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Vestibular information has been traditionally considered as a specialized input for basic orienting behaviours, such as oculo-motor adjustments, postural control and gaze orientation. However, in the past two decades a widespread ...
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Vestibular information has been traditionally considered as a specialized input for basic orienting behaviours, such as oculo-motor adjustments, postural control and gaze orientation. However, in the past two decades a widespread vestibular network in the human brain has been identified, that goes far beyond the low-level reflex circuits emphasized by earlier work. Because this vestibular cortical network is so widely distributed, it could, in principle, impact multiple neurocognitive functions in health and disease. This paper focuses on the relations between vestibular input, vestibular networks, and vestibular interventions by providing the authors' personal viewpoint on the state-of-the-art of vestibular cognitive neuropsychology, and its potential relevance for neurorehabilitation.
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The bilateral anatomical organization of the vestibular system provides three functional advantages: optimal differentiation of head motion and orientation, sensory substitution of a unilateral peripheral failure, and central comp...
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The bilateral anatomical organization of the vestibular system provides three functional advantages: optimal differentiation of head motion and orientation, sensory substitution of a unilateral peripheral failure, and central compensation of a peripheral or central vestibular tone imbalance. The structure is based on bilaterally ascending and descending pathways and at least four crossings: three in the brain stem and one in the cortex. The resulting sensorimotor functions can be subdivided into
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The aim of the present paper was to provide a comprehensive review of vestibular neuritis. This disorder was described for the first time by Ruttin in 1909 and Nylen coined the term vestibular neuritis in 1924. Dix and Hallpike ...
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The aim of the present paper was to provide a comprehensive review of vestibular neuritis. This disorder was described for the first time by Ruttin in 1909 and Nylen coined the term vestibular neuritis in 1924. Dix and Hallpike reported 100 cases with vestibular neuritis including cases with either single or multiple attacks of vertigo. A more restricted diagnostic criterion limited to a single severe attack of vertigo with a subsequent unilateral deficit in caloric response was adopted by the Japan Society For Equilibrium Research and Research Group for Vestibular Disorder of the Ministry of Health, Labour and Welfare of Japan. A human temporal bone histopathological study demonstrated severe atrophic changes of one or more nerve trunks of the superior vestibular nerve, with or without their associated sense organs. The above histological findings suggested viral infection rather than vascular occlusion. However, the cause of vestibular neuritis remains uncertain. Previous histopathological studies exhibited atrophic changes limited to the superior division of the vestibular nerve. In addition, recent studies revealed that some patients demonstrated vestibular dysfunction limited to the inferior division or superior/inferior division of the vestibular nerve. Antiviral agents (valacyclovir) have failed to demonstrate any improvement in vestibular neuritis-related vestibular function. Furthermore, the effectiveness of corticosteroids in the management of patients with vestibular neuritis has not been established. A Cochrane Database Systematic Review reported insufficient evidence to support the administration of corticosteroids to patients with vestibular neuritis in 2011.
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The vestibular center of the brainstem contains afferent and efferent vestibular neurons, which play an important role in information perception, processing, and sensory integration. Vestibular efferent neurons (VENs) can receive ...
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The vestibular center of the brainstem contains afferent and efferent vestibular neurons, which play an important role in information perception, processing, and sensory integration. Vestibular efferent neurons (VENs) can receive changes in vestibular afferent information and regulate peripheral vestibular function; however, it remains unclear how VENs change after vestibular afferent information increases or weakens. In this study, we used animal models with altered vestibular afferent information by electrically stimulating or destroying the vestibular medial nucleus (MVe). We confirmed the location of VENs in the brainstem by injecting five adult male Wistar rats in the vestibular region with a retrograde tracer. Following this, the MVe was stimulated electrically for 30min in 20 naive rats. Rats were anesthetized and euthanized 1, 3, 6, and 12h after stimulation. The MVe was electrolytically lesioned in another group (n=20); then, the rats were anesthetized and euthanized 1, 3, 5, and 7 days after lesioning. VENs were clearly identified dorsolateral to the genu of the facial nerve (g7) in coronal brainstem sections using choline acetyltransferase (ChAT) staining. The number of ChAT-positive VENs dorsolateral to g7 increased significantly on both sides compared with the control group 3 and 6h after electrical stimulation. The number of ChAT-positive VENs dorsolateral to g7 was significantly greater on both sides compared with controls 3 and 5 days after electrolytic lesion. In summary, we found that the number of ChAT-positive VENs was significantly increased following a change in the excitability of MVe neurons. This suggests that VENs can respond to changes in afferent vestibular information and feedback, and regulate the peripheral vestibule. In addition, this shows that acetylcholine is an important neurotransmitter that plays an important role in the perception and fine regulation of the vestibular system.
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Recent reports have suggested that hemispatial neglect may be a vestibular disorder at the cortical level, based on the similarities of symptoms and neural correlates between the two phenomena. If this is the case, peripheral vest...
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Recent reports have suggested that hemispatial neglect may be a vestibular disorder at the cortical level, based on the similarities of symptoms and neural correlates between the two phenomena. If this is the case, peripheral vestibulopathy may lead to hemispatial neglect. However, the etiology of hemispatial neglect in patients with unilateral peripheral vestibulopathy remains unclear. The aims of the present study were to investigate the following: (1) if unilateral peripheral vestibulopathy might cause hemispatial neglect, and if so, (2) whether hemispatial neglect in unilateral peripheral vestibulopathy might be induced by horizontal bias for eye position and body orientation or whether it is secondary to vestibular cortical dysfunction following unilateral peripheral vestibulopathy. Twenty-five consecutive patients with acute vestibular neuritis were recruited at the Dizziness Clinic of Pusan National University Hospital. All participants underwent neglect testing and measurements of horizontal bias for eye position and head and body orientation. Hemispatial neglect occurred in 32 % of patients with unilateral peripheral vestibulopathy. The frequency of contralesional neglect was equal to that of ipsilesional neglect. All patients with hemispatial neglect showed abnormal performance in bisection tasks. The incidence and severity of the horizontal bias of eye position and head and body orientation did not differ between patients with or without hemispatial neglect. Our study demonstrates that hemispatial neglect can develop after acute unilateral peripheral vestibulopathy. Hemispatial neglect after acute unilateral peripheral vestibulopathy may be attributed to damaged vestibular subnuclei, which receive afferents from both peripheral vestibular end organs and the vestibulocerebellum and project to the ipsilateral or contralateral thalamus and vestibular cortex.
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Structural and functional interconnections of the bilateral central vestibular network have not yet been completely delineated. This includes both ipsilateral and contralateral pathways and crossing sites on the way from the vesti...
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Structural and functional interconnections of the bilateral central vestibular network have not yet been completely delineated. This includes both ipsilateral and contralateral pathways and crossing sites on the way from the vestibular nuclei via the thalamic relay stations to multiple "vestibular cortex" areas. This study investigated "vestibular" connectivity in the living human brain in between the vestibular nuclei and the parieto-insular vestibular cortex (PIVC) by combined structural and functional connectivity mapping using diffusion tensor imaging and functional connectivity magnetic resonance imaging in 24 healthy right-handed volunteers. We observed a congruent functional and structural link between the vestibular nuclei and the ipsilateral and contralateral PIVC. Five separate and distinct vestibular pathways were identified: three run ipsilaterally, while the two others cross either in the pons or the midbrain. Two of the ipsilateral projections run through the posterolateral or paramedian thalamic subnuclei, while the third bypasses the thalamus to reach the inferior part of the insular cortex directly. Both contralateral pathways travel through the posterolateral thalamus. At the cortical level, the PIVC regions of both hemispheres with a right hemispherical dominance are interconnected transcallosally through the antero-caudal splenium. The above-described bilateral vestibular circuitry in its entirety takes the form of a structure of a rope ladder extending from the brainstem to the cortex with three crossings in the brainstem (vestibular nuclei, pons, midbrain), none at thalamic level and a fourth cortical crossing through the splenium of the corpus callosum.
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Abstract Background Although, vestibular syndrome is a common neurological presentation, little is known about the diagnostic value of cerebrospinal fluid (CSF) analysis in vestibular syndrome in dogs. Methods Medical records were...
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Abstract Background Although, vestibular syndrome is a common neurological presentation, little is known about the diagnostic value of cerebrospinal fluid (CSF) analysis in vestibular syndrome in dogs. Methods Medical records were retrospectively reviewed, and dogs with vestibular disease that had undergone magnetic resonance imaging of the head, CSF analysis and were diagnosed with central or peripheral vestibular syndrome were included. Disorders affecting the central vestibular system included meningoencephalitis of unknown origin (MUO), brain neoplasia, ischaemic infarct, intracranial empyema or metronidazole toxicity. Disorders affecting the peripheral vestibular system included idiopathic vestibular disease, otitis media/interna or neoplasia affecting the inner ear structures. Total nucleated cell concentration (TNCC), total protein concentration (TP) and cytologic assessment were recorded. Results A total of 102 dogs met the inclusion criteria. The sensitivity and specificity of increased CSF TNCC to differentiate central from peripheral vestibular syndrome was 49% and 90%, while the sensitivity and specificity of increased TP was 58% and 39%, respectively. The TNCC and TP in dogs with MUO were significantly higher than in dogs with idiopathic vestibular disease (p?=?0.000 and p?=?0.004). MUO was associated with lymphocytic pleocytosis, while idiopathic vestibular disease and ischaemic infarct were associated with the presence of activated macrophages or normal cytology (p?=?0.000). Conclusion Although consistent CSF abnormalities were observed in dogs with MUO, CSF analysis did not allow reliable differentiation between central and peripheral vestibular syndrome. CSF analysis is not reliable as the sole diagnostic technique in dogs with vestibular disease.
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The growing evidence of the need for pediatric vestibular evaluation, as well as the availability of successful treatment options for children, is attracting the attention of many professionals and sparking much interest in the de...
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The growing evidence of the need for pediatric vestibular evaluation, as well as the availability of successful treatment options for children, is attracting the attention of many professionals and sparking much interest in the development of pediatric balance centers in North America. Complete balance function assessment and rehabilitation in children requires specialized knowledge and practices of professionals in multiple disciplines. While individual specialists provide useful test information and recommendations for patients, the collaboration of specialists working in a multidisciplinary fashion allows the information to become more powerful, providing the patients and their families with a comprehensive plan. Currently, there are only a handful of pediatric balance centers in North America and most of the centers have been in existence less than 10 years. Thus, this new initiative is in its infancy. Educating oneself, administrators, referral sources, and interdisciplinary colleagues is crucial for gathering support for the enormous endeavor of developing such a center. There are many resources one can draw from, including the works found in this issue. Our hope is that this special Seminars in Hearing may serve as a companion guide to anyone interested in performing pediatric vestibular evaluations and/or developing a multidisciplinary pediatric balance center.
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