Vestibular Stimulation In Patients Research Articles

Tackling Insomnia Symptoms through Vestibular Stimulation in Patients with Breast Cancer: A Perspective Paper.

Insomnia symptoms are common among patients with breast cancer (BC; 20-70%) and are predictors of cancer progression and quality of life. Studies have highlighted sleep structure modifications, including increased awakenings and reduced sleep efficiency and total sleep time. Such modifications may result from circadian rhythm alterations consistently reported in this pathology and known as carcinogenic factors, including lower melatonin levels, a flattened diurnal cortisol pattern, and lower rest-activity rhythm amplitude and robustness. Cognitive behavioral therapy and physical activity are the most commonly used non-pharmacological interventions to counter insomnia difficulties in patients with BC. However, their effects on sleep structure remain unclear. Moreover, such approaches may be difficult to implement shortly after chemotherapy. Innovatively, vestibular stimulation would be particularly suited to tackling insomnia symptoms. Indeed, recent reports have shown that vestibular stimulation could resynchronize circadian rhythms and improve deep sleep in healthy volunteers. Moreover, vestibular dysfunction has been reported following chemotherapy. This perspective paper aims to support the evidence of using galvanic vestibular stimulation to resynchronize circadian rhythms and reduce insomnia symptoms in patients with BC, with beneficial effects on quality of life and, potentially, survival.

Postural control during galvanic vestibular stimulation in patients with persistent perceptual-postural dizziness.

Over the past years galvanic vestibular stimulation (GVS) has been increasingly applied to stimulate the vestibular system in health and disease, but not in patients with persistent postural-perceptual dizziness (PPPD) yet. We functionally tested motion perception thresholds and postural responses to imperceptible noisy (nGVS) and perceptible bimastoidal GVS intensities in patients with PPPD with normal vestibulo-ocular reflexes. We hypothesized that GVS destabilizes PPPD patients under simple postural conditions stronger compared to healthy controls. They were compared to healthy subjects under several conditions each with the eyes open and closed: baseline with firm platform support, standing on foam and cognitive demand (count backward). Low and high GVS intensities (range 0.8-2.8mA) were applied according to the individual thresholds and compared with no GVS. PPPD patients showed a reduced perception threshold to GVS compared to healthy control subjects. Median postural sway speed increased with stimulus intensity and on eye closure, but there was no group difference, irrespective of the experimental condition. Romberg's ratio was consistently lower during nGVS than in all other conditions. Group-related dissociable effects were found with the eyes closed in (i) the baseline condition in which high GVS elicited higher postural sway of PPPD patients and (ii) in the foam condition, with better postural stability of PPPD patients during perceptible GVS. Group and condition differences of postural control were neither related to anxiety nor depression scores. GVS may be helpful to identify thresholds of vestibular perception and to modulate vestibulo-spinal reflexes in PPPD, with dissociable effects with respect to perceptible and imperceptible stimuli. The sway increase in the baseline of PPPD may be related to an earlier transition from open- to closed-loop mode of postural control. In contrast, the smaller sway of PPPD in the foam condition under visual deprivation is in line with the known balance improvement under more demanding postural challenges in PPPD. It is associated with a prolonged transition from open- to closed-loop postural feedback control. It could also reflect a shift of intersensory weighting with a smaller dependence on proprioceptive feedback control in PPPD patients under complex tasks. In summary, GVS discloses differences between simple and complex balance tasks in PPPD.

Does galvanic vestibular stimulation decrease spasticity in clinically complete spinal cord injury?

The aim of this study was to determine changes in clinical and biomechanical measures of spasticity after administering galvanic vestibular stimulation in patients with a complete spinal cord injury (SCI). The spasticity in the lower limbs was assessed using the Modified Ashworth Scale and the pendulum test in seven SCI patients (grade A on the ASIA Impairment Scale) before (0), immediately after (0), and at 5 and 30 min after the real versus sham galvanic vestibular stimulation (15 s each, anode over the right mastoid). Overall, the changes in spasticity were not significantly different between the real and sham galvanic vestibular stimulation. However, the Modified Ashworth Scale and the pendulum test indicated a reduction in spasticity in two out of seven patients. The results suggest that galvanic vestibular stimulation may modify spasticity in some patients with complete SCI, presumably through the residual vestibulospinal influences. Future studies should determine clinical and neurophysiological profiles of responders versus nonresponders and optimize parameters of galvanic vestibular stimulation.

Can Postural Instability Respond to Galvanic Vestibular Stimulation in Patients with Parkinson's Disease?

ObjectiveGalvanic vestibular stimulation (GVS) activates the vestibular afferents, and these changes in vestibular input exert a strong influence on the subject’s posture or standing balance. In patients with Parkinson’s disease (PD), vestibular dysfunction might contribute to postural instability and gait disorders.MethodsCurrent intensity was increased to 0.7 mA, and the current was applied to the patients for 20 minutes. To perform a sham stimulation, the current intensity was increased as described and then decreased to 0 mA over the course of 10 seconds. The patient’s status was recorded continuously for 20 minutes with the patient in the supine position.ResultsThree out of 5 patients diagnosed with PD with postural instability and/or abnormal axial posture showed a reduction in postural instability after GVS. The score for item 12 of the revised Unified Parkinson’s Disease Rating Scale part 3 was decreased in these patients.ConclusionsThe mechanism of postural instability is complex and not completely understood. In 2 out of the 5 patients, postural instability was not changed in response to GVS. Nonetheless, the GVS-induced change in postural instability for 3 patients in our study suggests that GVS might be a therapeutic option for postural instability.

The Treatment of Peripheral Vestibular Dysfunction Using Caloric Vestibular Stimulation in Patients with Cerebral Hypertensive Crisis

Background: To verify the efficacy of caloric vestibular stimulation in patients with peripheral vestibular dysfunction after cerebral hypertensive crisis. Methods: Enrolled in the study were 60 patients with peripheral vestibular dysfunction caused by a cerebral hypertensive crisis, docu-mented by vestibulometry. Thirty patients underwent standard treatment plus caloric vestibular stimulation, and 30 control group patients received standard treatment alone. Results: After the two-week treatment course, the sensation of vertigo was observed in 40.0% ± 8.9% of treatment group patients compared with 80.0% ± 7.3% of control group patients (t = 3.46; p < 0.001). Spontaneous vestibular somatic reactions were found in 46.7% ± 9.1% of the study treatment group in contrast to 86.7% ± 6.2% of the control group (t = 3.63; p < 0.001). Spontaneous nystagmus was seen in 40.0% ± 8.9% of treatment group patients compared with 93.3% ± 4.6% of control subjects (t = 5.31; p < 0.001). Spontaneous vestibular vegetative reactions were observed in 33.3% ± 8.6% of patients receiving study treatment in contrast to 93.3% ± 4.6% of control group patients (t = 6.16; p < 0.001). Also, 53.3% ± 9.1% of study treatment group patients showed asymmetry of labyrinths compared with 86.7% ± 6.2% of patients from the control group (t = 3.03; p < 0.001). Conclusion: Caloric vestibular stimulation was shown to be an effective treatment for peripheral vestibular dysfunction in patients with cerebral hypertensive crisis. During the 14-day treatment of cerebral hypertensive crisis, complete labyrinthine function recovery occurred in 46.7% of treatment group patients who underwent caloric vestibular stimulation as opposed to 13.3% of control group patients who received standard treatment alone.

Altered resting state – functional connectivity in patients with bilateral vestibular failure

Background: Patients with bilateral vestibular failure (BVF) suffer from gait unsteadiness and oscillopsia. Brain imaging studies applying vestibular stimulation in patients with BVF have shown altered neural activity of cortical visual-vestibular interaction: decreased bilateral neural activity in the posterior insula and parietal operculum and decreased deactivations in the visual cortex. It is unknown how this affects functional connectivity in the resting brain.

The Vestibular Implant: Quo Vadis?

Objective: To assess the progress of the development of the vestibular implant (VI) and its feasibility short-term. Data sources: A search was performed in Pubmed, Medline, and Embase. Key words used were “vestibular prosth*” and “VI.” The only search limit was language: English or Dutch. Additional sources were medical books, conference lectures and our personal experience with per-operative vestibular stimulation in patients selected for cochlear implantation. Study selection: All studies about the VI and related topics were included and evaluated by two reviewers. No study was excluded since every study investigated different aspects of the VI. Data extraction and synthesis: Data was extracted by the first author from selected reports, supplemented by additional information, medical books conference lectures. Since each study had its own point of interest with its own outcomes, it was not possible to compare data of different studies. Conclusion: To use a basic VI in humans seems feasible in the very near future. Investigations show that electric stimulation of the canal nerves induces a nystagmus which corresponds to the plane of the canal which is innervated by the stimulated nerve branch. The brain is able to adapt to a higher baseline stimulation, while still reacting on a dynamic component. The best response will be achieved by a combination of the optimal stimulus (stimulus profile, stimulus location, precompensation), complemented by central vestibular adaptation. The degree of response will probably vary between individuals, depending on pathology and their ability to adapt.

Mechanisms of Vibration-Induced Nystagmus in Normal Subjects and Patients with Vestibular Neuritis

It has been reported that vibration applied either on the mastoid or on the sternocleidomastoid (SCM) muscles induces nystagmus in normal subjects or patients after unilateral vestibular neuritis (VN). The aims of the study were to characterize vibration-induced nystagmus (VIN) in normal and patient groups and to propose the mechanism of VIN. We recorded eye movements during unilateral 100-Hz vibration on the mastoid bone and SCM muscles in 22 normal subjects and 19 patients with unilateral VN. In normal subjects, the direction of slow-phase velocity (SPV) tended to be toward the vibrated side. Vibration on the right/left SCM muscles induced mean SPV of 1.7°/s, –1.9°/s toward the stimulated side in all normal subjects. Vibration on the right/left mastoid bone induced mean SPV of 1.5°/s, –0.4°/s toward the stimulated side in most of the normal subjects. Positive value means SPV to the right side. This directional preponderance to the vibrated side was statistically significant. Among the patients with VN, the slow phase of the VIN was directed towards the lesioned side, irrespective of whether vibration was applied on the lesioned or intact side. Vibration on the right/left mastoid bone induced mean SPV of –10.4°/s, –10.8°/s toward the lesioned side. Vibration on the right/left SCM induced mean SPV of –7.9°/s, –10.5°/s toward the lesioned side. The amplitude of SPV showed a significant correlation with the unilateral weakness of caloric test. Our results suggest that the proprioceptive stimulation plays a major role in producing VIN in normal subjects, while VIN is generated mostly by the vestibular stimulation in patients with unilateral VN, which helps us localize the lesion side. Vibration tests on the SCM muscles as well as on the mastoid are recommended and our hypothetic mechanisms of VIN are presented.

Response to Galvanic Vestibular Stimulation in Patients with Unilateral Vestibular Loss

This study sought to characterize various responses to galvanic vestibular stimulation (GVS) by comparing GVS-induced eye movements in healthy subjects and patients with vestibular function loss. The study also aimed to estimate the clinical significance of GVS tests. Finally, an effort was made to localize the primary excitation site of stimulation in the vestibular system. Three parameters of response to GVS, spontaneous nystagmus, galvanic stimulating nystagmus (GSN), and postgalvanic stimulating nystagmus (PGSN), were evaluated in 20 normal subjects and 14 patients with complete unilateral vestibular function loss resulting from labyrinthectomy or vestibular neurectomy using a three-dimensional video-electronystagmography technique. In normal subjects, GSN was detected in all subjects and was directed toward the negative electrode. PGSN was also detected but was directed toward the opposite electrode. When the negative electrode was attached to the intact side in unilateral vestibular loss subjects, GSN was always directed toward the negative electrode and PGSN was never observed. When the negative electrode was attached to the lesion side, however, GSN was detected in only one case, and PGSN was observed and directed to the intact side in 13 patients. The response to GVS in vestibular loss patients differed from that in normal subjects, which suggests that GVS could be useful for estimating the extent of vestibular function loss. The fact that the patterns of GVS response differed so significantly suggests that the primary site of excitation is not central but is instead the peripheral vestibular organ.

Vestibular stimulation affects dichotic lexical decision performance

We report an experimental attempt to shift, by vestibular stimulation, healthy subjects right ear advantage (REA) in a dichotic listening (DL) task with words and nonwords as stimuli. Forty right-handed men performed the task under two different conditions, once while sitting in a stationary turning chair (baseline) and once during sinusoidal rotation. In this latter condition, every other stimulation was received during maximal left-to-right (i.e., clockwise), every other during maximal right-to-left (i.e., counterclockwise) acceleration. There was a reliable REA for lexical decision accuracy in the baseline and right-to-left trials but not during left-to-right rotation. While right ear performance was unaffected by rotation, there were more correct lexical decisions to left ear targets exclusively during left-to-right turns (one-tailed P = 0.05). Since there were no parallel shifts in auditory thresholds under the different conditions, this effect is not due to any hypothetical auditory-vestibular interactions on a primary sensory level. The improvement in left ear DL performance, although small in our study, is comparable to the symptom-alleviating effect of caloric vestibular stimulation in patients with left-sided hemispatial neglect and interpreted as a consequence of a rotation-induced attentional shift towards the left hemispace.

Vegetative, EEG and nystagmic reactivity to vestibular stimulation in patients with cerebral vascular disorders.

Nystagmic, EEG and vegetative reactions i. e. digital plethysmogram, electrodermogram, rheoencephalogram, were investigated in 15 controls and in 42 patients with cerebro-vascular diseases. The frequency of autonomic, EEG and nystagmic reactions to vestibular stimuli was significantly different in patients with cerebro-vascular diseases from controls. That pointed to differentiated reactions depending on the type of lesion and on the site of connection between the vestibular afferents and oculomotor and autonomic efferents. It was also possible to distinguish the nonspecific orienting reflex, appearing at the beginning of ear irrigation and the vestibular reaction, appearing late, after the end of irrigation.