Symptom reduction in mal de débarquement syndrome with attenuation of the velocity storage contribution in the central vestibular pathways.

Background: The velocity storage mechanism of the central vestibular system is closely associated with the vestibulo-ocular reflex (VOR), but also contributes to the sense of orientation in space and the perception of self-motion. We postulate that mal de débarquement syndrome (MdDS) is a consequence of inappropriate sensory adaptation of velocity storage. The premise that a maladapted velocity storage may be corrected by spatial readaptation of the VOR has recently been translated into the development of the first effective treatment for MdDS.

Treatment of Gravitational Pulling Sensation in Patients With Mal de Debarquement Syndrome (MdDS): A Model-Based Approach.

Perception of the spatial vertical is important for maintaining and stabilizing vertical posture during body motion. The velocity storage pathway of vestibulo-ocular reflex (VOR), which integrates vestibular, optokinetic, and proprioception in the vestibular nuclei vestibular-only (VO) neurons, has spatio-temporal properties that are defined by eigenvalues and eigenvectors of its system matrix. The yaw, pitch and roll eigenvectors are normally aligned with the spatial vertical and corresponding head axes.

Predicting Vasovagal Responses: A Model-Based and Machine Learning Approach.

Vasovagal syncope () or neurogenically induced fainting has resulted in falls, fractures, and death. Methods to deal with are to use implanted pacemakers or beta blockers. These are often ineffective because the underlying changes in the cardiovascular system that lead to the syncope are incompletely understood and diagnosis of frequent occurrences of is still based on history and a tilt test, in which subjects are passively tilted from a supine position to 20° from the spatial vertical (to a 70° position) on the tilt table and maintained in that orientation for 10-15 min.

Readaptation Treatment of Mal de Debarquement Syndrome With a Virtual Reality App: A Pilot Study.

Mal de Debarquement syndrome (MdDS) is composed of constant phantom sensations of motion, which are frequently accompanied by increased sensitivity to light, inability to walk on a patterned floor, the sensation of ear fullness, head pressure, anxiety, and depression. This disabling condition generally occurs in premenopausal women within 2 days after prolonged passive motion (e.g.

The neural basis of motion sickness.

Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last 20 yr that the source of the signal generating motion sickness and its neural basis has been firmly established. Here, we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness and provide a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs, and the velocity storage integrator in the vestibular nuclei.

Adaptation of spatio-temporal convergent properties in central vestibular neurons in monkeys.

The spatio-temporal convergent (STC) response occurs in central vestibular cells when dynamic and static inputs are activated. The functional significance of STC behavior is not fully understood. Whether STC is a property of some specific central vestibular neurons, or whether it is a response that can be induced in any neuron at some frequencies is unknown.

Mal de Debarquement Syndrome: A Retrospective Online Questionnaire on the Influences of Gonadal Hormones in Relation to Onset and Symptom Fluctuation.

Introduction: Mal de Debarquement Syndrome (MdDS) is a condition characterized by a persistent perception of self-motion, in most cases triggered from exposure to passive motion (e.g., boat travel, a car ride, flights).

Hypothesis: The Vestibular and Cerebellar Basis of the Mal de Debarquement Syndrome.

The Mal de Debarquement syndrome (MdDS) generally follows sea voyages, but it can occur after turbulent flights or spontaneously. The primary features are objective or perceived continuous rocking, swaying, and/or bobbing at 0.2 Hz after sea voyages or 0.

Coding of Velocity Storage in the Vestibular Nuclei.

Semicircular canal afferents sense angular acceleration and output angular velocity with a short time constant of ≈4.5 s. This output is prolonged by a central integrative network, velocity storage that lengthens the time constants of eye velocity.

Treatment of the Mal de Debarquement Syndrome: A 1-Year Follow-up.

The mal de debarquement syndrome (MdDS) is a movement disorder, occurring predominantly in women, is most often induced by passive transport on water or in the air (classic MdDS), or can occur spontaneously. MdDS likely originates in the vestibular system and is unfamiliar to many physicians. The first successful treatment was devised by Dai et al.

Vestibular Activation Habituates the Vasovagal Response in the Rat.

Vasovagal syncope is a significant medical problem without effective therapy, postulated to be related to a collapse of baroreflex function. While some studies have shown that repeated static tilts can block vasovagal syncope, this was not found in other studies. Using anesthetized, male Long-Evans rats that were highly susceptible to generation of vasovagal responses, we found that repeated activation of the vestibulosympathetic reflex (VSR) with ±2 and ±3 mA, 0.

A Model of Blood Pressure, Heart Rate, and Vaso-Vagal Responses Produced by Vestibulo-Sympathetic Activation.

Blood Pressure (BP), comprised of recurrent systoles and diastoles, is controlled by central mechanisms to maintain blood flow. Periodic behavior of BP was modeled to study how peak amplitudes and frequencies of the systoles are modulated by vestibular activation. The model was implemented as a relaxation oscillator, driven by a central signal related to Desired BP.

Vasovagal oscillations and vasovagal responses produced by the vestibulo-sympathetic reflex in the rat.

Sinusoidal galvanic vestibular stimulation (sGVS) induces oscillations in blood pressure (BP) and heart rate (HR), i.e., vasovagal oscillations, as well as transient decreases in BP and HR, i.

The vasovagal response of the rat: its relation to the vestibulosympathetic reflex and to Mayer waves.

Vasovagal responses (VVRs) are characterized by transient drops in blood pressure (BP) and heart rate (HR) and increased amplitude of low-frequency oscillations in the Mayer wave frequency range. Typical VVRs were induced in anesthetized, male, Long-Evans rats by sinusoidal galvanic vestibular stimulation (sGVS). VVRs were also produced by single sinusoids that transiently increased BP and HR, by 70-90° nose-up tilts, and by 60° tilts of the gravitoinertial acceleration vector using translation while rotating (TWR).

Modeling spatial tuning of adaptation of the angular vestibulo-ocular reflex.

Gain adaptation of the yaw angular vestibular ocular reflex (aVOR) induced in side-down positions has gravity-independent (global) and -dependent (localized) components. When the head oscillation angles are small during adaptation, localized gain changes are maximal in the approximate position of adaptation. Concurrently, polarization vectors of canal-otolith vestibular neurons adapt their orientations during these small-angle adaptation paradigms.

Fos expression in neurons of the rat vestibulo-autonomic pathway activated by sinusoidal galvanic vestibular stimulation.

The vestibular system sends projections to brainstem autonomic nuclei that modulate heart rate and blood pressure in response to changes in head and body position with regard to gravity. Consistent with this, binaural sinusoidally modulated galvanic vestibular stimulation (sGVS) in humans causes vasoconstriction in the legs, while low frequency (0.02-0.

Tuning of gravity-dependent and gravity-independent vertical angular VOR gain changes by frequency of adaptation.

The gain of the vertical angular vestibulo-ocular reflex (aVOR) was adaptively increased and decreased in a side-down head orientation for 4 h in two cynomolgus monkeys. Adaptation was performed at 0.25, 1, 2, or 4 Hz.

Orientation adaptation of eye movement-related vestibular neurons due to prolonged head tilt.

Sixteen neurons, including vestibular-only (VO), eye-head velocity (EHV), and position-vestibular-pause (PVP) neurons sensitive to head tilt were recorded in the rostromedial and in superior vestibular nuclei. Projection of the otolith polarization vector to the horizontal plane (response vector orientation [RVO]) was determined before and after prolonged head orientation in side-down position. The RVO of VO neurons shifted toward alignment with the axis of gravity when the head was in the position of adaptation.

Sinusoidal galvanic vestibular stimulation (sGVS) induces a vasovagal response in the rat.

Blood pressure (BP) and heart rate (HR) were studied in isoflurane-anesthetized Long-Evans rats during sinusoidal galvanic vestibular stimulation (sGVS) and sinusoidal oscillation in pitch to characterize vestibular influences on autonomic control of BP and HR. sGVS was delivered binaurally via Ag/AgCl needle electrodes inserted over the mastoids at stimulus frequencies 0.008-0.

Spatial orientation of the angular vestibulo-ocular reflex (aVOR) after semicircular canal plugging and canal nerve section.

We investigated spatial responses of the aVOR to small and large accelerations in six canal-plugged and lateral canal nerve-sectioned monkeys. The aim was to determine whether there was spatial adaptation after partial and complete loss of all inputs in a canal plane. Impulses of torques generated head thrusts of ≈ 3,000°/s².

Complementary gain modifications of the cervico-ocular (COR) and angular vestibulo-ocular (aVOR) reflexes after canal plugging.

To determine whether the COR compensates for the loss of aVOR gain, independent of species, we studied cynomolgus and rhesus monkeys in which all six semicircular canals were plugged. Gains and phases of the aVOR and COR were determined at frequencies ranging from 0.02 to 6 Hz and fit with model-based transfer functions.

Dependence of the roll angular vestibuloocular reflex (aVOR) on gravity.

Little is known about the dependence of the roll angular vestibuloocular reflex (aVOR) on gravity or its gravity-dependent adaptive properties. To study gravity-dependent characteristics of the roll aVOR, monkeys were oscillated about a naso-occipital axis in darkness while upright or tilted. Roll aVOR gains were largest in the upright position and decreased by 7-15% as animals were tilted from the upright.