortical mastoidectomy performance and procedure duration.
Methods: University students (n=40) were randomized evenly into a rehearsal and control group. After watching a video tutorial on cortical mastoidectomy, participants completed the procedure on a virtual reality simulator as a pre-test. Participants completed a further 8 cortical mastoidectomies on the virtual reality simulator as training before drilling two 3-dimensional (3D) printed temporal bones. The rehearsal group received 3D printed bones they had previously operated on in virtual reality, while the control group received 2 new bones. Cortical mastoidectomy was assessed by 3 blinded graders using the Melbourne Mastoidectomy Scale.
Results: There was high interrater reliability between the 3 graders (intraclass correlation coefficient, r=0.8533, P < .0001). There was no difference in the mean surgical performance on the two 3D printed bones between the control and rehearsal groups (P=.2791). There was no significant difference in the mean procedure duration between the control and rehearsal groups for both 3D printed bones (P=.8709). However, there was a significant decrease in procedure duration between the first and second 3D printed bones (P < .0001).
Conclusion: In this study, patient-specific virtual reality rehearsal provided no additional advantage to cortical mastoidectomy performance by novice operators compared to generic practice on a virtual reality simulator. Further, virtual reality training did not improve cortical mastoidectomy performance on 3D printed bones, highlighting the impact of anatomical diversity and changing operating modalities on the acquisition of new surgical skills.
Migraine and vertigo are common complaints seen in clinical practice, and in a few such cases, we also find epileptic manifestations, including migraine-triggered seizures. Currently, patients presenting with vertigo and headache are diagnosed according to established diagnostic criteria for Meniere's disease, vestibular migraine, or vestibular migraine/Meniere's disease overlapping syndrome. In addition to using those diagnostic criteria and the patient's history, cervical vestibular evoked myogenic potential and auditory middle latency responses are useful tools to better understand the physiological background of these patients and also to confirm the diagnosis. Here we report 2 cases: 1 of vestibular migraine/ Meniere's disease overlapping syndrome and 1 of vestibular migraine with epileptic manifestations. Each patient showed potentiation (lack of habituation) in auditory middle latency response, and each showed endolymphatic hydrops in cervical vestibular evoked myogenic potential. The potentiation in auditory middle latency response might be attributable to neuronal hyperexcitability in those patients with migraine or epilepsy, and neurogenic inflammation caused by migraine episodes might affect inner ear function.
Background: Hearing loss is frequently associated with reduced postural control. This is possibly not only related to simultaneous pathophysiological changes within the hearing and vestibular system. The auditory input itself could provide helpful information for maintaining postural control. Previous studies of our group already showed that continuous or interrupted white noise can significantly improve postural control during gait conditions in young healthy individuals. The present study aimed at investigating if those effects are also active in the elderly.
Methods: Elderly volunteers (mean age 67 years) without any history of disorders to influence gait performance successfully completed 5 walking tasks under 4 different acoustic conditions. Angular sway velocity was measured close to the center of gravity with the Vertiguard® system.
Results: Significant changes in body sway velocity were found in 4 of 5 investigated tasks. Only "walking with turning head in rhythm" was not associated with any change in the acoustic input. The sway increased by 8.9% during "walking with open eyes" in the pitch direction and by 11.5% during "tandem walking" in the roll direction if ear protection was applied. The sway was reduced by 9.1% during "walking over barriers" in the pitch direction and by 16.7% in the roll direction during "walking with closed eyes" if a stationary source of continuous white noise was presented.
Conclusion: The data of the present study indicate that auditory information could significantly alter postural control during walking in the elderly. Continuous white noise seems to be helpful for maintaining balance in different walking tasks.
Background: This study aimed to investigate the outcomes of pediatric patients with acute mastoiditis while examining the role of intravenous steroid therapy, patient demographics, and serum inflammatory values as prognostic factors.
Methods: This study is a single-center retrospective observational study including 73 consecutive patients treated for acute mastoiditis in the course of the 10-year study period (January 2010 to December 2019).
Results: Data analysis showed that patients requiring surgical treatment (14%) had a 3-fold higher C-reactive protein value at admission compared to those treated conservatively (P < .001). Receiver operating characteristic analysis revealed that a C-reactive protein cut-off of ≥98.7 had a sensitivity and specificity of 100% and 74.6%, respectively, for predicting the need for surgery (area under the curve=0.927, P < .001). The duration of symptoms before hospitalization was nearly 2 days shorter in male patients (P=.031), and the use of intravenous steroid therapy significantly shortened the length of hospitalization (P=.023), by 1.4 days on average.
Conclusion: Intravenous steroid therapy may be useful in decreasing the length of hospital stay. Mastoiditis tends to present more severely in male patients, and monitoring C-reactive protein values during treatment correlated well with the need for surgery.
Background: This study investigates the test-retest reliability, aging effects, and differences in horizontal semicircular canals gain values between the head impulse paradigm and suppression head impulse paradigm.
Methods: Sixty healthy adult subjects aged 22-76-year-old (mean ± standard deviation=47.27 ± 18.29) participated in the head impulse paradigm and suppression head impulse paradigm using the video head impulse test. The Head impulse paradigm was used to assess all 6 semicircular canals, while suppression head impulse paradigm measured only the horizontal canals. Twenty subjects aged 22-40-year-old (25.25 ± 4.9) underwent a second session for the test-retest reliability.
Results: There were good test-retest reliability for both measures (right horizontal head impulse paradigm, intraclass correlation coefficient=0.80; left horizontal head impulse paradigm, intraclass correlation coefficient=0.77; right anterior head impulse paradigm, intraclass correlation coefficient=0.86; left anterior head impulse paradigm, intraclass correlation coefficient=0.78; right posterior head impulse paradigm, intraclass correlation coefficient=0.78; left posterior head impulse paradigm, intraclass correlation coefficient=0.75; right horizontal suppression head impulse paradigm, intraclass correlation coefficient=0.76; left horizontal suppression head impulse paradigm, intraclass correlation coefficient=0.79). The test-retest reliability for suppression head impulse paradigmanti-compensatory saccade latency and amplitude were moderate (right latency, intraclass correlation coefficient=0.61; left latency, intraclass correlation coefficient=0.69; right amplitude, intraclass correlation coefficient=0.69; left amplitude, intraclass correlation coefficient=0.58). There were no significant effects of age on head impulse paradigm and suppression head impulse paradigm vestibulo-ocular reflex gain values and suppression head impulse paradigmsaccade latency. However, the saccade amplitude became smaller with increasing age, P < .001. The horizontal suppression head impulse paradigm vestibuloocular reflex gain values were significantly lower than the head impulse paradigm for both sides (right, P = .004; left, P = .004).
Conclusion: There was good test-retest reliability for both measures, and the gain values stabilized with age. However, suppression head impulse paradigm anti-compensatory saccade latency and amplitude had lower test-retest reliability than the gain. The suppression head impulse paradigm vestibulo-ocular reflex gain was lower than the head impulse paradigm and its anti-compensatory saccade amplitude reduced with increasing age.
Background: Few investigations have been conducted on the clinical characteristics of the differential diagnosis of acoustic neuroma with acute sensorineural hearing loss and idiopathic sudden sensorineural hearing loss. The aim of the study was to investigate the clinical characteristics of the differential diagnoses between acoustic neuroma and idiopathic sudden sensorineural hearing loss.
Methods: The medical records of patients with acute sensorineural hearing loss (142 ears), including acoustic neuroma (19 ears) and idiopathic sudden sensorineural hearing loss (123 ears), who underwent audiometric and hematologic examinations and received systemic corticosteroid treatment, were retrospectively reviewed.
Results: Hematological examination revealed that the erythrocyte sedimentation rate and fibrinogen values were significantly higher in the idiopathic sudden sensorineural hearing loss group compared to the acoustic neuroma group. Although all patients received corticosteroid treatment, hearing thresholds at the initial examination and 3 months after corticosteroid treatment were significantly higher in the idiopathic sudden sensorineural hearing loss group compared to the acoustic neuroma group at all frequencies. However, hearing recovery was worse in the acoustic neuroma group compared to the idiopathic sudden sensorineural hearing loss group. Furthermore, speech discrimination and short increment sensitivity index tests were not significantly different between the acoustic neuroma and idiopathic sudden sensorineural hearing loss groups.
Conclusion: This is the first study to reveal that speech discrimination and short increment sensitivity index tests are not useful for the differential diagnoses between acoustic neuroma and idiopathic sudden sensorineural hearing loss, whereas erythrocyte sedimentation rate and fibrinogen, blood biomarkers of inflammation and blood viscosity, would be considered valuable. Furthermore, acoustic neuroma should be considered in cases where acute sensorineural hearing loss did not recover after corticosteroid treatment, although the initial hearing loss was mild.
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