Visual Input Is the Main Trigger and Parametric Determinant for Catch-Up Saccades During Video Head Impulse Test in Bilateral Vestibular Loss

Patients with vestibular deficit use slow eye movements or catch-up saccades (CUS) to compensate for impaired vestibulo-ocular reflex (VOR). The purpose of CUS is to bring the eyes back to the visual target. Covert CUS occur during high-velocity head rotation and overt CUS are generated after head rotation has stopped. Dynamic visual acuity is improved with an increased rate and gain of CUS. Nevertheless, the trigger and the parametric determinants of CUS are still under debate. To clarify the underlying mechanism, especially the visual contribution, we analyzed the number, amplitude and latencies of the CUS in relation with the extent of VOR deficiency. The head and eye movements were recorded in 17 patients with bilateral vestibular loss (BVL) and in 33 subjects with normal VOR gain using the Video Head Impulse Test (vHIT) in two conditions: with visible target and in darkness with an imaginary target. Our study shows that in darkness without visible target the number of CUS is significantly reduced and the relationship between the amplitude of CUS and gaze position error is lost. Results showed that there is a correlation between the number of CUS and the drop in VOR gain. CUS occurring during the head movement and when the head remained still were not always sufficiently accurate. Up to four consecutive CUS could be required to bring eyes back to the visible target. A positive correlation was found between the amplitude of overt saccades with visible target and the gaze position error, namely the remaining eye movement to reach the target. These results suggest that the visual inputs are the main trigger and parametric determinant of the CUS or at least the presence of a visual target is necessary in most cases for a CUS to occur

Influence of Visual and Vestibular Hypersensitivity on Derealization and Depersonalization in Chronic Dizziness

Objective: The aim of this study was to investigate the relation between visual and vestibular hypersensitivity, and Depersonalization/Derealization symptoms in patients with chronic dizziness.Materials and Methods: 319 adult patients with chronic dizziness for more than 3 months (214 females and 105 males, mean age: 58 years, range: 13–90) were included in this prospective cross-sectional study. Patients underwent a complete audio-vestibular workup and 3 auto questionnaires: Hospital Anxiety and Depression (HAD), Depersonalization/Derealization Inventory (DDI), and an in-house questionnaire (Dizziness in Daily Activity, DDA) assessing 9 activities with a score ranging from 0 (no difficulty) to 10 (maximal discomfort) and 11 (avoidance) to detect patients with visual and vestibular hypersensitivity (VVH, a score > 41 corresponding to mean + 1 standard deviation).Results: DDI scores were higher in case of VVH (6.9 ± 6.79, n = 55 vs. 4.2 ± 4.81, n = 256 without VVH, p < 0.001, unpaired t-test), migraine (6.1 ± 6.40, n = 110 vs. 4.0 ± 4.42, n = 208no migraine, p < 0.001, unpaired t-test), and motion sickness (6.8 ± 5.93, n = 41 vs. 4.4 ± 5.11, n = 277 no motion sickness, p < 0.01, unpaired t-test). Women scored DDI higher than men (5.1 ± 5.42, n = 213 vs. 3.9 ± 4.91, n = 105, respectively, p < 0.05, unpaired t-test). DDI scores were also related to depression and anxiety. DDI score was also higher during spells than during the basal state.Conclusion: During chronic dizziness, Depersonalization/Derealization symptoms seem to be related to anxiety and depression. Moreover, they were prominent in women, in those with visual and vestibular hypersensitivity, migraine, and motion sickness

Nonsyndromic bilateral and unilateral optic nerve aplasia: first familial occurrence and potential implication of CYP26A1 and CYP26C1 genes

Purpose: Optic nerve aplasia (ONA, OMIM 165550) is a very rare unilateral or bilateral condition that leads to blindness in the affected eye, and is usually associated with other ocular abnormalities. Although bilateral ONA often occurs in association with severe congenital anomalies of the brain, nonsyndromic sporadic forms with bilateral ONA have been described. So far, no autosomal-dominant nonsyndromic ONA has been reported. The genetic basis of this condition remains largely unknown, as no developmental genes other than paired box gene 6 (PAX6) are known to be implicated in sporadic bilateral ONA. Methods: The individuals reported underwent extensive ophthalmological, endocrinological, and neurologic evaluation, including neuroimaging of the visual pathways. In addition genomewide copy number screening was performed. Results: Here we report an autosomal-dominant form of nonsyndromic ONA in a Belgian pedigree, with unilateral microphthalmia and ONA in the second generation (II:1), and bilateral ONA in two sibs of the third generation (III:1; III: 2). No PAX6 mutation was found. Genome wide copy number screening revealed a microdeletion of maximal 363 kb of chromosome 10q23.33q23.33 in all affected individuals (II:1, III:1; III:2) and in unaffected I:1, containing three genes: exocyst complex component 6 (EXOC6), cytochrome p450, subfamily XXVIA, polypeptide 1 (CYP26A1), and cytochrome p450, subfamily XXVIC, polypeptide 1 (CYP26C1). The latter two encode retinoic acid-degrading enzymes. Conclusions: This is the first study reporting an autosomal-dominant form of nonsyndromic ONA. The diagnostic value of neuroimaging in uncovering ONA in microphthalmic patients is demonstrated. Although involvement of other genetic factors cannot be ruled out, our study might point to a role of CYP26A1 and CYP26C1 in the pathogenesis of nonsyndromic ONA. © 2011 Molecular Vision.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Discussion about Visual Dependence in Balance Control: European Society for Clinical Evaluation of Balance Disorders

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked FilesThe executive committee of the European Society for the clinical evaluation of balance disorders meets annually to address equilibrium problems that are not well understood. This is a review paper on discussions in the latest meeting we held. MATERIALS AND METHODS: Seeing patients with vestibular disorders who end up depending on visual information as part of their compensation process is a common clinical occurrence. However, this "visual dependence" can generate symptoms, which include nausea, sensations of imbalance, and anxiety. It is unclear how this develops, as symptoms can be widely variable from patient to patient. There are several triggering factors to this symptom set, and quantifying it in a given patient is extremely difficult Results: The committee agreed that the presence of this symptom set can be suggestive of vestibular pathology, but the pathology does not have to be present. As a result, there is no correlation between symptom severity and test results. CONCLUSION: Visual dependence can often be present in a patient, although little, if any, measurable pathology is present. It is important to emphasize that although we cannot accurately measure this with either standardized testing or pertinent questionnaires, "hypersensitive" patients have a genuine disease and their symptoms are not of psychiatric origin

Visual suppression of vestibular nystagmus

The realisation of combined movements of the head and eyes requires the capacity to modulate the vestibulo-ocular reflex (VOR) but the absence of sufficiently rapid visual feed back results in an open loop function. This reflex must be modulated by other mechanisms. Two options are discussed. A modulation of the gain of the reflex loop is not satisfactory for small combined movements of the head and eyes as it would no longer permit the effective compensation for unexpected perturbations of movement of the head. An additive mechanism modifying the VOR through the addition of an other ocular movement is limited by the constrictions of latency, speed and amplitude of such movement. According to experimental conditions, varying complementary effect of the two mechanisms seems to result in maximum efficiency. This paper attempts to include the mechanism of the ocular fixation index (OFI) among the models of study. The OFI applied to a pendular test is, by the nature of its stimulus, more physiologic and more capable of being integrated into existing models. In the usual conditions of the test, the additive model is probably dominant with a preponderant role in the ocular pursuit system. But whatever may be the part of each mechanism, the OFI is not only dependant on the integrity of the floccular inhibition of the VOR but on the numerous cortical and subcortical structures involved in the realisation of voluntary ocular movements. This information should encourage clinicians to investigate the ocular movements of patients presenting vertigo, particularly those with visual instability on head movements.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Séance dédiée: « de quelques sens »

Reliable knowledge of one's space is a prerequisite for effective action, and only sensory experience, although not alone sufficient, can provide access to knowledge of reality. All the different sensory modalities help to make sense of this mental construct, but visual information, when available, is predominant. This requires stable images and constant updating of one's awareness of gaze direction and position in space at the moment of acquisition. The vestibular system is sensitive to angular and linear accelerations and thus acts as a reference for stability - an inertial base which stabilizes and characterizes the gaze direction and encodes the subject's movement tracking. In clinical practice, loss of these capacities induces eye drift, nystagmus, oscillopsia, vertical eye misalignment and a shift in the representation of mental space, leading to dizziness, translational illusions, integration path error, and " senseless "perceptions of the self in space. The reaction time of the eye and of mental image stabilization is of the order of a few tens of milliseconds. Recent tools for vestibular exploration allow us to measure this reactivity, which is a determining factor for quality of life. The video head impulse test, dynamic visual acuity, and cervical vestibular evoked myogenic potentials explore the structures involved in gaze and image stabilization, while subjective visual vertical and ocular vestibular evoked myogenic potentials provide an approach to the utricular contribution. This clinical and instrumental semiology sometimes proves more sensitive than the most advanced and accurate medical imaging methods, but rational listening and multidisciplinary skills on the part of the physician remain necessary to identify "self in space " perceptual alterations.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Les troubles de l'équilibration

Balance disorders may result from an impairment of one of the sensorial modalities involved in the perception of the self-location in space: Vestibular, proprioception and vision, a deficit of the neuronal multisensorial integration, a less effective motor or loco-motor system, the medication side effects or psychological interferences. The basic examination of a dizzy patient implies the assessment of these different aspects. The balance is not restricted to à set of reflexes. It is a distinctive expression of the sixth sense :The sense of orientation. For every moving being, to go around in circles is ineffective to find new sources of food or avoid a predator. So, the ability of self-orientation in space is a primitive, unconscious function, critical to stay alive and closely related to the limbic system. The experience of the mobility, that required the spatial memory, which evolved towards the episodic memory, could be considered as the foundation of our thought.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Les syndromes vestibulaires centraux

The aim of this topic is on one hand to pick out the semiological features which can quickly show the way of central nervous system lesions related to the vestibular system and on the other hand to describe these main central vestibular syndromes. A particular attention is carried to central otolithics syndromes which often remain undiagnosed. They induce imbalance, non rotatory vertigo, intolerance to linear acceleration and most often there is no nystagmus on examination. Neurophysiological diagram are restricted to a minimum useful to the clinician.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Neuro-ophthalmological symptoms in vertigo and dizziness

The vestibular and visual systems are closely linked in the genesis of vertigo and dizziness. An examination of these two systems is helpful in the search for an aetiological diagnosis. In ENT, this double approach can also help to avoid certain ophthalmological pitfalls such as the mistaken idea that a squint cannot be of vestibular origin, that the absence of diplopia symptoms is enough to exclude any recent oculomotor paresis, or even that eyelid asymmetry is not relevant to diagnosing dizziness. This paper is intended to help in understanding the neuro-ophthalmological aspects of the guidelines. It is sometimes limited to defining certain terms. However, on the whole, it covers diagnostic procedures.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Adaptation du système nerveux central aux corrections optiques.

Wearing spectacles imply an adjustment of the visual perception and eye movements. The visual cortex accounts for this plasticity, including at the adulthood, especially by the shift or the sprading of the receptor fields and the adjustment of the sensitivity of the primary visual cortex cells to spatial orientation and movement. The cerebellum modulates the vestibulo-ocular reflex gain. The adjustment latencies range from a few minutes to several days according to the disturbancy severity, the drug interferences and the age and medical history of the subject. Neurotrophins seem to be essential for this adjustment and might become an efficient tool to extend the plasticity period.SCOPUS: ar.jinfo:eu-repo/semantics/publishe