Suppression Of Vestibulo-ocular Reflex Research Articles

Does spectacle use lead to vestibular suppression?

Laboratory experiments indicate that changes in retinal image size result in adaptive recalibration or suppression of the vestibulo-ocular reflex. Myopia correction with spectacles or contact lenses also leads to retinal image size changes, and may bring about similar vestibulo-ocular reflex alterations. A hypothesis-generating preliminary investigation was conducted. In this cross-sectional study, findings of electronystagmography including bithermal caloric testing were compared between 17 volunteer myopes using spectacles or contact lenses and 17 volunteer emmetropes (with no refractive error). Bilateral hypoactive caloric responses were demonstrated in 6 of 11 spectacle users, in 1 of 6 contact lens users and in 1 of 17 emmetropes. Hypoactive caloric responses were significantly more likely in spectacle users than in emmetropes (p < 0.01; relative risk = 9.3). A significant proportion of myopes using spectacles have vestibulo-ocular reflex suppression, as demonstrated by the caloric test. This has implications for the interpretation of electronystagmography and videonystagmography results, and highlights spectacle use as a possible cause of vestibular impairment. Further corroboration of these findings is warranted, with more precise and direct vestibulo-ocular reflex tests such as rotational tests and the head impulse test.

Cerebellar Control of Ocular Movements: Application to the Topographical Diagnosis of Cerebellar Lesions

Over the last decade, substantial information on cerebellar oculomotor control has been provided by the use of sophisticated neuroanatomical, neurophysiological, and imaging techniques. We now know that an intact cerebellum is a prerequisite for normal oculomotor performance. This review clarifies the current knowledge on structure-function correlations of the cerebellum in relation to ocular movements and allows them to be applied to topographical diagnosis of cerebellar lesions. The cerebellar regions most closely related to oculomotor function are: (1) the flocculus/paraflocculus for VOR suppression, cancellation, smooth pursuit eye movement and gaze-holding, (2) the nodulus/ventral uvula for velocity storage and low frequency prolonged vestibular response, and (3) the dorsal oculomotor vermis (declive VI, folium VII) and the posterior portion of the fastigial nucleus (fastigial oculomotor region) for saccades and smooth pursuit initiation. Symptomatically, defects in the flocculus/parflocculus cause saccadic pursuit, downbeat nystagmus, and impairments to visual suppression of the VOR. Lesions of the nodulus/uvula reveal as periodic alternating nystagmus. Lesions of the oculomotor vermis and the fastigial nucleus can induce saccadic dysmetria, while fastigial nucleus lesions may also cause ocular flutter/opsoclonus. A detailed knowledge of cerebellar anatomy and the physiology of eye movements enables localization of lesions to specific areas of the cerebellum.

Chapter 4 - Multisensory integration in balance control

This chapter provides an introduction to the topic of multisensory integration in balance control in, both, health and disease. One of the best-studied examples is that of visuo-vestibular interaction, which is the ability of the visual system to enhance or suppress the vestibulo-ocular reflex (VOR suppression). Of clinical relevance, examination of VOR suppression is clinically useful because only central, not peripheral, lesions impair VOR suppression. Visual, somatosensory (proprioceptive), and vestibular inputs interact strongly and continuously in the control of upright balance. Experiments with visual motion stimuli show that the visual system generates visually-evoked postural responses that, at least initially, can override vestibular and proprioceptive signals. This paradigm has been useful for the study of the syndrome of visual vertigo or vision-induced dizziness, which can appear after vestibular disease. These patients typically report dizziness when exposed to optokinetic stimuli or visually charged environments, such as supermarkets. The principles of the rehabilitation treatment of these patients, which use repeated exposure to visual motion, are presented. Finally, we offer a diagnostic algorithm in approaching the patient reporting oscillopsia - the illusion of oscillation of the visual environment, which should not be confused with the syndrome mentioned earlier of visual vertigo.

Association between vestibulo-ocular reflex suppression, balance, gait, and fall risk in ageing and neurodegenerative disease: protocol of a one-year prospective follow-up study.

BackgroundFalls frequency increases with age and particularly in neurogeriatric cohorts. The interplay between eye movements and locomotion may contribute substantially to the occurrence of falls, but is hardly investigated. This paper provides an overview of current approaches to simultaneously measure eye and body movements, particularly for analyzing the association of vestibulo-ocular reflex (VOR) suppression, postural deficits and falls in neurogeriatric risk cohorts. Moreover, VOR suppression is measured during head-fixed target presentation and during gaze shifting while postural control is challenged. Using these approaches, we aim at identifying quantitative parameters of eye-head-coordination during postural balance and gait, as indicators of fall risk.Methods/DesignPatients with Progressive Supranuclear Palsy (PSP) or Parkinson’s disease (PD), age- and sex-matched healthy older adults, and a cohort of young healthy adults will be recruited. Baseline assessment will include a detailed clinical assessment, covering medical history, neurological examination, disease specific clinical rating scales, falls-related self-efficacy, activities of daily living, neuro-psychological screening, assessment of mobility function and a questionnaire for retrospective falls. Moreover, participants will simultaneously perform eye and head movements (fixating a head-fixed target vs. shifting gaze to light emitting diodes in order to quantify vestibulo-ocular reflex suppression ability) under different conditions (sitting, standing, or walking). An eye/head tracker synchronized with a 3-D motion analysis system will be used to quantify parameters related to eye-head-coordination, postural balance, and gait. Established outcome parameters related to VOR suppression ability (e.g., gain, saccadic reaction time, frequency of saccades) and motor related fall risk (e.g., step-time variability, postural sway) will be calculated. Falls will be assessed prospectively over 12 months via protocols and monthly telephone interviews.DiscussionThis study protocol describes an experimental setup allowing the analysis of simultaneously assessed eye, head and body movements. Results will improve our understanding of the influence of the interplay between eye, head and body movements on falls in geriatric high-risk cohorts.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-015-0447-5) contains supplementary material, which is available to authorized users.

Vestibulo-ocular reflex suppression during head-fixed saccades reveals gaze feedback control.

Previous experiments have shown that the vestibulo-ocular reflex (VOR) is partially suppressed during large head-free gaze (gaze = eye-in-head + head-in-space) shifts when both the eyes and head are moving actively, on a fixed body, or when the eyes are moving actively and the head passively on a fixed body. We tested, in human subjects, the hypothesis that the VOR is also suppressed during gaze saccades made with en bloc, head and body together, rotations. Subjects made saccades by following a target light. During some trials, the chair rotated so as to move the entire body passively before, during, or after a saccade. The modulation of the VOR was a function of both saccade amplitude and the time of the head perturbation relative to saccade onset. Despite the perturbation, gaze remained accurate. Thus, VOR modulation is similar when gaze changes are programmed for the eyes alone or for the eyes and head moving together. We propose that the brain always programs a change in gaze using feedback based on gaze and head signals, rather than on separate eye and head trajectories.

5.脊髄小脳変性症

Spinocerebellar degeneration (SCD) is a progressive ataxia disease that can affect the spine, the cerebellum, the nervous system and the muscles. Recently, many of the dominantly inherited ataxias have been renamed Spinocerebellar Ataxia or SCA. The SCAs are usually followed by a number which indicates that the ataxia is caused by a specific genetic defect. New subtypes are found each year based on ongoing genetic studies. We now distinguish more than 60 SCA subtypes. In general, the main features of the clinical presentation of the patient with SCA are family history suggestive of autosomal-dominant traits, adult onset, mostly between 30-50 years, cerebellar ataxia with signs and symptoms of extra-cerebellar involvement in the majorities of cases, slow progression resulting in progressive impairment and variable phenotypes within one family. The patients frequently reveal unsteadiness of gait associated with nystagmus. Brainstem and cerebellar lesions affect physiological eye movements, e.g., saccade, smooth pursuit and VOR suppression. For this, some of them visit the otolaryngologist at their first hospital visit. To distinguish the SCA diseases from other peripheral vestibular disorder, it is necessary for otolaryngologists to understand the characteristics of the SCA diseases.

Applications of neuromodulation to explore vestibular cortical processing; new insights into the effects of direct current cortical modulation upon pursuit, VOR and VOR suppression.

Functional imaging, lesion studies and behavioural observations suggest that vestibular processing is lateralised to the non-dominant hemisphere. Moreover, disruption of interhemispheric balance via inhibition of left parietal cortex using transcranial direct current stimulation (tDCS) has been associated with an asymmetric suppression of the vestibulo-ocular reflex (VOR). However, the mechanism by which the VOR was modulated remains unknown. In this paper we review the literature on non-invasive brain stimulation techniques which have been used to probe vestibular function over the last decade. In addition, we investigate the mechanisms whereby tDCS may modulate VOR, e.g. by acting upon pursuit, VOR suppression mechanisms or direct VOR modulation. We applied bi-hemispheric parietal tDCS in 11 healthy subjects and only observed significant effects on VOR gain (tdcs * condition p=0.041) - namely a trend for VOR gain increase with right anodal/left cathodal stimulation, and a decrease with right cathodal/left anodal stimulation. Hence, we suggest that the modulation of the VOR observed both here and in previous reports, is directly caused by top-down cortical control of the VOR as a result of disruption to interhemispheric balance, likely parietal.

A Method to Monitor Eye and Head Tracking Movements in College Baseball Players

This study had two purposes. The first was to develop a method to measure horizontal gaze tracking errors (based on synchronized eye and head tracking recordings) as subjects viewed many pitched balls. The second was to assess horizontal eye, head, and gaze tracking strategies of a group of Division 1 college baseball players. Subjects viewed, but did not swing a bat at, tennis balls projected by a pneumatic pitching machine. Subjects were to call out numbers and the color of these numbers (black or red) on the balls. The trajectory of each pitch was very predictable. Eye and head movements were monitored with a video eye tracker and an inertial sensor, respectively, and these movements were synchronized with ball position using an analog recording device. Data were analyzed for 15 subjects. Eye rotation, head rotation, gaze errors (GEs), and unsigned gaze errors (UGEs) were calculated at various elapsed times. On average, subjects tracked the pitched ball with the head throughout the pitch trajectory, while the eye was moved very little until late in the pitch trajectory. On average, gaze position matched the target position throughout the pitch trajectory. There was some variability in the mean amplitudes of head and eye movement between subjects. However, the eye and head were related by a common rule (partial rotational vestibulo-ocular reflex suppression) for all subjects. Although the mean amplitudes of the GE and UGE varied between subjects, these means were not consistent with anticipatory saccades for any subject. On average, Division 1 college players tracked the pitched ball primarily with the head and maintained gaze close to the ball throughout much of the pitch trajectory. There was variability between subjects regarding the head and eye movement amplitudes and GEs, but, overall, all subjects maintained gaze close to the ball throughout the pitch trajectory despite the fact that these individuals were not batting.

6.脊髄小脳変性症

Spinocerebellar degeneration (SCD) is an inherited neurological disorder characterized by the slow degeneration of the brainstem and cerebellum. The Motor Ataxia Research Group has reported that there are more than 36,000 patients in Japan. Previously, SCD was classified by the clinical symptoms so that it was hard to make a distinct diagnosis. After the 1990s, SCD was identified genetically and has been classified into more than 60 different types. This classification has facilitated our approach to the restricted neuronal function of the brain stem and cerebellum. Usually the diagnosis comes after examination by a neurologist, which includes a physical exam, family history, MRI scanning of the brain and spine, and spinal tap. However, the patients frequently reveal unsteadiness of gait associated with nystagmus that could be also observed in the patients with peripheral vestibular impairment. For this, one third of the SCD patients visit otolaryngologists at their first hospital visit. For an accurate diagnosis, an eye movement examination is necessary. Brainstem and cerebellar lesions affect physiological eye movements, e.g., saccade, smooth pursuit and VOR suppression. Eye gains during those physiological eye movements in SCD patients are significantly lower than controls. Although it is not necessary for them to be an expert, otolaryngologists should understand the role of the brain stem and cerebellum, especially how they affect movements of the eye.

脊髄小脳失調症3型 (Machado-Joseph 病) における神経耳科学的所見

In recent years, a definitive diagnosis of spinocerebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), has become possible at an early stage with the development of a gene analysis method. We retrospectively investigated the otoneurological findings of 56 patients (male, 23 patients; female, 33 patients) who had been definitively diagnosed as having SCA3/MJD by gene information retrieval at Tokyo Metropolitan Neurological Hospital. In SCA3/MJD patients, the incidence of abnormal oto-neurological findings, e.g., upgaze palsy, gaze nystagmus, impaired optokinetic nystagmus (OKN), smooth pursuit, and saccade, reduced bilateral vestibulo-ocular reflex (VOR), and impaired visual suppression of VOR, was high. 12 of 56 patients had horizontal gaze palsy, so that those 12 cases were excluded from the later investigation. The reduced bilateral VOR performed by caloric response with cold and/or iced water was observed in 31 of 56 ears within six years of the disease; however, it was observed in all 32 ears of patients who had developed SCA3/MJD more than six years previously. Therefore, reduced bilateral VOR is considered to be a very useful biomarker of SCA3/MJD in clinical diagnosis, especially at six years or more since the onset of the disease. Moreover, the otoneurological findings in the markedly reduced VOR group (six patients) and normal VOR group (six patients) within six years after onset of the disease was investigated. In the markedly reduced VOR group, the incidence of upgaze palsy was higher, the impaired visual suppression of VOR was more advanced, and the mean maximum slow phase velocity of OKN was lower in comparison with the normal VOR group. It could indicate that the brainstem dysfunctions were more severe in the markedly reduced VOR group than in the normal VOR group. This may account for the fact that the bilateral VOR dysfunction in patients with SCA3/MJD may be due to a disorder in the central vestibular system originating from the VOR pathways.

Neuro-ophthalmology of movement disorders

Movement disorders commonly present with ocular features. The purpose of this review is to outline neuro-ophthalmologic findings that can help in diagnosis, treatment and determining prognosis in patients with movement disorders. Common movement disorders with ophthalmic symptoms include extrapyramidal disorders such as Parkinson disease-associated dry eye, decreased blink rate, and vergence dysfunction, and progressive supranuclear palsy-related lid retraction, frequent square-wave jerks and supranuclear gaze palsy. Multisystem atrophy can present with gaze-evoked horizontal or positional downbeat nystagmus and impaired vestibulo-ocular reflex suppression. Genetic disorders such as Huntington disease produce increased saccadic latencies and impaired suppression of saccades to presented stimulus, whereas Wilson disease is associated with saccadic pursuits, increased antisaccade latencies and decreased pursuit gain. Whipple's disease can present with supranuclear gaze palsy and characteristic oculomasticatory myorrhythmia. Movement disorders commonly present with ocular features. Knowledge of these ocular symptoms can assist the ophthalmologist in diagnosis and treatment of movement disorders.

14. Vestibular modulation of theta band oscillations in human pedunculopontine nucleus

Background and aims: The pedunculopontine nucleus (PPN) is a new deep brain stimulation (DBS) target, thought to be particularly for useful in ameliorating gait disturbance in Parkinson’s disease. Recent evidence shows a prominent theta (4–7 Hz) rhythm in the PPN (Tsang et al., Neurology, 2010; Simon et al., J. Neurophysiol., 2010; Shimamoto et al., JNNP, 2010). Given that theta activity is modulated by vestibular signals elsewhere in the brain, e.g. hippocampus, (Shin, Synapse, 2010; Chen et al., Neuroimage, 2010), we assessed whether vestibular signals modulate PPN theta activity. Methods: We recorded local field potentials (LFPs) in three patients with implanted bilateral subthalamic nucleus (STN) and PPN DBS electrodes at 2000 Hz and filtered at 0.5–500 Hz at rest and during passive, yaw-plane whole body rotations (i.e., vestibular stimulation) at 0.2 and 0.4 Hz with eyes closed and then open with manifest vestibular ocular reflex activation (i.e., nystagmus) and then with VOR suppression (VORS). Frequency power spectra and the average power across a 1–1000 Hz frequency range were obtained. Results: PPN LFPs showed significant modulation during vestibular activation (rotations) compared to rest with power changes ca. four times larger than those found in the STN. The PPN LFP was dominated by theta (4–7 Hz) activity which was enhanced during all tasks compared to rest (including eyes open vs. closed at rest) except for VORS where there was a clear reduction in theta activity and this was more prominent for ‘fast’ (i.e., 0.4 Hz rotations) rotations. The pattern of theta activity was the same for right and left PPN including task-dependent modulation. To rule out the possibility that this theta activity was purely driven by nystagmus, we recorded LFPs during optokinetic nystagmus (OKN). OKN was associated with a decrease of theta power compared to rest. Conclusions: This is the first demonstration of vestibular modulation of PPN activity (in either animals or humans). Human PPN activity is increased during vestibular activation with a relative suppression of theta during VORS. This pattern of a reduction of activity during VORS compared to VOR is seen in the vestibular nuclei. Thus, the PPN may represent an important component of vestibular processing within the brainstem. We speculate that given the role of the vestibular system in balance and posture, PPN DBS may be work to improve gait and balance control via vestibular circuits.

15. Functional mapping of monaural auditory brainstem responses

Background and aims: The pedunculopontine nucleus (PPN) is a new deep brain stimulation (DBS) target, thought to be particularly for useful in ameliorating gait disturbance in Parkinson’s disease. Recent evidence shows a prominent theta (4–7 Hz) rhythm in the PPN (Tsang et al., Neurology, 2010; Simon et al., J. Neurophysiol., 2010; Shimamoto et al., JNNP, 2010). Given that theta activity is modulated by vestibular signals elsewhere in the brain, e.g. hippocampus, (Shin, Synapse, 2010; Chen et al., Neuroimage, 2010), we assessed whether vestibular signals modulate PPN theta activity. Methods: We recorded local field potentials (LFPs) in three patients with implanted bilateral subthalamic nucleus (STN) and PPN DBS electrodes at 2000 Hz and filtered at 0.5–500 Hz at rest and during passive, yaw-plane whole body rotations (i.e., vestibular stimulation) at 0.2 and 0.4 Hz with eyes closed and then open with manifest vestibular ocular reflex activation (i.e., nystagmus) and then with VOR suppression (VORS). Frequency power spectra and the average power across a 1–1000 Hz frequency range were obtained. Results: PPN LFPs showed significant modulation during vestibular activation (rotations) compared to rest with power changes ca. four times larger than those found in the STN. The PPN LFP was dominated by theta (4–7 Hz) activity which was enhanced during all tasks compared to rest (including eyes open vs. closed at rest) except for VORS where there was a clear reduction in theta activity and this was more prominent for ‘fast’ (i.e., 0.4 Hz rotations) rotations. The pattern of theta activity was the same for right and left PPN including task-dependent modulation. To rule out the possibility that this theta activity was purely driven by nystagmus, we recorded LFPs during optokinetic nystagmus (OKN). OKN was associated with a decrease of theta power compared to rest. Conclusions: This is the first demonstration of vestibular modulation of PPN activity (in either animals or humans). Human PPN activity is increased during vestibular activation with a relative suppression of theta during VORS. This pattern of a reduction of activity during VORS compared to VOR is seen in the vestibular nuclei. Thus, the PPN may represent an important component of vestibular processing within the brainstem. We speculate that given the role of the vestibular system in balance and posture, PPN DBS may be work to improve gait and balance control via vestibular circuits.

The oculogyral illusion: retinal and oculomotor factors

Subjects in a dark chamber exposed to angular acceleration while viewing a head-fixed target experience motion and displacement of the target relative to their body. Competing explanations of this phenomenon, known as the oculogyral illusion, have attributed it to the suppression of the vestibulo-ocular reflex (VOR) or to retinal slip. In the dark, the VOR evokes compensatory eye movements in the direction opposite to body acceleration. A head-fixed visual target will tend to suppress these eye movements. The VOR suppression hypothesis attributes the oculogyral illusion to the signals that prevent reflexive deviation of the eyes from the target thus resulting in apparent target displacement in the direction of acceleration. The retinal slip hypothesis attributes the illusion to inadequate fixation of the target with the eyes being involuntarily deviated in the direction opposite acceleration, the retinal slip being interpreted as target displacement in the direction of acceleration. Another possibility is that the illusion could arise from a change in the representation of the perceived head midline. To evaluate these three alternative hypotheses, we tested 8 subjects at 4 acceleration rates (2, 10, 20, 30°/s²) in each of three conditions: (a) fixate and point to a target light; (b) fixate to the target light and point to the head midline; (c) look straight ahead in the dark. The displacement magnitude of the oculogyral illusion was least at 2°/s²≈2° and was ≈10° at the other acceleration rates. The presence of the target light significantly attenuated eye movements relative to the dark condition, but eye movements were still present at the 10, 20, and 30°/s² accelerations. The eye velocity profiles in the dark at different acceleration rates did not show a one-to-one inverse mapping to the magnitude of the oculogyral illusion at those rates. The perceived head midline was not significantly displaced at any of the acceleration rates. The oculogyral illusion thus has at least two contributing factors: the suppression of nystagmus at low acceleration rates and at higher acceleration rates, a partial suppression coupled with an integration of the drift of the eyes with respect to the fixation target.

POD06 Human pedunculopontine nucleus displays vestibular reactivity

We recorded local field potentials (LFPs) in a patient with implanted bilateral subthalamic nucleus (STN) and pedunculopontine nucleus (PPN) deep brain stimulation (DBS) electrodes at 2 kHz and filtered at...

Eye movement recordings to investigate a supranuclear component in chronic progressive external ophthalmoplegia: a cross-sectional study

BackgroundIt has been postulated that eye movement disorders in chronic progressive external ophthalmoplegia (CPEO) have a neurological as well as a myopathic component to them.AimTo investigate whether there is a...

Altered vision during motion: an unusual symptom of cerebellar dysfunction, quantifiable by a simple clinical test

To report a series of patients with cerebellar dysfunction and altered vision during motion, and to quantify their visual impairment in motion with a simple clinical test. Twenty consecutive patients suffering from cerebellar dysfunction and altered vision during motion were examined between 1994 and 2007. A control group consisted of 20 age- and sex-matched healthy people. All patients had a full neuro-ophthalmic examination. Near visual acuity (NVA) was measured at rest (static NVA) and during chair rotation (dynamic NVA). Distance visual acuity (DVA) was measured at rest (static DVA) and during rotation of the patient's head (dynamic DVA). Only four of the 20 patients reported altered vision during motion spontaneously. The remaining 16 patients admitted this unusual visual disturbance only when asked specifically. All patients exhibited abnormal eye movements, including saccadic smooth pursuit (20/20), dysmetric saccades (15/20), nystagmus (19/20) and impaired suppression of vestibulo-ocular reflex (VOR) (20/20). During rotation of the examination chair (dynamic NVA), the drop in NVA averaged 5.6 lines (range 1-10 lines). During rotation of the patient's head (dynamic DVA), the drop in DVA averaged only 2.5 lines (range 0-10 lines). For the control group, there was no significant drop in NVA under dynamic conditions. Patients with cerebellar dysfunction rarely complain spontaneously of altered vision during motion. However, specific questioning may bring up this unusual symptom. The use of a simple clinical test, consisting of NVA measurement during rotation of the examination chair (dynamic NVA), allows practitioners to quantify the level of visual impairment in patients presenting altered VOR modulation.

Anatomical correlates of ocular motor deficits in cerebellar lesions

Humans are able to stabilize the images of moving targets on the retina by means of smooth pursuit eye movements. After the pontine level, all smooth pursuit pathways pass through the cerebellum. Previous animal studies gave evidence that two specific lesion sites within the cerebellum cause smooth pursuit disorders: those of the flocculus/paraflocculus and the vermis including lobule VI, VII, the uvula and the deep cerebellar nuclei. To date, there have been only a few lesion studies in patients with smooth pursuit disorders that do not allow direct comparison with a control group. In the present study, new lesion mapping techniques determined which cerebellar structures were involved in patients with deficits of smooth pursuit eye movements, slow phase of optokinetic nystagmus (OKN) and fixation suppression of vestibulo-ocular reflex, i.e. in eye movements that are considered to belong to the smooth pursuit system. The aim was to elucidate whether there is an anatomical and clinical link between these different eye movement disorders. Seventeen patients with acute, mainly unilateral cerebellar infarctions and an intact gain of the smooth pursuit system were compared with 11 patients with cerebellar lesions and deficient gain of sinusoidal smooth pursuit eye movements by means of lesion-mapping imaging. In addition, lesion analyses were conducted in subgroups with impaired fixation suppression of vestibulo-ocular reflex and deficient gain of the slow phase of the OKN. The uvula and partly the vermal pyramid were found to be the structures commonly damaged in patients with deficient gain of the horizontal sinusoidal smooth pursuit eye movement, of the slow phase of the OKN and impaired fixation suppression of vestibulo-ocular reflex; and were less involved in patients with intact smooth pursuit system. The present data give evidence for an anatomical link between sinusoidal smooth pursuit eye movements, fixation suppression of vestibulo-ocular reflex and the slow phases of OKN implying that the uvula and the vermal pyramid are important structures for generating slow phases within the smooth pursuit network in humans.

Head‐Shaking Nystagmus in Central Vestibulopathies

Mechanisms of head-shaking nystagmus (HSN) require further exploration in central vestibular disorders. To determine whether impaired uvulonodular inhibition over the velocity storage of the vestibulo-ocular reflex (VOR) is the mechanism of ipsilesional HSN in lateral medullary infarction (LMI), 17 patients with ipsilesional HSN and LMI underwent measurements of the VOR gains during low-frequency sinusoidal harmonic accelerations, and the time constants (TC) of the VOR and tilt suppression of the post-otatory nystagmus during step-velocity rotation. Compared with normal controls, the patients showed increased VOR gains without difference between ipsi- and contralesional rotations, while the VOR TCs were decreased without directional asymmetry during step-velocity rotation. In contrast, the patients showed impaired tilt suppression of the postrotatory nystagmus, and the impairment of tilt suppression was more severe after contralesional than ipsilesional rotation. The asymmetric tilt suppression may generate ipsilesional HSN by increasing contralesional velocity storage during head shaking, and may be ascribed to disruption of ipsilesional nodulo-uvular inhibition of the velocity storage mechanism.

Oculomotor function in multiple system atrophy: Clinical and laboratory features in 30 patients

We reviewed the clinical and laboratory oculomotor features in 30 patients with probable multiple system atrophy (MSA), 22 with MSA-P and 8 with MSA-C. Six patients were also examined post mortem, MSA being confirmed in four and excluded in two (Parkinson's disease and progressive supranuclear palsy). Clinical examination showed the following abnormalities; excessive square wave jerks--21 of 30 patients; mild vertical supranuclear gaze palsy--8 of 30; gaze-evoked nystagmus--12 of 30 patients, three of whom had no extraocular evidence of cerebellar dysfunction; positioning downbeat nystagmus--10 of 25; mild or moderate saccadic hypometria--22 of 30; impaired ("broken up") smooth pursuit--28 of 30; reduced VOR suppression--16 of 24. Electro-oculography and caloric testing did not add significant extra information. In patients presenting with an akinetic-rigid syndrome it can be difficult to differentiate idiopathic Parkinson's disease from MSA-P and other causes of atypical parkinsonism. Our findings suggest that the presence of excessive square wave jerks, mild-moderate hypometria of saccades, impaired VOR suppression, spontaneous nystagmus or positioning downbeat nystagmus may be oculomotor "red flags" or clues to the presence of MSA. Further, the presence of clinically slow saccades, or moderate-to-severe gaze restriction, suggests a diagnosis other than MSA.