Vestibular Perception following Acute Unilateral Vestibular Lesions.

Little is known about the vestibulo-perceptual (VP) system, particularly after a unilateral vestibular lesion. We investigated vestibulo-ocular (VO) and VP function in 25 patients with vestibular neuritis (VN) acutely (2 days after onset) and after compensation (recovery phase, 10 weeks). Since the effect of VN on reflex and perceptual function may differ at threshold and supra-threshold acceleration levels, we used two stimulus intensities, acceleration steps of 0.5°/s(2) and velocity steps of 90°/s (acceleration 180°/s(2)). We hypothesised that the vestibular lesion or the compensatory processes could dissociate VO and VP function, particularly if the acute vertiginous sensation interferes with the perceptual tasks. Both in acute and recovery phases, VO and VP thresholds increased, particularly during ipsilesional rotations. In signal detection theory this indicates that signals from the healthy and affected side are still fused, but result in asymmetric thresholds due to a lesion-induced bias. The normal pattern whereby VP thresholds are higher than VO thresholds was preserved, indicating that any 'perceptual noise' added by the vertigo does not disrupt the cognitive decision-making processes inherent to the perceptual task. Overall, the parallel findings in VO and VP thresholds imply little or no additional cortical processing and suggest that vestibular thresholds essentially reflect the sensitivity of the fused peripheral receptors. In contrast, a significant VO-VP dissociation for supra-threshold stimuli was found. Acutely, time constants and duration of the VO and VP responses were reduced - asymmetrically for VO, as expected, but surprisingly symmetrical for perception. At recovery, VP responses normalised but VO responses remained shortened and asymmetric. Thus, unlike threshold data, supra-threshold responses show considerable VO-VP dissociation indicative of additional, higher-order processing of vestibular signals. We provide evidence of perceptual processes (ultimately cortical) participating in vestibular compensation, suppressing asymmetry acutely in unilateral vestibular lesions

Peaks and Troughs of Three-Dimensional Vestibulo-ocular Reflex in Humans

The three-dimensional vestibulo-ocular reflex (3D VOR) ideally generates compensatory ocular rotations not only with a magnitude equal and opposite to the head rotation but also about an axis that is collinear with the head rotation axis. Vestibulo-ocular responses only partially fulfill this ideal behavior. Because animal studies have shown that vestibular stimulation about particular axes may lead to suboptimal compensatory responses, we investigated in healthy subjects the peaks and troughs in 3D VOR stabilization in terms of gain and alignment of the 3D vestibulo-ocular response. Six healthy upright sitting subjects underwent whole body small amplitude sinusoidal and constant acceleration transients delivered by a six-degree-of-freedom motion platform. Subjects were oscillated about the vertical axis and about axes in the horizontal plane varying between roll and pitch at increments of 22.5° in azimuth. Transients were delivered in yaw, roll, and pitch and in the vertical canal planes. Eye movements were recorded in with 3D search coils. Eye coil signals were converted to rotation vectors, from which we calculated gain and misalignment. During horizontal axis stimulation, systematic deviations were found. In the light, misalignment of the 3D VOR had a maximum misalignment at about 45°. These deviations in misalignment can be explained by vector summation of the eye rotation components with a low gain for torsion and high gain for vertical. In the dark and in response to transients, gain of all components had lower values. Misalignment in darkness and for transients had different peaks and troughs than in the light: its minimum was during pitch axis stimulation and its maximum during roll axis stimulation. We show that the relatively large misalignment for roll in darkness is due to a horizontal eye movement component that is only present in darkness. In combination with the relatively low torsion gain, this horizontal component has a relative large effect on the alignment of the eye rotation axis with respect to the head rotation axis

Deficient high-acceleration vestibular function in patients with polyneuropathy

BACKGROUND: Unsteadiness during standing and walking is a frequent complaint of patients with polyneuropathy (PNP). OBJECTIVE: To determine whether balance disorders in patients with PNP may be caused by reduced proprioceptive input from the feet alone or whether impaired vestibular input, resulting from involvement of the vestibular nerve, can be an additional factor. METHODS: A total of 37 patients (mean age 65 years +/- 12 SD; 12 women) with electrodiagnostically confirmed PNP (predominantly axonal: 18; predominantly demyelinating: 19) underwent horizontal search-coil head-impulse testing, which assesses the high-acceleration vestibulo-ocular reflex (VOR). RESULTS: Relative to a healthy comparison group, the gains (eye velocity divided by head velocity) of the horizontal VOR were reduced in 27 of 37 patients (unilateral: 13; bilateral: 14). The percentages of patients with unilateral or bilateral VOR deficits were not significantly different between patients with axonal or demyelinating PNP. CONCLUSIONS: Two thirds of patients with axonal or demyelinating polyneuropathy (PNP) showed unilateral (approximately 50%) or bilateral (approximately 50%) gain reductions of the horizontal high-acceleration vestibulo-ocular reflex. This finding suggests that, in many patients with PNP, the neuropathic process includes the vestibular nerve. Such information is highly relevant for subsequent physical therapy, since vestibular exercise improves balance control and reduces disability

Absence of gravity-dependent modulation of straight sinus flow velocity in healthy humans

The influence of whole-body positions on the cerebral blood flow in normal subjects is unclear. Blood flow in cerebral veins and sinuses is continuous, pulsatile and proportional to cerebral blood flow. We examined young healthy volunteers to evaluate peak mean flow velocity (vm) in the straight sinus (SS) assessed by transcranial Doppler sonography in predefined variations of the whole-body pitch position relative to gravity in the presence of a normal (normocarbia) and an impaired (hypercarbia) cerebral autoregulation. A 2 MHz ultrasound probe was fixed with a headband nearby the protuberantia occipitalis externa. Fifteen subjects were seated in a motorized three-dimensional turntable. Vm-SS, blood pressure and heart rate were monitored in five whole-body pitch positions from upright (0 degrees ) to "20 degrees head-hanging" (110 degrees ): 0, 30, 60, 90 and 110 degrees . The experiment was repeated during the inspiration of 5% CO2. Of 15 subjects, 14 showed reliable ultrasound data; the results of one subject with movement artifacts were excluded. Vm-SS values under normocarbia (hypercarbia) were 23.9 +/- 4.2 cm/s (40.9 +/- 6.7 cm/s) at 0 degrees , 23.1 +/- 5.0 cm/s (38.0 +/- 5.0 cm/s) at 30 degrees , 24.9 +/- 5.1 cm/s (39.9 +/- 3.3 cm/s) at 60 degrees , 29.2 +/- 8.5 cm/s (41.0 +/- 4.7 cm/s) at 90 degrees and 27.0 +/- 11.6 cm/s (43.6 +/- 12.1 cm/s) at 110 degrees . Vm-SS measured under normocarbia (p = 0.09) and hypercarbia (p = 0.25) were not affected while subjects were positioned from upright toward "20 degrees head-hanging", whereas blood pressure and heart rate decreased (p < 0.01). Our results suggest that changes of whole-body position from upright to "20 degrees head-hanging" do not alter cerebral blood flow in healthy subjects

Vestibular and auditory deficits in fabry disease and their response to enzyme replacement therapy

Progressive hearing (pHL) and vestibular (pVL) loss are frequent deficits in Fabry disease (FD). Recently, enzyme replacement therapy (ERT) with human alpha-galactosidase A has become available. Here, we investigate the association between pHL and pVL in FD and their ERT responses. Pure tone audiometry (PTA) and head impulse testing (HIT) were administered at baseline in 47 patients (25 male, 18-60 y; 22 female, 17-74 y), of whom 24 also received caloric irrigation (CI). Of the 47 patients, 38 (24 male) were tested both before and during ERT (follow- up or = 18 months of ERT, pVL was significantly smaller than at baseline (ANOVA for HIT: p 0.05). We conclude that pHL and pVL prevalences are similar in FD. To detect pVL, HIT is more sensitive than CI. We speculate that pHL and pVL emerge from lesions within the vestibulocochlear labyrinth, because no specific patterns of vestibulo-cochlear deficits were observed, as expected if lesions were more proximal along the inferior or superior branch of the vestibulo-cochlear nerve or labyrinthine artery. Finally, ERT stabilizes auditory and even improves vestibular function

Recovery of the High-Acceleration Vestibulo-ocular Reflex After Vestibular Neuritis

Vestibular neuritis (VN) usually leads to a sudden gain asymmetry of the high-acceleration horizontal vestibulo-ocular reflex (VOR). We asked whether this asymmetry decreases over time indicating peripheral recovery and/or central compensation. The horizontal VOR during rapid rotational head impulses to both sides was recorded with search coils in 37 patients at different time periods (1–240 weeks) after the onset of VN. In ten patients, sequential measurements were performed. Gains of the VOR during head impulses toward the ipsilesional side significantly increased after the initial drop (average gains: < 1 week: 0.35; 1–4 weeks: 0.33; 4–40 weeks: 0.55; 40–240 weeks: 0.50). Gains on the contralesional side, however, were only slightly reduced and showed no significant change. We conclude that, in contrast to patients after hemilabyrinthectomy or unilateral vestibular neurectomy, the ocular response to ipsilesional rotations in patients after VN improves over time. This finding suggests that ipsilesional recovery is peripheral or, if central, depends on spared peripheral function. The physiology of linear and nonlinear VOR pathways predicts a considerable gain reduction for contralesional head impulses if central compensation mechanisms are not engaged. Thus, the relatively preserved gain on the contralesional side can be explained only by central “upregulation”. Apparently, for high accelerations of the head, effective central compensation after VN does not aim to balance the gains of the VOR but tries to boost the contralesional gain close to normal