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This study utilized cervical vestibular-evoked myogenic potentials tests (cVEMP) and ocular vestibular-evoked myogenic potentials tests (oVEMP) to investigate the vestibulocollic and vestibuloocular reflex arcs and to evaluate cerebellar and brainstem involvement) in essential tremor (ET). Eighteen cases with ET and 16 age- and gender-matched healthy control subjects (HCS) were included in the present study. Otoscopic and neurologic examinations were performed on all participants, and both cervical and ocular VEMP tests were performed. Pathological cVEMP results were increased in the ET group (64.7%) compared to the HCS (41,2%; p > 0.05). The latencies of P1 and N1 waves were shorter in the ET group than in HCS (p = 0.01 and p = 0.001). Pathological oVEMP responses were significantly higher in the ET group (72.2%) compared to the HCS (37.5%; p = 0.01). There was no statistically significant difference in oVEMP N1-P1 latencies between groups (p > 0.05). Because the ET group had high pathological responses to the oVEMP, but not the cVEMP, the upper brainstem pathways may be more affected by ET. [ABSTRACT FROM AUTHOR]

BACKGROUND: Ground-based studies have reported shifts of the vestibulo-ocular reflex (VOR) slow phase velocity (SPV) axis toward the resultant gravito-inertial force vector. The VOR was examined during eccentric roll rotation before, during and after an 8-day orbital mission. On orbit this vector is aligned with the head z-axis. Our hypothesis was that eccentric roll rotation on orbit would generate horizontal eye movements. METHODS: Two subjects were rotated in a semi-supine position with the head nasal-occipital axis parallel to the axis of rotation and 0.5 m off-center. The chair accelerated at 120 deg/s2 to 120 deg/s, rotated at constant velocity for one minute, and then decelerated to a stop in similar fashion. RESULTS: On Earth, the stimulation primarily generated torsional VOR. During spaceflight, in one subject torsional VOR became horizontal VOR, and then decayed very slowly. In the other subject, torsional VOR was reduced on orbit relative to pre- and post-flight, but the SPV axis did not rotate. CONCLUSION: We attribute the shift from torsional to horizontal VOR on orbit to a spatial orientation of velocity storage toward alignment with the gravito-inertial force vector, and the inter-individual difference to cognitive factors related to the subjective straight-ahead. [ABSTRACT FROM AUTHOR]

The cervico-ocular reflex (COR) has a low gain in normal animals. In this study, we determined whether COR gain increases were specific to the low/midband frequency range, which is the range over which the angular vestibulo-ocular reflex (aVOR) is compromised by plugging. The gain and phase of the yaw and pitch COR and aVOR were compared in normal monkeys and those with all six semicircular canals or only the lateral canal plugged. During experiments animals sat with the body fixed to a chair and the head fixed in space. The body was oscillated about body-yaw and body-pitch axes over a frequency range of 0.05–6 Hz, with amplitude <10°. For normal animals, both yaw and pitch eye velocities were compensatory to the relative velocity of the head with respect to the body. The gains were 0.1–0.2 at frequencies below 1 Hz and decreased to zero as stimulus frequency increased above 1 Hz. Canal-plugged animals had COR gains close to 1.0 at low frequencies, decreasing to ≈0.6 at 0.5 Hz and to 0.2 for stimulus frequencies above 3 Hz. The phase of eye velocity was 180° relative to head-re-body velocity at frequencies below 0.5 Hz and shifted toward 270° as frequencies were increased to 4 Hz. This study demonstrates that adaptation of COR gain is tuned to a frequency range at which the aVOR is compromised by the canal plugging. [ABSTRACT FROM AUTHOR]

Introduction: The vestibulo-ocular reflex (VOR) is an important part of the neurologicalexamination of the patient with coma when determining brainstem function. VOR istested via the oculocephalic reflex (OCR) and the oculovestibular reflex (OVR), or coldcalorics. It has been noted that sedative medications, such as opioids and benzodiazepines,can diminish or abolish the VOR.Methods: We performed a chart review on three patients noted to have absent VOR atinitial neurological assessment as an isolated finding.Results: The three patients ranged in age from 45-74 years. Two patients presented withintentional drug overdoses, whereas the third patient had a complicated course postcardiacsurgery and received sedative drugs. All three patients initially had absent responses toOCR and cold calorics bilaterally. However, all other brainstem functions were normal atthe initial examination. All three patients regained both OCR and OVR within 24 hoursafter sedative medication had been removed.Conclusion: Sedatives may selectively and transiently abolish the VOR, altering theclinical examination; this is to be considered in the examination of a patient with coma. [ABSTRACT FROM AUTHOR]

This study determined whether dependence of angular vestibuloocular reflex (aVOR) gain adaptation on gravity is a fundamental property in three dimensions. Horizontal aVOR gains were adaptively increased or decreased in two cynomolgus monkeys in upright, side down, prone, and supine positions, and aVOR gains were tested in darkness by yaw rotation with the head in a wide variety of orientations. Horizontal aVOR gain changes peaked at the head position in which the adaptation took place and gradually decreased as the head moved away from this position in any direction. The gain changes were plotted as a function of head tilt and fit with a sinusoid plus a bias to obtain the gravity-dependent (amplitude) and gravity-independent (bias) components. Peak-to-peak gravity-dependent gain changes in planes containing the position of adaptation and the magnitude of the gravity-independent components were both approximately 25%. We assumed that gain changes over three-dimensional space could be described by a sinusoid the amplitude of which also varied sinusoidally. Using gain changes obtained from the head position in which the gains were adapted, a three-dimensional surface was generated that was qualitatively similar to a surface obtained from the experimental data. This extends previous findings on vertical aVOR gain adaptation in one plane and introduces a conceptual framework for understanding plasticity in three dimensions: aVOR gain changes are composed of two components, one of which depends on head position relative to gravity. It is likely that this gravitational dependence optimizes the stability of retinal images during movement in three-dimensional space. [ABSTRACT FROM AUTHOR]

The ionotropic glutamate receptorδ2 subunit (GluRδ2) is selectively expressed in cerebellar Purkinje cells and is implicated in long-term depression, synaptic formation and elimination. To study the effect of GluRδ2 deficiency on motor control, we measured the vestibulo-ocular reflex (VOR) and optokinetic response (OKR) induced by sinusoidal rotation of the animal and/or the surrounding screen in two GluRδ2 mutant mice: a GluRδ2 knockout mouse (δ2–/–) and alurchermouse with a point mutation in the GluRδ2 gene resulting in loss of all Purkinje cells.δ2–/– showed significantly higher VOR gain in the dark (VORD) than in the wild-type. Inδ2–/–, the VOR gain in light was lower than that in the dark. The phase of OKR lagged more inδ2–/– than inlurcherand wild-type mice. Both mutant mice failed to change the VORD or OKR gain adaptively in response to sustained vestibular and/or visual stimulation. Basal properties of VOR and OKR changed little by lesion of the flocculus, but they changed substantially by lesion of the inferior olivary nuclei (IO). The abnormal VOR gain and OKR phase delay were clearly reduced inδ2–/– by the latter lesion. Our results indicate that failures in the GluRδ2-dependent synaptic regulation affect motor performance more severely than loss of cerebellar cortical outputs. This study suggests that the anomalies inδ2–/– are dependent on inputs from IO and that GluRδ2 deficiency changed properties of not only the cerebellar cortex but also the brainstem neuronal pathways controlling reflex eye movements during development. [ABSTRACT FROM AUTHOR]

The gain of the vestibulo-ocular reflex (VOR) normally depends on the distance between the subject and the visual target, but it remains uncertain whether vergence angle can be linked to changes in VOR gain through a process of context-dependent adaptation. In this study, we examined this question with an adaptation paradigm that modified the normal relationship between vergence angle and retinal image motion. Subjects were rotated sinusoidally while they viewed an optokinetic (OKN) stimulus through either diverging or converging prisms. In three subjects the diverging prisms were worn while the OKN stimulus moved out of phase with the head, and the converging prisms were worn when the OKN stimulus moved in-phase with the head. The relationship between the vergence angle and OKN stimulus was reversed in the fourth subject. After 2 h of training, the VOR gain at the two vergence angles changed significantly in all of the subjects, evidenced by the two different VOR gains that could be immediately accessed by switching between the diverged and converged conditions. The results demonstrate that subjects can learn to use vergence angle as the contextual cue that retrieves adaptive changes in the angular VOR. [ABSTRACT FROM AUTHOR]