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Anatomy and Physiology of Balance
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Nishchay Mehta, Andrew Forge, Jonathan Gale
The vestibular system is housed in the labyrinth of each ear. The main components of the vestibular system are three semicircular canals and two otolith organs (utricle and saccule). The three semicircular canals (superior, posterior, and lateral) detect angular acceleration in orthogonal planes. The utricle and saccule detect linear acceleration in primarily horizontal and vertical planes, respectively, as well as head position in relation to gravity.
Dizziness
Published in Henry J. Woodford, Essential Geriatrics, 2022
The labyrinthine structures form a key part of the peripheral vestibular system. They include three semi-circular canals that contain sensory structures and fluid (seeFigure 13.2). They are able to detect rotational movement. Benign paroxysmal positional vertigo (BPPV) is caused by free-floating debris within these semi-circular canals that causes inappropriate activation of the sensory structures. It presents as acute episodes of short-lasting vertigo (seconds to minutes) often induced by specific movements such as rolling over in bed or looking up to hang out washing. There may be associated nausea and vomiting. It can be diagnosed by the Hallpike test – seeFigure 13.3. It is best treated by the Epley manoeuvre – a series of movements that transfer the debris within the semi-circular canal into the utricle where it no longer causes any symptoms.7
Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
The utricle and saccule sense linear acceleration of the head. Both are expansions of the membranous labyrinth and contain a macula, which consists of hair cells covered by an otolithic membrane (lying on top of the hair cells) and otoconia (composed of calcium carbonate crystals or otoliths) on the surface. The movement of the otoliths deflects the hair cells.
The value of vestibular evoked myogenic potential and electrocochleography in unexplained aural fullness
Published in Acta Oto-Laryngologica, 2022
A study on Menière’s disease (MD) reported that EH was significantly associated with the disappearance of cVEMP [15]. It has been reported that 54% of MD patients had absence of cVEMP responses to clicks on the affected side. A recent study showed that the sensitivity and specificity of cVEMP is 50.0% and 48.9%, respectively [16]. A simple abnormal finding, such as absence of responses or decreased amplitudes, does not always indicate the existence of EH. In our study, we observed that absence of responses or a decreased VEMP amplitude existed in 38.9% of patients with unexplained aural fullness. This result indicated that unexplained aural fullness in 38.9% of patients might be associated with EH. In addition, we found that the proportion of patients with an abnormal oVEMP was significantly greater than cVEMP in 54 patients with unexplained aural fullness. This finding indicated that hydrops in the utricle might be more common than the saccule in these patients. Maheu et al. [13] reported that the ECochG SP/AP area ratio was greater in unexplained aural fullness ears than healthy ears. However, in our study, it showed that there was no significant difference in EcochG abnormal rate between patients with unexplained aural fullness and healthy volunteers. Moreover, we found that the VEMP abnormal rate was greater than the EcochG abnormal rate in 54 patients with unexplained aural fullness. This result suggested that EH in patients with unexplained aural fullness was not common in the membranous cochlea, but common in the utricle or saccule.
Comparison of furosemide-loading cervical vestibular-evoked myogenic potentials with magnetic resonance imaging for the evaluation of endolymphatic hydrops
Published in Acta Oto-Laryngologica, 2020
Ko Shiraishi, Noriko Ohira, Takaaki Kobayashi, Mitsuo Sato, Yasuhiro Osaki, Katsumi Doi
The MRI data were evaluated by two specialized neurotologists, who were blinded to the clinical progress of the patients. Differences in their evaluations were resolved by discussion until a final decision was reached. The degree of EH in the vestibule and cochlea was assessed by visual comparison of the hypointense signal areas of each part (cochlea, saccule, utricle) of the endolymphatic space versus the hyperintense signal of the perilymphatic space in the axial plane according to the criteria reported by Kahn et al. [13]. The degree of cochlear hydrops was categorized as none or grade I, when the area of the endolymphatic space exceeded the area of the scala vestibule. We did not consider the cochlear duct to be pathological when its area was less than that of the scala vestibule, because 30% of healthy subjects may present with this finding. The degree of saccular hydrops was defined as none; grade I, when the saccule appeared larger or equal to the utricle, surrounded by perilymphatic space; or grade II, when the saccule touched the oval window, without surrounding perilymphatic space. The degree of utricular hydrops was defined as none; grade I, herniation of the utricle in the nonampullated part of the lateral semicircular canal; or grade II, when there was no surrounding perilymphatic space.
Comparing the sensitivity and specificity of cervical vestibular-evoked myogenic potentials and electrocochleography in the diagnosis of Ménière’s disease
Published in International Journal of Audiology, 2019
Faten Saeed Obeidat, Steven Lewis Bell
In 1861, Prosper Ménière described a new disease that affected the inner ear, which was characterised by episodic spells of vertigo lasting several minutes and was associated with tinnitus, ear fullness, and fluctuating hearing loss (Stapleton and Mills 2008). It is believed to be caused by an abnormal accumulation of endolymph fluid termed endolymphatic hydrops (EH) most often in the cochlear duct and the sacculus followed by the utricle and the semi-circular canals, respectively based on evidence from human temporal bones studies (Merchant, Adams, and Nadol 2005), although hydrops alone does not explain the mechanism underlying all the clinical symptoms of the disease, including the progression of hearing loss and the frequency of vertigo attacks (Rauch, Merchant, and Thedinger 1989). It has been shown that whilst all patients with Ménière’s disease (MD) symptoms in life show evidence of EH in at least one ear post-mortem, there are also patients with EH without signs or symptoms of MD (Merchant, Adams, and Nadol 2005; Rauch, Merchant, and Thedinger 1989). This suggests that pre-existing hydrops is not directly responsible for the symptoms of MD, but it can merely be an epiphenomenon of the pathophysiological mechanism of the disease (Merchant, Adams, and Nadol 2005).