Infrared Video Frenzel Goggles allow for observing the eyes in the dark without the patient focusing on a target , enlarge the eyes on a screen for easier viewing and records the eye movements for repeated playback. VNG video nystagmography software converts the eye movement into a computer generated signal, also increasing the likelihood of an accurate diagnosis. As with most vestibular equipment, this equipment is expensive and found in limited locations, usually clinics that specialize in vestibular testing and treatment.
Other computerized testing exists, such as caloric testing which tests the horizontal canals at a very slow frequency , VEMP vestibular evoked myogenic potential testing and rotary chair testing hallmark for confirming deficits in both vestibular systems to test other portions of the vestibular system or to confirm a suspected diagnosis.
Since there are direct connections from the inner ears to the eyes and brain, injuries or deficiencies in any number of these structures can produce dysfunction in balance, hearing and abnormal eye movements.
Testing exists to evaluate the response of the eyes in order to determine if there is dysfunction in the peripheral, central or both vestibular systems. Childs L. Assessing vestibular dysfunction. Exploring treatments of a complex condition. Rehab Management [serial online]. July ;23 6 Hain, Timothy, MD. Accessed July 5, Mann, Michael, PhD. Accessed online July 5, Balaban, Carrey, PhD. University of Pittsburgh. Volume 1. May , Anatomy The human inner ear contains two divisions: the hearing auditory component—the cochlea, and a balance vestibular component—the peripheral vestibular system.
Peripheral in this context refers to a system that is outside of the central. Infections of the Inner Ear Vestibular neuritis and labyrinthitis are disorders resulting from an infection that inflames the inner ear or the nerves connecting the inner ear to the brain.
This inflammation disrupts the transmission. Vestibular and auditory symptoms and signs can result from a dehiscence opening in the bone overlying the superior semicircular canal of the inner ear. This clinical syndrome—superior semicircular canal dehiscence syndrome SSCD —was first described by. The quality of information your website provides is amazing. Scientific Study Peripheral Vestibular System. View This Section's Articles. What is Vestibular? Article Summary The peripheral vestibular system includes the organs of the inner ear, also known as the labyrinth, which contains two primary structures: the cochlea, responsible for hearing, and the vestibular apparatus, responsible for maintaining balance, stability and spatial orientation.
Download PDF. Figure 1. Figure 2. Figure 3. Figure 4. Facebook 0 Tweet 0 Pin 0 LinkedIn 0. View References. Labyrinthitis and Vestibular Neuritis. VeDA is a nonprofit that relies on donations to support our education and advocacy efforts. Your support makes a real difference. The receptor cells may shift due to the endolymph inertia shift. At the movement acceleration stage, it will be the maximum one.
While rotating the head with steady speed, the endolymph shift gradually decreases, and in 15—20 s of rotation it attains the background properties. If to stop movement, the cupula shift turns the cupula toward the opposite side. If to compare duration of the caloric test, or the bilateral caloric cold and heat stimulation as well as the post-rotation nystagmus after rotating to the left and right, we should assess the symmetry or asymmetry of vestibular functions [ 1 ].
An adequate stimulus of the otolith organ results in acceleration or slowing down at the straight-line movements. As the gravity force is a linear acceleration, the otolith receptors perceive head inclination movements regarding the earth gravity force vector. Absent action of the gravity force onto the otolith organ at null gravity causes significant disturbance in the body, which are thoroughly studied by cosmic medicine.
The sensitivity of otolith hairy cells to linear acceleration is determined by the mass of heavy calcium crystals—otoliths. Elliptic sacs of the otolith organ, situated close to horizontal plane, are more sensitive to acceleration within this plane.
Spheric sacs are located in almost vertical plane, so they are more sensitive to acceleration and slowing down within a vertical plane. It is necessary to stress that the head movements are the combined ones, i. Due to joint functioning of four otolith organs and six semicircular canals, it is possible to perceive complex movements in space [ 11 , 13 , 14 ]. The nystagmus subtypes are the most valuable specific and objective characteristics of acute peripheral, chronic, or acute progressing central VD.
The nature of these nystagmuses has not been understood completely. It is supposed that the standard tone of the eye-moving muscles is supported by the impulses of similar symmetric force which derive from the both labyrinths. When we irritate the labyrinth, there appears reflex asymmetry from the eye-moving muscles, expressed as a gradual turning away of the eyes toward the muscle hypertonia side, with gradual nystagmus component developing. Gradual turning away of the eyes causes instant response from the central cortex parts, so the eyes turn to the previous position.
This is how a quick component of the spontaneous or other nystagmus may appear. The confirmation of cortex genesis of quick nystagmus component is its absence in the case of unconsciousness or narcosis. The slow nystagmus component is preserved in these cases. The nystagmus direction is determined by its quick component [ 12 ]. There are three stages of spontaneous nystagmus: in the first phase, when the nystagmus is manifested when the eyes turn away toward the quick component side; in the second phase, when the eyes move toward the quick component or when a person looks straightforward; in the third phase, when the eyes look toward the quick component, straightforward and to the opposite side [ 13 ].
The studies established that the peripheral or labyrinth-borne spontaneous nystagmus, as a rule, by its intensity is a small- or medium-swinging; by its direction the nystagmus may be horizontal or horizontal-rotating and rhythmical, with distinctly changing quick and slow phases [ 12 ].
Peripheral nystagmus in the acute stage lasts from the first 2—3 hours to 2—3 days, being directed toward acute stimulation of the labyrinth receptor structures. With gradual labyrinth depression, the nystagmus changes its direction toward the healthy side. In the case of the VD acute stage of peripheral syndrome type, the spontaneous horizontal or horizontal-rotating nystagmus is accompanied with sensory subjective sensation, horizontal vertigo toward labyrinth hyperreflexia side and, in the case of depression, toward the opposite intact side.
So, shifts in statics and movement coordination, keeping to the vector laws, are observed the same, directed toward stimulation side or toward the healthy side in depression. The specific acute vestibular symptoms are accompanied by considerable general discomfort, manifested dually; its first manifestation is characterized by nausea, vomiting, and vascular disorders associated with sympatho-adrenergic crisis.
Here we may observe increased arterial pressure, tachycardia, hyperemia, and skin dryness, as well as dry oral mucosa. Its second manifestation is characterized by decreased arterial pressure, bradycardia, pale skin and mucosa, extreme sweating, and salivation [ 13 , 14 ]. The acute vestibular syndrome requires urgent medical aid. As the authors observe [ 14 , 15 , 16 ], the peripheral vestibular syndrome is characterized by high capacity for compensating the affected functions due to central regulating mechanisms.
In 2—4 weeks the spontaneous nystagmus decreases in intensity and then disappears completely. At the same time, vertigo decreases; kinetic and then static equilibrium functions are restored. The pressure changes and pathological disorders in purulent and non-purulent processes in the external ear and tympanic membranes cause problems with the sound-conducting function of the middle ear.
These pathological changes through the helix window and vestibule may migrate onto the ear labyrinth. In the labyrinth, under the effect of these conditions, the content and shift of endolymph movement may be changed.
These endolymph changes lead to the VS receptor structure impairment, and finally they result in sensorineural deafness and vestibular dysfunction. In the case of the acute central vestibular syndrome pathology of the cerebellopontine angle or the pons bodies , there may be other characteristics of spontaneous nystagmus observed.
It may be large-swinging or medium-swinging. It may develop within various planes: the vertical, diagonal, horizontal, or multiple. In some cases, spontaneous nystagmus is defined as a tonic-clonic or tonic with prolonged average angular speed of the slow stage of nystagmus or decrease of its frequency.
Spontaneous nystagmus in the case of the central vestibular syndrome is continuous and may progress in intensity [ 12 ]. Benign paroxysmal positional vertigo BPPV is the most frequent cause of light-headedness. Its treatment has become possible due to application of the original correction methods. The main sign of the BPPV is short-lasting vertigo attacks, which appear when a person abruptly changes his head position related to the gravity vector, for example, changing from the vertical onto the horizontal position, when a person lies down, or vice versa, when he gets up, or upturns in the bed, or abruptly throws his head back.
These attacks of vertigo more often appear in the morning after sleep. They are mostly manifested when the person first changes body position after sleep. They are weakened with repeated head movements. The patient quite often shows himself, from what side vertigo appears [ 1 , 4 , 10 , 12 ]. If the vertigo and nystagmus are horizontally or horizontally rotating directed, this shows us that the horizontal lateral semicircular canal is affected.
The provoking moment may be when a patient inclines his head toward the affected ear side. The vertigo may be accompanied with nausea and vomiting. The attack appears after a person moves his head, in 1—2 s and lasts for 30—60 s. Vertigo and nystagmus depend on the head movement. If a person looks upward, vertigo and nystagmus are vertical.
Vertical nystagmus in this case evidences about excitement of receptors of the posterior semicircular canal. BPPV may develop at any age, most often from 50 to 70 years, affecting women twice as often as men. It may develop after prolonged bed stay, particularly after craniocerebral traumas [ 11 , 14 , 16 , 17 ]. The diagnosis is established due to position tests.
When there are no effective method of the primary disease treatment, it is always possible to relieve the vertigo, related to the BPPV [ 12 , 15 ]. According to the cupulolothiasis theory, which was histologically confirmed, in the ampulla of the posterior canal, which is located lower than the other canals, otoliths may deposit more frequently. They, due to various reasons, leave the otolith membrane and stick to the cupula walls. The cupula walls with otoliths become heavy. They become a sensor of linear acceleration instead of the sensor of the angular one though this theory cannot explain many peculiarities of nystagmus [ 4 ].
The canalolithiasis theory explains the positional nystagmus signs. Otoliths, according to this theory, do not stick but freely float in the endolymph. As they narrow or obstruct the canal diameter, they cause positional vertigo. As they travel along the canal, otoliths disrupt free shift of the endolymph from the utricle or to the utricle. This theory allows predicting the direction, latent period, and duration of the nystagmus, as well as the changes of its characteristics at various positional maneuvers [ 4 ].
There are two types of them: related to canalolithiasis more widespread and a rarer one, cupulolithiasis. Identification of the lateral semicircular canal BPPV is characterized by some features which were earlier considered to be characteristics of the central positional vertigo. In the case of the lateral semicircular canal canalolithiasis, the patient experiences vertigo when he turns his head to sides, being supine. Changing the position from the supine onto the sitting one and vice versa is not accompanied with significant symptoms.
Exacerbations with the lateral canal BPPV are less prolonged than those with the posterior canal affected. The cause of lateral canal BPPV as a canalithiasis type is the invasion of aggressive otoliths in this canal. Remissions are often observed in patients with lateral canal BPPV as otoliths can easily leave the lateral canal during head movements.
On the contrary, otoliths do not move from the posterior canal independently due to the anatomical position it is located below all other canals. A quick result from the maneuvers testifies to the lateral canal BPPV. BPPV anterior canal is used very rarely [ 4 , 6 , 17 ]. In the case of left posterior semicircular canal dysfunction, the test will first cause an increased and then decreased nystagmus that occurs after a short latent period.
After returning to the starting position, the nystagmus will change the direction [ 15 , 16 , 17 ]. A number of positional maneuvers have been developed to treat BPPV.
They are aimed at removing conglomerates of otoliths from semicircular canals. At present, maneuvers developed by Brandt and Daroff and Semont and Epley maneuvers are used. Within the theory of canalolithiasis, Brandt and Daroff were the first to come up with a set of exercises, including head movements that destroy the otolith conglomerates. Their fragments move to the other sections of the labyrinth, where they may be stationary.
Therefore, they do not affect the function of semicircular canals [ 4 ]. In case of relapses, it is recommended to repeat the maneuver that was more effective at the first attack [ 12 , 14 ]. Vestibular neuronitis is a common cause after BPPV peripheral vestibular disease. Clinically, it is manifested by vertigo in the direction of a healthy ear, by spontaneous nystagmus of a horizontally rotary direction to a healthy ear.
Functional tests check various degrees of hyporeflexia to the affected ear and postural abnormalities toward a healthy ear. It is considered that vestibular neuronitis is of viral etiology. It is recommended to prescribe glucocorticoids at first as they effectively reduce functional disorders and have a strong anti-inflammatory effect. In addition, they accelerate the central mechanisms of vestibular compensation for postural disorders. Antiviral drugs are less effective [ 10 ].
During an acute attack in the excitation phase in the affected labyrinth, there occurs a strong vertigo of the horizontal direction with horizontal nystagmus, postural disorders, and significant vestibulo-vegetative pathological reactions.
At the same time, there is a strong noise in the affected ear, hearing loss, feeling of pawning and fullness in it, and the phenomena of sound discomfort on enhanced sound stimuli. In the phase of inhibition of the labyrinth, vertigo and nystagmus change the direction toward a healthy labyrinth.
Postural disorders gradually settle, and vestibulo-vegetative pathological reactions disappear. Within functional stimulation, hyporeflection of the nystagmus is fixed from the side of the affected labyrinth.
At the same time, noise, stuffiness, and fullness in the ear decrease, and the effects of sound discomfort are reduced. These facts indicate a common mechanism of the processes of excitation and inhibition in both sensory systems in this disease [ 6 , 10 , 18 , 19 ]. An acute attack of vestibular dysfunction lasts from 30 minutes to 3—4 hours and recurs at different intervals.
Long-term betahistine treatment is often prescribed to prevent attacks and reduce their manifestation. However, the causes of its occurrence have not been fully understood [ 11 , 12 , 18 ]. Migrainous vertigo is the most common form of spontaneous recurrent systemic vertigo. It occurs at any age, from preschoolers to older adults. Family history is often noted, indicating the contribution of genetic factors.
It occurs with an aura less often than without an aura. During the attack, transient symptoms occur, such as atrial fibrillation, unilateral paresthesia, and aphasia. These symptoms are often preceded by headaches. Migraine-associated vertigo increases when the position of the head changes. The duration of symptomatic episodes when positional nystagmus can be detected may take several days. Relapses occur more frequently than BPPV. Migrainous vertigo is referred to as central positional vertigo [ 2 , 3 , 5 , 19 ].
But it is a sign of a serious disease that is associated with structural damage of central divisions of the vestibular system and lobes of the cerebellum. Therefore, central lesion should be excluded first of all in patients with positional vertigo. The most reliable differential feature of BPPV and central positional vertigo is the direction of positional nystagmus.
In the case of BPPV, by stimulation in the plane of a certain canal, positional nystagmus characteristic for this canal is typical. When stimulating horizontal lateral canalis semicircularis, horizontal positional nystagmus always occurs.
The direction of the central positional nystagmus is often not correlated with the stimulating canal. Pure vertical or rotary nystagmus is a sign of central vestibular disorder. In patients with central vertigo, in the absence of changes in MRI, it is possible to suspect a migrainous or other vertigo [ 14 , 16 , 19 ].
Our own experience [ 20 , 21 ] of vestibular examinations for more than three decades of participants of Chornobyl nuclear power plant accident indicates that the patients had vestibular and sensorineural dysfunction. These two dysfunctions are characterized by a predominant disorder in the central brain stem and subcortical structures.
The priority of changes preclinical and early clinical in the central departments of the vestibular and auditory systems, the dependence of the degree of manifestation on the dose, and duration of radiation exposure indicate the parallelism of the common mechanism under the influence of the radiation factor. The occurrence of deterministic radiation effects of these dysfunctions by the type of central syndrome in radiation doses greater than 0. The membranous labyrinth of the inner ear consists of three semicircular ducts horizontal, anterior and posterior , two otolith organs saccule and utricle , and the cochlea which is discussed in the chapter on Auditory System: Structure and Function.
Figure These sensory organs respond to angular acceleration. In Figure This expansion proceeds from the inner ear as it sits in the head, to a sketch of the horizontal semicircular duct, to a detail of the ampulla.
In the outline of the single horizontal semicircular duct the angle has changed, and what was initially horizontal is now seen as a vertically-oriented duct on the computer screen. The ampulla is a localized dilatation at one end of the semicircular duct.
A patch of innervated hair cells is found at the base of the ampulla in a structure termed a crista meaning crest. The crista contains hair cells with stereocilia oriented in a consistent direction. The cupula, a thin vane, sits atop this crest, filling the lumen of the semicircular duct. The stereocilia of the hair cells are embedded in the gelatinous cupula. By pressing the "play button" in Figure As the head rotates in one direction, inertia of the fluid causes it to lag, and hence generate relative motion in the semicircular duct in the direction opposite that of the head movement.
This moving fluid bends the broad vane of the cupula. The stereocilia of the hair cells are bent because they are embedded in the gelatinous cupula. Shearing of the hair cells opens potassium channels, as discussed at the beginning of the auditory section See Figure Then, press PLAY to watch the reaction to head movement. There are three pairs of semicircular ducts, which are oriented roughly 90 degrees to each other for maximum ability to detect angular rotation of the head.
Each slender duct has one ampulla. When the head turns, fluid in one or more semicircular ducts pushes against the cupula and bends the cilia of the hair cells. Fluid in the corresponding semicircular duct on the opposite side of the head moves in the opposite direction.
The basic transduction mechanism is the same in the auditory and vestibular systems See Figure A mechanical stimulus bends the cilia of the hair cells. Fine thread-like tip links connect to trap doors in the adjacent cilium. Hair cells in the vestibular system are slightly different from those in the auditory system, in that vestibular hair cells have one tallest cilium, termed the kinocilium. Bending the stereocilia toward the kinocilium depolarizes the cell and results in increased afferent activity.
Bending the stereocilia away from the kinocilium hyperpolarizes the cell and results in a decrease in afferent activity. The semicircular ducts work in pairs to detect head movements angular acceleration. A turn of the head excites the receptors in one ampulla and inhibits receptors in the ampulla on the other side. Then press PLAY to watch the reaction to head movement. Begin by pressing "expand" to show details from the horizontal semicircular ducts on both sides of the head. Beneath the ampullae are new details, which highlight the orientation of the stereocilia in both cristae and their outputs.
The kinocilia are oriented in the direction of the ampullae ampullo fugal within the ducts on both sides. The two sides are mirror images. There is a constant low level of ionic influx into the body of the hair cells, so there is a steady-state receptor potential and a spontaneous low-level discharge of afferent activity. These neutral neurophysiological properties are shown in graphs below each ampulla.
By pressing the "play" button you will see an animation of this. A constant low level of spontaneous activity keeps all the muscles slightly and equally contracted, causing the eyes to look straight ahead.
When the head turns, inertia causes the fluid to move more slowly than the head, generating relative fluid motion in the semicircular duct in the opposite direction of the head turn. This moving fluid, shown by arrows in the lumens of the semicircular duct, bends the hair cells on both sides of the head.
Because the two sides are mirror images, the stereocilia are bent toward their kinocilium on one side and away from their kinocilium on the other side.
Shearing of the stereocilia toward the kinocilium causes a depolarization of the receptor potential and an increase in afferent action potentials. There is an opposite effect on the other side — a decrease in afferent activity. These counteracting bilateral changes in afferent activity affect the vestibular and occulomotor nuclei.
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