Voluntary suppression of neck reflexes during passive head-on-trunk rotations - reflex gain control vs. proprioceptive feedback

Normal subjects can completely eliminate resistance upon imposed head-on-trunk rotations when they are asked to relax. It is not, however, clear how neck reflexes to stretch can be voluntarily suppressed. Reflexive responses might be modified by adjusting the gain of the reflex loop through descending control. Theoretically, necessary corrections upon interfering disturbances during coordinated motor performace requiring the interplay of relaxation/activation may be missing if muscle relaxation is taking place exclusively by this mechanism. It has been alternatively proposed, that sensory information from the periphery may be allowed to "neutralize" neck reflexes if it is fed back with opposite sign to the structures driving the reflexes. Six healthy subjects were asked to relax while subjected to head-on-trunk rotations generated by a head motor. After any initial resistance had completely subsided, the head was unexpectedly exposed to "ramp-and-hold" perturbations of up to 2○ amplitude and 0.7 s duration. Resistance to stretch consistently reappeared thereupon suggesting that stretch reflex gain had not been set to zero during the previously achieved complete relaxation. Resistance to perturbations under these circumstaces was compared to the forces generated when the same "ramp-and-hold" displacements were delivered unpredictably to the head held stationary. A quantitative model of neck proprioceptive reflexes suppression has been thus constructed. Gain scheduling or "motor set" cannot sufficiently account for the voluntary reflex suppression during slow passive head rotations. Instead, we propose as underlying mechanism the "neutralization" of the controlling servo by means of continuous feedback tracking displacement and force signals from the periphery.

Report of oscillopsia in ataxia patients correlates with activity, not vestibular ocular reflex gain

BACKGROUND: Patients with cerebellar ataxia report oscillopsia, “bouncy vision” during activity, yet little is known how this impacts daily function. The purpose of this study was to quantify the magnitude of oscillopsia and investigate its relation to vestibulo-ocular reflex (VOR) function and daily activity in cerebellar ataxia. METHODS: 19 patients diagnosed with cerebellar ataxia and reports of oscillopsia with activity were examined using the video head impulse test (vHIT), Oscillopsia Functional Index (OFI), and clinical gait measures. Video head impulse data was compared against 40 healthy controls. RESULTS: OFI scores in ataxia patients were severe and inversely correlated with gait velocity (r = –0.55, p < 0.05), but did not correlate with VOR gains. The mean VOR gain in the ataxic patients was significantly reduced and more varied compared with healthy controls. All patients had abnormal VOR gains and eye/head movement patterns in at least one semicircular canal during VHIT with passive head rotation. CONCLUSIONS: Patients with cerebellar ataxia and oscillopsia have impaired VOR gains, yet severity of oscillopsia and VOR gains are not correlated. Patients with cerebellar ataxia have abnormal oculomotor behavior during passive head rotation that is correlated with gait velocity, but not magnitude of oscillopsia.

Relationship between vestibulo-ocular reflex gain and dizziness handicap inventory score to predict effectiveness of vestibular rehabilitation

Background and Aim: Evaluating the effective­ness of vestibular rehabilitation (VR) in patients with vestibular lesions has always been a challe­nge. The questionnaires that are used for this pur­pose mostly show the degree of vestibular dis­ability rather than providing information about improvement of vestibular dysfunction. This study aimed to evaluate whether video head imp­ulse test (vHIT) that is used for the examination of vestibulo-ocular reflex (VOR), is a useful method for predicting the effectiveness of VR and has a correlation with dizziness handicap inventory (DHI) score. Methods: Participants were 42 patients with unilateral peripheral vestibular hypofunction (UPVH) undergoing VR. Patients were assessed before and after rehabilitation by the vHIT in all ipsilesional and contralesional semicircular can­als (SCCs) and the DHI. The changes in DHI score and VOR gain before and after rehabili­tation, were shown as ΔDHI and ΔVOR and their correlation was evaluated. Results: VOR gain from ipsilesional and contra­lesional SCCs was improved significantly after VR. There was a significant strong negative correlation between ΔVOR gain from ipsile­sional SCCs and ΔDHI score but no significant correlation was found between the ΔDHI score and ΔVOR gain from contralesional SCCs. Conclusion: vHIT test is a useful tool to evaluate the effectiveness of VR. VOR gain is correlated with the DHI score. Therefore, the improvement in vHIT results in all three SCCs after VR may be a good predictor of the degree of improvement in dizziness-related disability. Keywords: Vestibular rehabilitation; follow-up; unilateral vestibular hypofunction; video head impulse test; dizziness handicap inventory

The Effect of Different Head Movement Paradigms on Vestibulo-Ocular Reflex Gain and Saccadic Eye Responses in the Suppression Head Impulse Test in Healthy Adult Volunteers

Objective: This study aimed to identify differences in vestibulo-ocular reflex gain (VOR gain) and saccadic response in the suppression head impulse paradigm (SHIMP) between predictable and less predictable head movements, in a group of healthy subjects. It was hypothesized that higher prediction could lead to a lower VOR gain, a shorter saccadic latency, and higher grouping of saccades.Methods: Sixty-two healthy subjects were tested using the video head impulse test and SHIMPs in four conditions: active and passive head movements for both inward and outward directions. VOR gain, latency of the first saccade, and the level of saccade grouping (PR-score) were compared among conditions. Inward and active head movements were considered to be more predictable than outward and passive head movements.Results: After validation, results of 57 tested subjects were analyzed. Mean VOR gain was significantly lower for inward passive compared with outward passive head impulses (p &lt; 0.001), and it was higher for active compared with passive head impulses (both inward and outward) (p ≤ 0.024). Mean latency of the first saccade was significantly shorter for inward active compared with inward passive (p ≤ 0.001) and for inward passive compared with outward passive head impulses (p = 0.012). Mean PR-score was only significantly higher in active outward than in active inward head impulses (p = 0.004).Conclusion: For SHIMP, a higher predictability in head movements lowered gain only in passive impulses and shortened latencies of compensatory saccades overall. For active impulses, gain calculation was affected by short-latency compensatory saccades, hindering reliable comparison with gains of passive impulses. Predictability did not substantially influence grouping of compensatory saccades.

Episodic Vestibulocerebellar Ataxia Associated with a CACNA1G Missense Variant

Episodic vestibulocerebellar ataxias are rare diseases, frequently linked to mutations in different ion channels. Our objective in this work was to describe a kindred with episodic vestibular dysfunction and ataxia, associated with a novel <i>CACNA1G</i> variant. Two individuals from successive generations developed episodes of transient dizziness, gait unsteadiness, a sensation of fall triggered by head movements, headache, and cheek numbness. These were suppressed by carbamazepine (CBZ) administration in the proband, although acetazolamide and topiramate worsened instability, and amitriptyline and flunarizine did not prevent headache spells. On examination, the horizontal head impulse test (HIT) yielded saccadic responses bilaterally and was accompanied by cerebellar signs. Two additional family members were asymptomatic, with normal neurological examinations. Reduced vestibulo-ocular reflex gain values, overt and covert saccades were shown by video-assisted HIT in affected subjects. Hearing acuity was normal. Whole-exome sequencing demonstrated the heterozygous <i>CACNA1G</i> missense variant c.6958G&#x3e;T (p.Gly2320Cys) in symptomatic individuals. It was absent in 1 unaffected member (not tested in the other asymptomatic individual) and should be considered likely pathogenic. <i>CACNA1G</i> encodes for the pore-forming, α1G subunit of the T-type voltage-gated calcium channel (VGCC), in which currents are transient owing to fast inactivation, and tiny, due to small conductance. Mutations in <i>CACNA1G</i> cause generalized absence epilepsy and adult-onset, dominantly inherited, spinocerebellar ataxia type 42. In this kindred, the aforementioned <i>CACNA1G</i> variant segregated with disease, which was consistent with episodic vestibulocerebellar ataxia. CBZ proved successful in bout prevention and provided symptomatic benefit in the proband, probably as a result of interaction of this drug with VGCC. Further studies are needed to fully determine the vestibular and neurological manifestations of this form of episodic vestibulocerebellar ataxia. This novel disease variant could be designated episodic vestibulocerebellar ataxia type 10.

Vestibular Rehabilitation after Vestibulopathy Focusing on the Application of Virtual Reality

Human postural control is regulated by the vestibular, somatosensory, and visual systems. These types of sensory information are integrated in the central nervous system to ascertain the body’s position in space. Proper functioning of the vestibular, somatosensory, and visual senses is necessary for the body to maintain equilibrium. Bilateral vestibulopathy (BVP) is a condition in which bilateral peripheral vestibular function is reduced. Its treatment includes vestibular rehabilitation (VeR), balance training, counseling, treating the underlying cause, and avoiding further damage to the vestibular system. As VeR is often tedious for patients, patient motivation is required or patients may drop out of the program. To solve this problem, in recent years, there have been increasing reports of VeR using virtual reality, which increases vestibulo-ocular reflex gain and decreased dizziness by inducing adaptation. In this review, we discuss VeR, particularly for BVP, and VeR using virtual reality.

Autonomous Purkinje cell activation instructs bidirectional motor learning through evoked dendritic calcium signaling

The signals in cerebellar Purkinje cells sufficient to instruct motor learning have not been systematically determined. Therefore, we applied optogenetics in mice to autonomously excite Purkinje cells and measured the effect of this activity on plasticity induction and adaptive behavior. Ex vivo, excitation of channelrhodopsin-2-expressing Purkinje cells elicits dendritic Ca2+ transients with high-intensity stimuli initiating dendritic spiking that additionally contributes to the Ca2+ response. Channelrhodopsin-2-evoked Ca2+ transients potentiate co-active parallel fiber synapses; depression occurs when Ca2+ responses were enhanced by dendritic spiking. In vivo, optogenetic Purkinje cell activation drives an adaptive decrease in vestibulo-ocular reflex gain when vestibular stimuli are paired with relatively small-magnitude Purkinje cell Ca2+ responses. In contrast, pairing with large-magnitude Ca2+ responses increases vestibulo-ocular reflex gain. Optogenetically induced plasticity and motor adaptation are dependent on endocannabinoid signaling, indicating engagement of this pathway downstream of Purkinje cell Ca2+ elevation. Our results establish a causal relationship among Purkinje cell Ca2+ signal size, opposite-polarity plasticity induction, and bidirectional motor learning.

Absence of a vergence-mediated vestibulo-ocular reflex gain increase does not preclude adaptation

BACKGROUND: The gain (eye-velocity/head-velocity) of the angular vestibuloocular reflex (aVOR) during head impulses can be increased while viewing near-targets and when exposed to unilateral, incremental retinal image velocity error signals. It is not clear however, whether the tonic or phasic vestibular pathways mediate these gain increases. OBJECTIVE: Determine whether a shared pathway is responsible for gain enhancement between vergence and adaptation of aVOR gain in patients with unilateral vestibular hypofunction (UVH). MATERIAL AND METHODS: 20 patients with UVH were examined for change in aVOR gain during a vergence task and after 15-minutes of ipsilesional incremental VOR adaptation (uIVA) using StableEyes (a device that controls a laser target as a function of head velocity) during horizontal passive head impulses.A 5 % aVOR gain increase was defined as the threshold for significant change. RESULTS: 11/20 patients had >5% vergence-mediated gain increase during ipsi-lesional impulses. For uIVA, 10/20 patients had >5% ipsi-lesional gain increase. There was no correlation between the vergence-mediated gain increase and gain increase after uIVA training. CONCLUSION: Vergence-enhanced and uIVA training gain increases are mediated by separate mechanisms and/or vestibular pathways (tonic/phasic).The ability to increase the aVOR gain during vergence is not prognostic for successful adaptation training.