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Common otology viva topics
Published in Joseph Manjaly, Peter Kullar, Advanced ENT Training, 2019
VOR suppression test: The brain is able to suppress the VOR when tracking a moving target with head and eyes moving together. Testing for this involves the patient's arms outstretched and being asked to fixate on thumbs whilst the patient's chair is oscillated. This can also be performed with VNG using a laser light. This is an assessment of the vestibulocerebellum, in particular the flocculus and paraflocculus, although it is a non-specific assessment.
Ototoxicity
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
Exposure to high concentrations of organic solvents induce acute, reversible narcosis and neurotoxicity, but the possibility of ototoxic damage was initially recognized from the unusually high number of workers in the chemical industry who showed a hearing loss, and from case reports of hearing deficits in solvent abusers.186 The effects of solvents may be exacerbated by concurrent exposure to high noise levels, or the converse, i.e. noise-induced hearing loss becoming more pronounced with concomitant exposure to certain solvents presenting a significant occupational hazard.187,188 Vestibular dysfunction may also follow from exposure to organic solvents but this may result from specific effects on vestibulo-oculomotor pathways in the vestibulocerebellum rather than from effects in the inner ear.188 This would be classified as neurotoxicity rather than ototoxicity for the definitions used in this chapter.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Several authors equate the flocculonodular lobe with the vestibulocerebellum (e.g., Brod, p. 295 [Fig. 5–1], K&S, p. 510; MarMar, p. 85), but several others also include a few additional structures—e.g., part of the uvula (W&G, p. 382), the lingula (w&w, p. 913–914, 918), or the entire “dorsal vermis [= lingula, central lobule, culmen, declive, folium, and tuber]” (FitzG, p. 94–95). Although Matzke and Foltz equate the spmocerebellum with the anterior lobe (1983, p. 87), several other authors include portions of the posterior lobe as well (e.g., MarMar, p. 85; Heim, p. 215–216) and may not even include the lateralmost portions of the anterior lobe (e.g., B&K, p. 168; K&S, p. 510; Brod, p. 295 [Fig. 5–1], 296). Matzke and Foltz also equate the pontocerebellum with the posterior lobe (1983, p. 87), but most other consulted authors exclude some of the posterior lobe (e.g., MarMar, p. 85; Heim, p. 216) and often include a lateral portion of the anterior lobe as well (e.g., K&S, p. 510; B&K, p. 168; Brod, p. 295 [Fig. 5–1]).
The ‘worm’ in our brain. An anatomical, historical, and philological study on the vermis cerebelli
Published in Journal of the History of the Neurosciences, 2023
In clinical neuroanatomy, the vestibulocerebellum regulates balance and eye movements; the spinocerebellum regulates body and limb movements (see Figure 8). Lesions of the vermis, therefore, affect vestibular connexions and impair the balance of the trunk (truncal ataxia, see Clarke et al. 2009, 28–30). Classically, the spinocerebellum receives somatosensory input from ascending spinal pathways, but part of the vermis seems to receive input from the cerebral cortex, too (Coffman, Dum, and Strick 2011). According to other recent research, the posterior vermis is the anatomical substrate of the limbic cerebellum. Lesions may result in cognitive disturbances, even in personality changes (the “cerebellar cognitive affective syndrome,” first described in Brain by Schmahmann and Sherman in 1998; for a recent review, see Schmahmann 2019). However, the fact that working memory and visual-spatial memory can also be affected should not provoke nostalgic reminiscences of the cell doctrine: Memory is represented in multiple regions of the brain.
Current perspectives on galvanic vestibular stimulation in the treatment of Parkinson’s disease
Published in Expert Review of Neurotherapeutics, 2021
Soojin Lee, Aiping Liu, Martin J. McKeown
Postural instability is one of the main disabling symptoms largely refractory to L-dopa in PD. The cerebellum plays a critical role in postural control and gait through its close connection with the vestibular system. The vestibulocerebellum (the flocculonodular lobe and adjacent parts of the caudal cerebellar vermis) receives a substantial amount of its input from the vestibular nuclei and is involved in the regulation of posture and equilibrium as well as the vestibulo-ocular reflex – a reflex to generate eye movements for stabilization of retinal images during head movements [72]. Thus, GVS could subserve some of the vestibulocerebellar functions altered in PD through this pathway. Notably, the postural instability in PD is closely associated with dysfunction of vestibular processing [71] and can be improved by vestibular rehabilitation [73].
The challenges faced by clinicians diagnosing and treating infantile nystagmus Part I: diagnosis
Published in Expert Review of Ophthalmology, 2021
Eleni Papageorgiou, Irene Gottlob
A child with vestibular dysfunction may also present with nystagmus. In those cases, additional neurological symptoms, such as vertigo, vomiting, hearing loss, or ataxia. Vestibular nystagmus may result from impairment of the peripheral (labyrinth, vestibular nerve) or central vestibular pathways [133,134]. Peripheral vestibular nystagmus is usually associated with vestibular neuritis, Meniere’s disease, and benign paroxysmal positional vertigo. Peripheral vestibular nystagmus obeys Alexander’s law. Nystagmus is more pronounced in the direction of the fast phase and decreases but never reverses in the direction of the slow phase. Another distinguishing feature of acquired horizontal vestibular nystagmus is that it’s direction changes to upbeat nystagmus in upgaze. In contrast congenital nystagmus remains horizontal in upgaze [135]. Additionally, peripheral vestibular nystagmus increases with occlusion and dampens during fixation. It is often incompletely suppressed in light, can be evoked by non-upright head positions, and is also associated with head movements and anomalous head postures. Central vestibular nystagmus is not influenced by visual fixation, and usually results from lesions of the vestibulocerebellum (i.e., flocculus, nodulus, and vermis) or associated connections within the brainstem [136]. Downbeat nystagmus is the most common type of central vestibular nystagmus, while upbeat nystagmus is much less common. Etiologies include brainstem and cerebellar processes such as infarcts, demyelination, neurodegenerative disorders, intoxication, neoplasms, or Chiari malformations [137].”