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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 first-order sensory neurons of the vestibular pathway are bipolar cells located in Scarpa's ganglion (vestibular ganglion), in the fundus of the internal auditory meatus. The vestibular portion of the membranous labyrinth is divided into two sections: kinetic labyrinth (formed by the semicircular canals), and the static labyrinth (formed by the saccule and utricle). The vestibular bipolar neurons send peripheral projections to the hair cells in the semicircular canals, saccule, and utricle. Their central projections are to the four vestibular nuclei in the brainstem (lateral, medial, superior, and inferior) located in the caudal pons and rostral medulla. From the vestibular nuclei, central fibers are projected to the nuclei of the CNs responsible for extraocular movements (through the medial longitudinal fasciculus), the spinal cord (via the lateral and medial vestibulospinal tracts), and the flocculonodular lobe of the cerebellum.37
Anatomy of the Cochlea and Vestibular System: Relating Ultrastructure to Function
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
The maculae of the utricle and saccule are flat sheets of epithelium that are oriented at right angles to each other (Figure 47.2a), the utricle in the anterior–posterior plane, the saccule in the superior–inferior. The utricular macula is approximately U-shaped and the saccular macula, in mammals, is almost S-shaped (Figure 47.3a,b). The cristae ampullares of the semicircular canals are saddle-shaped epithelial mounds (Figure 47.3c) contained within swellings, the ampullae, which open to the utricle at one end. The cell bodies of the nerves that innervate the sensory cells of the vestibular system are collected together in Scarpa’s or vestibular ganglion, which is just external to the medial wall of the inner ear (Figure 47.2a).
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Only Carpenter and Sutin were noted to label the myelinated cell body explicitly as an “axon” (1983, p. 92 [Fig. 4–41]). However, some other authors do use phrasing that suggests it is functionally axonic. For example, Williams and Warwick state that “The vestibular nerve supplies the utricle, the saccule and the … semicircular ducts. The vestibular ganglion … is situated in the trunk of the nerve …. On the distal side of the ganglion the nerve divides. …” (1980, p. 1213)
White Matter Hyperintensities (WMH) and clinical outcome after vestibular neuritis
Published in Neurological Research, 2022
Huimin Fan, Jing Feng, Melissa Wills, Liying Wang, Xiaomeng Chen, Xiaokun Geng, Yuchuan Ding
In our study, we found that only 8 (18.6%) patients have a history of preceding or accompanying viral infection. Therefore, the cause of VN is not completely understood at the present, as viral infection is evidently not responsible for all cases. The leading hypothesis involves reactivation of a latent neurotropic virus[16]. The hypothesis is based on the findings of HSV type 1 DNA in human vestibular and other cranial nerve ganglia on autopsy[17] and the finding of Herpes simplex virus type 1 in the saliva of the patients with Vestibular Neuronitis[18]. Interestingly, there is no intrinsic difference in HSV-1 infection or virion production between superior and inferior VN. In our study, the superior VN subtype was identified in 31 of 43 patients (72.1%). Only 1 of 43 patients (2.3%) demonstrated exclusively inferior VN affecting saccule function, implying that other factors such as length and width of the bony canal containing the ganglia and nerves may account for the greater involvement of the superior vestibular ganglion. Other possible mechanisms include autoimmune[19] and microvascular ischemic insults to the vestibular labyrinth[20]. These patients had not been tested for the detailed etiology of neuritis in our study, which is a retrospective study. Future investigations of VN should include exploration of these etiologies.
Evolution of Meniere’s Disease from MD 1.0, via MD 1.5, to MD 2.0
Published in Acta Oto-Laryngologica, 2019
An inner ear test battery comprising audiometry, and cVEMP, ocular VEMP (oVEMP) and caloric tests has recently been utilized for mapping the hydropic territory in MD patients [4]. Using this test battery to study the localization and prevalence of hydrops formation revealed that the declining function in the cochlea, saccule, utricle and semicircular canals mimics the declining sequence of hydrops formation in temporal bone studies [5,6]. However, loss of hair cell population was demonstrated in the saccular and utricular macula with increasing age [7]. Further, declining in the number of vestibular ganglion cells and degeneration in the vestibular afferent neurons were also identified in the elderly. Hence, it is hard to interpret whether absent oVEMP or cVEMP in an elder MD patient is caused by aging effect or progression of MD. This study utilized an inner ear test battery in elder MD patients to investigate the evolution of MD.
Noise exposure as a risk factor for acoustic neuroma: a systematic review and meta-analysis
Published in International Journal of Audiology, 2019
Zuwei Cao, Fei Zhao, Helena Mulugeta
Early studies have suggested possible biological mechanisms for the association between AN and noise exposure. Mechanical damage induced by noise exposure may destroy the hair cells in the Organ of Corti and the eighth Cranial Nerve (Hamernik et al. 1984; Bohne et al. 2007). During repair, DNA errors may occur during cell division, leading to disordered proliferation of cells (Fisher et al. 2014). An alternative possible mechanism is that loud noise exposure can damage the Styria Vascularise and lead to a mixing of cochlear fluids by changing the tight cell junction of the Reticular Lamina (Henderson and Hamernik 1995), and consequently causing the hair cells to be immersed in fluid with a nonphysiological complement of electrolytes. Because electrolyte balance is very important for maintaining normal function of the nerve cells, the damage induced by this electrolyte disequilibrium could lead to degeneration of the eighth Cranial Nerve, and consequently, the Schwann cells as the supporting cells of the nerve system may lose the ability to protect the auditory nerve fibres (Hours et al. 2009). Indeed some animal studies have shown that free radicals that can cause DNA damage were found in vestibular ganglion cells after exposure to loud acoustic stimulation (Van Campen et al. 2002; Watanabe et al. 2004). This suggests that noise could be responsible for the development of AN (Hours et al. 2009). Lastly, nerve growth factors may be induced by loud noise and subsequently contribute to tumorigenesis (Hamernik et al. 1984; Lesser and Pollak 1990).