scholarly journals Perceived Vertical and Lateropulsion: Clinical Syndromes, Localization, and Prognosis

2000 ◽  
Vol 14 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Thomas Brandt ◽  
Marianne Dieterich

We present a clinical classification of central vestibular syndromes according to the three major planes of action of the vestibulo-ocular reflex: yaw, roll, and pitch. The plane-specific syndromes are determined by ocular motor, postural, and percep tual signs. Yaw plane signs are horizontal nystagmus, past pointing, rotational and lat eral body falls, deviation of perceived straight-ahead to the left or right. Roll plane signs are torsional nystagmus, skew deviation, ocular torsion, tilts of head, body, and perceived vertical in a clockwise or counterclockwise direction. Pitch plane signs are upbeat/downbeat nystagmus, forward/backward tilts and falls, deviations of the per ceived horizon. The thus defined vestibular syndromes allow a precise topographic analysis of brainstem lesions according to their level and side. Special emphasis is placed on the vestibular roll plane syndromes of ocular tilt reaction, lateropulsion in Wallenberg's syndrome, thalamic and cortical astasia and their association with roll plane tilt of perceived vertical. Recovery is based on a functionally significant central compensation of a vestibular tone imbalance, the mechanism of which is largely un known. Physical therapy may facilitate this central compensation, but this has not yet been proven in prospective studies. Key Words: Visual vertical—Lateropulsion— Vestibulo-ocular reflex—Central vestibular syndromes.

Author(s):  
Carlo Canepa-Raggio

57-year-old male patient with a 30-year history chronic cough, balance difficulties (most noticeable in the dark), ataxia and sensory neuropathy. There was also evidence of orthostatic hypotension and hypohydrosis. Examination revealed downbeat nystagmus, an abnormal visually-enhanced vestibulo-ocular reflex, length-dependent sensory neuropathy, high-stepping tandem ataxia and bilateral dysmetria. MRI brain shows marked vermian cerebellar atrophy (more noticeable in lobes VI and VIIa/b) and nerve conduction studies reveal absent sensory conductions (ganglionopathy). Genetic testing for Friedrich’s ataxia, spinocerebellar ataxia and hereditary motor sensory neuropathy (Charcot-Marie-Tooth disease) were all negative. Sural nerve biopsy showed pattern of severe loss of myelinated fibres. This patient was diagnosed with cerebellar ataxia, neuronopathy (ganglionopathy) and vestibular areflexia with autonomic dysfunction. Keywords: ataxia, neuronopathy, vestibular areflexia, autonomic dysfunction.


Neurology ◽  
2020 ◽  
Vol 95 (17) ◽  
pp. e2409-e2417
Author(s):  
Sun-Uk Lee ◽  
Hyo-Jung Kim ◽  
Jeong-Yoon Choi ◽  
Ji-Soo Kim

ObjectiveTo determine the mechanism of ictal downbeat nystagmus in Ménière disease (MD), we compared the head impulse gain of the vestibulo-ocular reflex (VOR) for each semicircular canal between patients with (n = 7) and without (n = 70) downbeat nystagmus during attacks of MD.MethodsWe retrospectively analyzed the results of video-oculography, video head-impulse tests, and cervical vestibular-evoked myogenic potentials (VEMPs) in 77 patients with definite MD who were evaluated during an attack.ResultsPure or predominant downbeat nystagmus was observed in 7 patients (9%) with unilateral MD during the attacks. All 7 patients showed spontaneous downbeat nystagmus without visual fixation with a slow phase velocity ranging from 1.5 to 11.2°/s (median 5.4, interquartile range 3.7–8.5). All showed a transient decrease of the head impulse VOR gains for the posterior canals (PCs) in both ears (n = 4) or in the affected ear (n = 3). Cervical VEMPs were decreased in the affected (n = 2) or both ears (n = 2) when evaluated during the attacks. Downbeat nystagmus disappeared along with normalization of the VOR gains for PCs after the attacks in all patients. During the attacks, the head impulse VOR gains for the PC on the affected side were lower in the patients with ictal downbeat nystagmus than in those without (Mann-Whitney U test, p < 0.001), while the gains for other semicircular canals did not differ between the groups.ConclusionDownbeat nystagmus may be observed during attacks of MD due to an asymmetry in the vertical VOR or saccular dysfunction. MD should be considered in recurrent audiovestibulopathy and ictal downbeat nystagmus.


1999 ◽  
Vol 9 (2) ◽  
pp. 135-144 ◽  
Author(s):  
J.H.J. Allum ◽  
T. Ledin

The centrally controlled compensation for a reduced horizontal vestibulo-ocular reflex (VOR) gain caused by a unilateral afferent deficit is usually studied following a selective surgical procedure which completely lesions the vestibular nerve or blocks the horizontal semicircular canal. The more common, unilateral, vestibular deficit encountered clinically, is a partial loss of peripheral vestibular function, following which peripheral recovery and/or central compensation may occur. We investigated changes of the VOR gain in response to a sudden, idiopathic, unilateral vestibular deficit in 64 subjects by examining the responses to low-frequency, whole-body, rotations about an earth vertical axis with different accelerations (5, 20 and 40 deg / sec 2 ) during in- and out-patient visits separated by 4 months in an attempt to identify changes brought about by peripheral recovery and by central compensation processes. Peripheral function was assumed to be measured by the response to caloric irrigation. It improved some 30% between the two visits. VOR responses for rotations towards the deficit side also improved between the two visits. Most improvement occurred for 20 deg / sec 2 accelerations. However, the correlation coefficient between rotation and caloric responses was always less than 0.6. Unlike caloric responses which improved over time, responses for rotations to the intact side did not change between the visits. For this reason, the majority of observed VOR rotation responses were nearly symmetrical at the time of the second visit, despite being below normal levels. These findings suggest that both peripheral recovery and central compensation processes help restore symmetrical VOR function for head rotations after a partial unilateral vestibular deficit. However the improvement of VOR response symmetry, particularly to slow ( < 40 deg / sec 2 ) accelerations, is largely independent of the recovery of peripheral sensitivity.


Neurology ◽  
2017 ◽  
Vol 89 (24) ◽  
pp. 2476-2480 ◽  
Author(s):  
Seo-Young Choi ◽  
Hyo-Jung Kim ◽  
Ji-Soo Kim

Objective:To determine the role of the medial longitudinal fasciculus (MLF) in conveying vestibular signals.Methods:In 10 patients with isolated acute unilateral internuclear ophthalmoplegia (INO) due to an acute stroke, we performed comprehensive vestibular evaluation using video-oculography, head impulse tests with a magnetic search coil technique, bithermal caloric tests, tests for the ocular tilt reaction, and measurements of subjective visual vertical and cervical and ocular vestibular evoked myogenic potentials (VEMPs).Results:The head impulse gain of the vestibulo-ocular reflex (VOR) was decreased invariably for the contralesional posterior canal (PC) (n = 9; 90%) and usually for the ipsilesional horizontal canal (n = 5; 50%). At least one component of contraversive ocular tilt reaction (n = 9) or contraversive tilt of the subjective visual vertical (n = 7) were common along with ipsitorsional nystagmus (n = 5). Cervical or ocular VEMPs were abnormal in 5 patients.Conclusions:The MLF serves as the main passage for the high-acceleration VOR from the contralateral PC. The associations and dissociations of the vestibular dysfunction in our patients indicate variable combinations of damage to the vestibular fibers ascending or descending in the MLF even in strokes causing isolated unilateral INO.


1989 ◽  
Vol 98 (3) ◽  
pp. 191-195 ◽  
Author(s):  
Marcel E. Norré ◽  
Gabriel Forrez ◽  
Ann Beckers

The influence of vestibular dysfunction upon the vestibulospinal reflex (VSR) in two common peripheral syndromes was investigated by two types of posturographic examination: “static” posturography, recording and analyzing the postural sway in stance, and “kinetic” posturography, recording the stepping in place test. The influence of the dysfunction was examined outside the attacks, ie, between attacks and not during or immediately after an attack, in patients with Meniere's disease and in others with a sudden vestibular loss syndrome, “neuronitis.” However, in both syndromes the influence of the dysfunction was obvious only in some patients; this indicates that central adaptation intervened in the other patients. In this way, central compensation related to the VSR was assessed and compared with compensation for the vestibulo-ocular reflex assessed by the rotation tests. Discordance was shown in a number of cases, ie, a number of cases showed compensation for one reflex, but not for the other. Comparison of the results of both posturographic methods also showed discordance. Normal performance in the walking test could not always be correlated with normal performance in the standing test and vice versa.


2020 ◽  
pp. 10.1212/CPJ.0000000000000951
Author(s):  
Itaru Hayakawa ◽  
Yuichi Abe ◽  
Masaya Kubota

Downbeat nystagmus occurs as a result of an impaired vestibulo-ocular reflex1. From animal experiments, the Purkinje cells of the flocculonodular and parafloccular lobes of the cerebellum (also known as the “vestibular cerebellum”) are known to negatively regulate the upward rotation of the eyes via feed-forward inhibitory neural circuitry to the vertical vestibulo-ocular reflex [Supplemental figure 1,links.lww.com/CPJ/A199) 2. Although various eye movement abnormalities have been described in congenital and acquired cerebellar disorders, there have been few reports of pure downbeat nystagmus in cerebellitis.Here we report a quite impressive pure downbeat nystagmus in an adolescent female with acute cerebellitis. The electro-oculography of the patient provided compelling evidence that the downbeat nystagmus is indeed the result of feed-forward inhibition to the vestibulo-ocular reflex. Our case may add new insights into the current literature on cerebellar control of eye movement.


2020 ◽  
Author(s):  
Christina Zeeh ◽  
Ümit S. Mayadali ◽  
Anja K.E. Horn

Abstract The Y-group plays an important role in the generation of upward smooth pursuit eye movements and contributes to the adaptive properties of the vertical vestibulo-ocular reflex. Malfunction of this circuitry may cause eye movement disorders, such as downbeat nystagmus. To characterize the neuron populations in the Y-group, we performed immunostainings for cellular proteins related to firing characteristics and transmitters (calretinin, GABA-related proteins and ion channels) in brainstem sections of macaque monkeys that had received tracer injections into the oculomotor nucleus. Two histochemically different populations of premotor neurons were identified: The calretinin-positive population represents the excitatory projection to contralateral upgaze motoneurons, whereas the GABAergic population represents the inhibitory projection to ipsilateral downgaze motoneurons. Both populations receive a strong supply by GABAergic nerve endings most likely originating from floccular Purkinje cells. All premotor neurons express nonphosphorylated neurofilaments and are ensheathed by strong perineuronal nets. In addition, they contain the voltage-gated potassium channels Kv1.1 and Kv3.1b which suggests biophysical similarities to high-activity premotor neurons of vestibular and oculomotor systems. The premotor neurons of Y-group form a homogenous population with histochemical characteristics compatible with fast-firing projection neurons that can also undergo plasticity and contribute to motor learning as found for the adaptation of the vestibulo-ocular reflex in response to visual-vestibular mismatch stimulation. The histochemical characterization of premotor neurons in the Y-group allows the identification of the homologue cell groups in human, including their transmitter inputs and will serve as basis for correlated anatomical-neuropathological studies of clinical cases with downbeat nystagmus.


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