Patients with non-compensated vestibular dysfunction frequently complain of the ability to maintain dynamic visual acuity during activities which require the movement of the head. When this occurs the patient is experiencing oscillopsia, which is the symptom resulting from a non-functional vestibulo-ocular reflex (VOR). To measure the presence of oscillopsia, tests of dynamic visual acuity (DVA) may be used. A recent test of DVA has been reported which is administered while patients are walking on a treadmill. Although this test has been shown to be useful in evaluating DVA in patients, there are several disadvantages to treadmill use. These include physical space, cost and accessibility. Additionally, walking at the required treadmill speed to produce sufficient head movement may pose difficulties and be medically contraindicated for patients with certain health risks. The purpose of this study was to evaluate a different method to measure DVA in patients which would not require the use of the treadmill, but instead utilize a volitional head movement to reveal oscillopsia. In this study, patients performed the DVA test in two conditions: (1) walking on a treadmill, and (2) seated on a chair volitionally moving the head. In this study, DVA was tested in both conditions with 15 adults with normal vestibular function, and 16 adults with vestibular impairment. Results revealed that both methods, treadmill walking and volitional head movement, appeared equivalent for measuring DVA in normal subjects and vestibular impaired subjects. The lack of finding a significant main effect of method, and interactions that include method, supports the equivalence of volitional head movement to a treadmill approach for the measurement of DVA.

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Description:With age and impairment due to neurodegenerative processes, the nervous system expresses symptoms of dizziness and imbalance with a dramatic increase in fall risk. While the fall risk of older individuals is well-known, the symptoms for patients with peripheral nervous system (PNS) pathology and central nervous system (CNS) degeneration are less well-known and manifest as vestibulo-ocular and vestibulo-spinal impairment. Emerging research shows a clear dysfunction in vestibular physiology in these populations, which adversely affects gaze and postural control and increases fall risk. This session will discuss the pathophysiology of vestibular function in the context of aging and PNS/CNS damage, critical examination tools, and research-based recommendations to augment vestibular motor learning in these patient populations. The presenters will use case studies to illustrate characteristic deficits in vestibular function and guide clinical decision making regarding examination and treatment. Learning Objectives:1 . Describe the natural aging process as it relates to vestibulo-ocular and vestibulospinal function. 2. Discuss the evidence for vestibular damage within 2 model neurodegenerative diseases. 3. Describe the research evidence for motor learning within the vestibulo-ocular and vestibulospinal pathways in the context of aging and neurodegeneration. 4. Identify crucial examination tools and treatment methods to measure and improve gaze and gait stability in patients with a variety of neurodegenerative diseases.

Le récepteur aux hydrocarbures aromatiques (AhR) est un facteur de transcription de la famille bHLH/PAS, activé par différents ligands exogènes dont les hydrocarbures aromatiques polycycliques ou halogénés (dioxines). A ce titre, il est décrit historiquement comme un récepteur de xénobiotiques dont le principal rôle est l’élimination de ces composés via la régulation des enzymes du métabolisme des xénobiotiques. Toutefois, des études récentes menées à l’aide de modèles souris invalidées pour le AhR, suggèrent indirectement que cette protéine régule des fonctions endogènes, notamment dans le système nerveux de mammifères dans lequel aucun rôle du AhR n’a jusqu’à présent été démontré. Nous avons donc utilisé le modèle de souris C57BL/6J AhR-/- pour mener à la fois des études comportementales et mécanistiques afin de déterminer ce rôle. Tout d’abord, nous avons identifié un défaut oculomoteur chez les souris AhR-/-, caractérisé par des mouvements spontanés horizontaux. En étudiant l’ensemble des circuits neurosensoriels potentiellement impliqués dans ce nystagmus pendulaire, nous avons montré que son origine est liée à des déficits du système visuo-moteur. De plus, en caractérisant et comparant les profils d’expression génique des cervelets de souris AhR+/+ et AhR-/- traitées ou non par de la 2,3,7,8 TétraChloroDibenzo-p-Dioxine (TCDD), nous avons montré que ce polluant, ligand du AhR, perturbait les fonctions endogènes du récepteur. Cet effet de « perturbation endogène » a été retrouvé dans un autre organe et est associé à une toxicité (fibrose hépatique). Cette étude a permis d’identifier de nouvelles fonctions physiologiques du AhR dans le système nerveux des souris, de caractériser un nouveau modèle animal de nystagmus pendulaire et ouvre de nouvelles perspectives de travail en neurotoxicologie. / The AhR is a basic helix-loop-helix Per/ARNT/Sim family (bHLH-PAS) transcription factor which is activated by many diverse compounds including polyphenols and aromatic hydrocarbons such as 2,3,7,8 TétraChloroDibenzo-p-Dioxin (TCDD). Initially, the AhR was described as a ubiquitous xenobiotic-activated transcription factor which promotes the elimination of xenobiotics by regulating the expression of genes involved in xenobiotic metabolism. However, mouse AhR knockout models have demonstrated that the AhR also regulates other normal physiological functions. In particular, functioning of the nervous system of mammals, previously unexplored in this respect, might depend upon the activity of the AhR. We, thus, performed behavioral and gene expression studies in AhR-/- mice to discover these functions. We, first, found that AhR-/- mice exhibit an oculomotor deficit which is characterized by spontaneous horizontal pendular eye movements that are probably due to a deficit in the visuo-motor circuitry. Second, we found that the cerebellar gene expression profiles of AhR-/- as compared to AhR+/+ mice resembled those of AhR+/+ mice treated with TCDD (the ligand with the highest affinity for the AhR). This suggests that TCDD disrupts some normal physiological functions of the AhR in the nervous system. Third, AhR-/- mice and AhR+/+ treated with TCDD both develop liver fibrosis. This further suggests a role for the AhR in normal liver function. In conclusion, this study reveals new physiological functions for the AhR in the mouse nervous system and describes a new model of pendular nystagmus. Moreover, the results also provide novel research perspectives in the field of neurotoxicology.

Athletic potential is one of the most complex human traits. An elite athlete is produced from a complex interaction of an innumerable number of traits exhibited by the athlete. However, it’s not clear whether these traits are innate, allowing the athlete to excel, or, alternatively, are a consequence of practice. To be successful, athletes rely heavily on sensory information from the visual and vestibular systems. This study investigated the relationship eye movement control has with innate athleticism by comparing the saccadic and Vestibulo-Ocular Reflex (VOR) responses of former, no longer practicing, elite athletes against their age and gender matched counterparts who were non-elite or non-athletes. Results showed subjects who participated in athletic activities longer (regardless of type or level achieved), showed both significantly better VOR suppression capabilities, as well as higher head velocities while suppressing their VOR. Although, these results are correlative in nature, they do not support the potential that VOR suppression is a learned trait of athletes. A longitudinal study would be required to assess this relationship fully.

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The human vestibulo-ocular reflex (VOR) stabilizes gaze during head movement. The reflex is typically tested in a clinic or laboratory using passive rotations or artificial stimuli which measure the amount of damage the vestibular apparatus has suffered. However, during everyday activities the vestibular system is stimulated by active, self generated head movements. Head movements are often rapid and associated with the goal of achieving either gaze-fixation or re-fixation. Patients who complain of on-going symptoms will typically identify a particular position or movement that aggravates their symptoms in their everyday life. There is a need to identify objective parameters which correlate with the subjective complaints of patients whose symptoms persist after vestibular damage. In the first study, a gaze-refixation task, patients who complain of ongoing symptoms (poorly-compensated), during rapid head turns, after unilateral vestibular de-afferentation (uVD) were compared with those who did not have the same complaints (well-compensated) and normal subjects. Well- and poorly-compensated groups were sorted according to responses on a standardized questionnaire. All subjects were then located in a real-world, non-laboratory environment in which poorly-compensated subjects reported experiencing symptoms. Each subject’s head, eye and gaze displacement and velocity, head rotation frequency and blink or eye-lid closure were measured and analysed and compared between ipsi- and contra-lesional head rotations within and between subject groups. When subjects are able to generate their own active head rotations it has been suggested that a number of vestibular and extra-vestibular strategies might be employed to compensate for an impaired VOR. In subsequent studies, high resolution scleral search coils were used to identify the compensatory mechanisms used during active head rotations during a gaze-fixation task. A corrective saccade is typically observed during passive ipsilesional head rotations or “impulses” and might be potentiated during rapid, active or self-generated head rotations. The conditions which predict or contribute to the generation of the rapid, corrective eye movement were investigated. The results were compared with responses to passive head impulses of matched velocity and acceleration to determine if active head impulses could be used to identify a lesioned vestibular apparatus as is routinely clinically achieved with passive head impulses.

The human vestibulo-ocular reflex (VOR) stabilizes gaze during head movement. The reflex is typically tested in a clinic or laboratory using passive rotations or artificial stimuli which measure the amount of damage the vestibular apparatus has suffered. However, during everyday activities the vestibular system is stimulated by active, self generated head movements. Head movements are often rapid and associated with the goal of achieving either gaze-fixation or re-fixation. Patients who complain of on-going symptoms will typically identify a particular position or movement that aggravates their symptoms in their everyday life. There is a need to identify objective parameters which correlate with the subjective complaints of patients whose symptoms persist after vestibular damage. In the first study, a gaze-refixation task, patients who complain of ongoing symptoms (poorly-compensated), during rapid head turns, after unilateral vestibular de-afferentation (uVD) were compared with those who did not have the same complaints (well-compensated) and normal subjects. Well- and poorly-compensated groups were sorted according to responses on a standardized questionnaire. All subjects were then located in a real-world, non-laboratory environment in which poorly-compensated subjects reported experiencing symptoms. Each subject’s head, eye and gaze displacement and velocity, head rotation frequency and blink or eye-lid closure were measured and analysed and compared between ipsi- and contra-lesional head rotations within and between subject groups. When subjects are able to generate their own active head rotations it has been suggested that a number of vestibular and extra-vestibular strategies might be employed to compensate for an impaired VOR. In subsequent studies, high resolution scleral search coils were used to identify the compensatory mechanisms used during active head rotations during a gaze-fixation task. A corrective saccade is typically observed during passive ipsilesional head rotations or “impulses” and might be potentiated during rapid, active or self-generated head rotations. The conditions which predict or contribute to the generation of the rapid, corrective eye movement were investigated. The results were compared with responses to passive head impulses of matched velocity and acceleration to determine if active head impulses could be used to identify a lesioned vestibular apparatus as is routinely clinically achieved with passive head impulses.

In this study we examined dynamic visual acuity as a functional testing of the vestibulo- ocular reflex. Two groups were examined: 22 healthy seniors and 22 healthy young people as controls. We used two types of situations for testing: while walking on a treadmill at a speed of 2, 4 and 5 kmph, and with a subject's head passively moved in yaw and pitch plane. Visual acuity was measured with optotype charts (for the walking test it was a standard Snellen optotype chart at 6 m distance, for the test of head moves it was a Jaeger chart at 30 cm distance). The values obtained in these ways we related to values of a subject's static visual acuity, measured in the same conditions, just before the dynamic situations were examined. We found significant difference of dynamic visual acuity in senior group within each condition tested. We also found a significant decline as for difference of dynamic visual acuity in the senior group compared to young subjects - in the walking test at 4 and 5 kmph and in both head-moving conditions. These results indicate age-related impairment in function of vestibulo-ocular reflex. Based on our results, the test of passive head moves appears to be more suitable for ordinary clinical examination of dynamic visual acuity.