Head-shaking nystagmus - a "central" pattern

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Identifier Central_Head_Shaking_Nystagmus
Title Head-shaking nystagmus - a "central" pattern
Subject Abnormal Head Shaking, Jerk Nystagmus, Vestibular Nystagmus
Creator Kemar Green, DO, Department of Neurology, Michigan State University; Daniel R. Gold, D.O. Departments of Neurology, Ophthalmology, Neurosurgery, Otolaryngology - Head & Neck Surgery,The Johns Hopkins School of Medicine
Description Evaluating for nystagmus provoked by head-shaking, so-called head-shaking nystagmus (HSN), should be performed in all patients with complaints of dizziness or vertigo, regardless of the chronicity. The maneuver is performed by passively moving the head horizontally (can also be performed vertically) at 2 Hz for about 15 cycles, and can help in differentiation of peripheral versus central etiologies. Peripheral vestibular loss - e.g., in a patient with right sided vestibular neuritis, spontaneous left-beating nystagmus (LBN) is seen acutely, and over time only mild fixation removed LBN will be appreciated. Because of Ewald's second law which states that ampullopetal endolymph flow will cause greater stimulation than ampullofugal flow within the horizontal canals, head-shaking will lead to transient, but clinically meaningful, asymmetric vestibular afferents even after central compensation has occurred. With a subacute or chronic right unilateral vestibulopathy, fixation-removed LBN is seen and will increase following horizontal head-shaking. Central vestibular conditions - e.g., velocity storage mechanisms are normally present to assist in the prolongation of labyrinthine semicircular canal inputs. Since the mechanical properties of the cupula and endolymph within each semicircular canal is such that vestibular afferents would cease firing after just a few seconds of sustained rotational stimuli, a central mechanism must be in place to prolong these signals. It is mainly thought that central patterns of HSN relate to dysfunction of the central velocity storage mechanisms. Lesions causing central HSN usually involve the GABA-ergic inhibitory projections from nodulouvular regions to vestibular nucleus, which can result in the disinhibition of velocity storage. Central patterns include 1) unusually robust HSN elicited by weak head-shaking, 2) nystagmus that reverses direction after head-shaking (e.g., LBN becomes RBN), biphasic HSN, 3) strong HSN in patients without clear unilateral vestibular loss, or 4) perverted HSN (e.g., vertical nystagmus after horizontal head-shaking, usually downbeat and associated with floccular lesions). Shown here is a 70-year-old man with vague episodes of lightheadedness that were not clearly vestibular, who despite having a normal vestibulo-ocular reflex on the left side (i.e., no left sided unilateral vestibular loss), had very strong and persistent right-beating HSN. Although this is considered to be a "central" pattern of HSN, there were no cerebellar, ocular motor or vestibular abnormalities and brain MRI was normal (with particular attention to the nodulus/uvula and vestibular nuclei), so the etiology of his lightheadedness and "central" HSN remained elusive during his initial evaluation.
Publisher Spencer S. Eccles Health Sciences Library, University of Utah
Date 2018-02
Format video/mp4
Rights Management Copyright 2018. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
Collection Neuro-ophthalmology Virtual Education Library: NOVEL http://NOVEL.utah.edu
Language eng
ARK ark:/87278/s61c5vkg
Setname ehsl_novel_gold
Date Created 2018-02-07
Date Modified 2018-02-07
ID 1295175
Reference URL https://collections.lib.utah.edu/ark:/87278/s61c5vkg
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