Vestibular System Research Paper

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1. Introduction

Throughout the evolution of life on the planet Earth the phenomena of light and gravity have played a compelling role in the development of many biological mechanisms. While the intensity of light changes from day to night, gravity remains constant and omnipresent at all times. For any being on Earth it remains impossible to escape from its influence for more than a few seconds. Indeed such transitions into weightlessness, or free-fall, provide pleasant sensational experiences as when the baby is thrown up in the air, the child playing on the swing or the more courageous who test their limits while bungee jumping or sky diving.

The gravitational force, which is directed to the Earth’s center and is equivalent to an acceleration with a magnitude of 9.81 ms−2 corresponding to the acceleration of a formula I racing car with 700–900 hp, represents a unidirectional force for all biological organisms, no matter how primitive, and thus provides the fundamental reference for ‘spatial orientation.’ For the neurophysiological circuitry of the sensorymotor system, gravity may be considered as a constant background offset or bias signal.

2. Anatomy Of The Vestibular Organs

Any movement in three-dimensional space involves accelerational components that are compounded with gravity. In order to cope with such continual reorientation, each organism requires adequate sensory organ to transduce the magnitude and direction of the concomitant acceleration. In single cell organisms and plants, this organ is situated within the cell, whereas in higher organisms more sophisticated sensory organs have been developed, namely the vestibular organs in the inner ear.

The basic principle for the measurement of acceleration is that of a heavy body, lying either on a sensitive surface, for example, the endolymphatic reticulum of the cell or the inner cell membrane, or embedded in a gelatinous membrane coupled with sensory hair bundles that are sensitive to flexion. The tip of a plant root possesses a relatively primitive sensory organ. This provides the root with information on the direction of gravity, enabling correct growth— usually deeper into the earth (a figure for such a type in a cress root can be found in Volkmann et al. 1986). More complex examples of sensory organs for the measurement of linear accelerations are the open systems, which employ foreign bodies (e.g., sand particles used by crabs), and sealed systems with selfmade bodies, typically calcium carbonate crystal structures. In the fish these consist of single bodies (otoconia) in each organ, while birds and mammals usually have multiple particles (otoconia) embedded in a gelatinous membrane (Fig. 1).

Vestibular System Research Paper

While a sensory organ that signals linear acceleration (otolith organ) may be adequate for those organisms that move relatively slowly and in a linear fashion, for faster moving species and particularly those that utilise three-dimensional space the transduction of linear acceleration must be complemented with the measurement of rotation. Accordingly, in the vertebrates a system of three, approximately orthogonal, semicircular ducts or canals has evolved to signal rotations around any arbitrary axis (Fig. 2). These canals are filled with liquid, so-called endolymph, and are sealed in a domelike enlargement (the ampulla) by a membrane-like structure (the cupula) projecting from a sensory epithelium on a crest (crista ampullaris) into the cupular structure are a multitude of sensory hairs (Fig. 3). When the head is rotated the inertial moment is counteracted by the viscosity of the semicircular canal liquid, producing pressure on the cupula and thus causing the sensory hairs to be sheared in the opposite direction. This, in turn, results in hyper respectively hypoactivity of the sensory cell, according to the direction of hair deflection.

Vestibular System Research Paper

The human vestibular organs are embedded in a fluid-filled bony labyrinth in the temporal bone (Fig. 4) adjacent to the hearing organ, or cochlea. Common to both vestibular and hearing organs are two fluid compartments containing respectively the perilymph and the endolymph. The vestibular labyrinth consists of two organs for the transduction of linear acceleration, the macula utriculi and macula sacculi, and a set of three semicircular canals, namely the horizontal, anterior, and posterior, which function as sensors of rotation. In the upright position the macula utriculi is more or less aligned to transduce any linear acceleration in the horizontal plane while the macula sacculi is effectively aligned to the vertical plane.

Vestibular System Research Paper

The function of this part of the vestibular organ is not yet exactly defined; it may also be responsible for the sensory transduction of very low frequency sound waves. From an ontogenetic viewpoint, the cochlea is an evagination of the sacculus. In principle the sensory hair cells in the cochlea function identically to those of the vestibular organ, although the general structure is optimised for acoustic transduction.

The vestibular labyrinths in the right and left inner ear can be regarded as mirror images. While each labyrinth is able to measure all naturally occurring linear and angular accelerations, they are neurally interconnected to complement one another, to some extent analogous to a push-pull amplifier. While the head is stationary a steady signal of typically 80–100 impulses per second is present on the afferent nerve connecting the vestibular organ to the vestibular nuclei in the central nervous system. During a head rotation to the right, this impulse rate from the right labyrinth increases while the impulse rate from the left labyrinth decreases (i.e. pulse frequency modulation). This is illustrated in Fig. 4. This push-pull principle provides increased sensitivity and permits accurate bi-directional measurement.

Vestibular System Research Paper

Such information is transferred via the bipolar vestibular nerve to the central vestibular nuclei in the brainstem. The ganglion Scarpae of this nerve is situated within the inner auditory canal. Its peripheral branch synapses to the primary vestibular sensory cells, the central branch to the cells of the vestibular nuclei, where the information is relayed to many efferent fibers.

3. Physiology Of The Vestibular System

The neural circuitry in the vestibular nuclei of the brainstem have three principal functions, namely the integration of vestibular information with that from the visual and the proprioceptive systems related to motion in space, the stabilization of the visual field, and third, the stabilization of body posture and locomotion. All of these tasks function autonomously without the need of our conscious intervention. Only in those situations where there is a disorder in the sensory information, occurring through sensory mismatch or through disease, do we become aware by way of motion sickness or dizziness with symptoms such as ataxia or tendency to fall to one side, or disturbance of the visual field. In the following chapters the major physiological functions—and the associated dysfunctions—of the central vestibular system, and thereafter of the peripheral vestibular system, are described.

4. Integration Of Motion-Related Sensory Information

Several sensory systems—namely the visual, the vestibular, the proprioceptive, and the auditory—contribute to the maintenance of spatial orientation. In principle one can say that all stereo systems responding to motion in three-dimensional space are involved to some degree in the integrative process in the central vestibular nuclei. This multisensory flow of information is essential for coordinated motion in space. Afferent nerve fibres from each of the named sensory systems converge to the nerve cells in the vestibular nuclei. This means, for example, that motion perception in the vestibular area in the cortex (parietoinsular vestibular cortex, PIVC) is induced by real motion or by regarding a moving visual field.

One can play with this phenomenon by looking at a fast running river from a bridge, or by watching clouds on a windy day while lying on a meadow. It takes about 20 seconds until one has the impression that the water, respectively the clouds are standing still and the observer is moving. This effect is due to the fact that when different sensory information converge to a single cell there is no possibility at this level to distinguish a optical from a vestibular stimulation.

Visual, or optical, motion perception is mainly mediated from the peripheral retinal field. Thus, a stronger intensity is reached when the entire field-of-view is stimulated. For clinical testing a stripe pattern or other strongly contrasting presentation (e.g., large format projection of city skyline) moving at angular velocites of up to 90 degs−1 is employed. This is known as ‘optokinetic stimulation.’

In the human there is a second component of the optical system for motion perception which must be taken into account. This is mediated by the central area in the retina known as the fovea, which provides high-resolution focussed imaging. The afferent information from this area is relayed to the vestibular nuclei via separate pathways. Clinical stimulation of the fovea is performed with more slowly moving objects (<40 degs−1 ), typically by means of visible point targets or a pendulum.

Brain diseases affecting any of the described systems generally produce disturbances in spatial perception or orientation.

Somatosensory perception of motion or gravity originates from receptors distributed throughout the body, even from the intestines. The neural information from these receptors is relayed either directly, or via mossy or climbing fibres to Purkinje cells in the cerebellum, and in turn via inhibitory connections, to the vestibular nuclei.

One feels gravity with the receptors of the plantar surface of the foot when standing upright, with the sensors in the back when lying down or when accelerated in a car. One can feel the change of gravity with the receptors in the intestinum, e.g. when a cable railway runs over a pillar.

The main sensory inputs converging to cells in the vestibular nuclei stem from the visual, vestibular and somatosensory receptors. When we move actively in our habitat all of these components are well matched and concur with a correct sensory perception. However, the situation can be very different during passive motion when the sensory inputs no longer necessarily match correctly, that is, a sensory mismatch occurs.

Such a sensory mismatch can be experienced by a car passenger who, while driving along a hilly and curved road, simultaneously reads a newspaper. The optical system will indicate that one is stationary (stable image of the newspaper) while the vestibular system, the somatosensory, and the acoustic systems will indicate the movement of the vehicle. The same situation occurs in an aircraft. The cabin compartment of the plane presents a stable optical environment for the passenger, but the vestibular organs trans-duce the plane’s motion during curves and landing manoeuvres.

When such a sensory mismatch, or conflict, cannot be resolved quickly and correctly a crisis known as ‘motion sickness’ occurs, which is accompanied by a series of symptoms, namely paleness, tiredness with yawning, stomach awareness, outbreak of sweat, nausea, and vomiting.

The vestibular system uses nausea and vomiting as an emergency outlet instead of pain as is the case for all other sensory systems. The reason for this is unknown, but we do know that there would be no fairground machines if the vestibular system would elicit pain when being overstimulated.

Strictly speaking, to avoid motion sickness one must prevent the occurrence of the precipitative sensory mismatch. One should not make fast head movements while the whole body is subject to passive motion. The combination of fast active and passive motion is associated with the outbreak of motion sickness. There is also a wide interindividual variability in susceptibility to motion sickness within the same provocative situation.

Goethe was hypersensitive to motion sickness. He described his problems during his Italian journey on a ship cruise from Napoli to Palermo on the island of Sicily. He was very angry, not only because of his own motion sickness, but also about the fact that his companion was not affected and furthermore was enjoying his food.

One reason for this variability may lie in the difference in mass of otoconia between the right and left labyrinths, which lead to asymmetrical afferent input to the central vestibular nuclei.

Normally, during our active movement repertoire this difference is well-compensated on a neural level. However, during passive motion this asymmetry could potentially introduce a sensory mismatch and therefore play a role in the elicitation of motion sickness. While it has proved difficult to measure the effective mass of otoconia in mammals, it has been possible to measure the mass of the single otoconial stones in fish. In a measurement series performed with the trout, salmon, and xiphophoris Helleri right-to-left differences of up to 76 percent were found (Scherer et al. 1997).

In the case of a sensory conflict (mismatch) in the area of the central vestibular nuclei hierarchical structures of the brain come into play. As we know the visual system dominates over the vestibular and within the vestibular system the evolutionary older otolith organs dominate over the semicircular canals.

One can notice this hierarchical principle when sitting in a stationary train in the railway station. When a neighbouring train starts to move one immediately gets the impression that one’s own train has started to move and that the other train is stationary. In this case of different sensory input (optical: moving; vestibular and somatosensory: stationary) the dominant visual system determines the percept.

5. Stabilization Of Upright Body Posture

Together with the cerebellum, the vestibular system contributes substantially to the stabilisation of body posture during locomotion. The vestibulo-spinal tract emerges from the lateral vestibular nucleus in the brainstem and runs unilaterally to the spinal motoneurons of the extensor muscles (Fig. 5). When a person turns to the right, the stimulus to the right vestibular organ leads to an increase of the afferent firing rate on the nerve fibres leading to the vestibular nuclei; simultaneously the firing rate on the nerve fibres from the left vestibular organ decreases. At the same time the visual system signals the rotation of the surrounding, that is, to the left during a head turn to the right. The afferent signal from the retina converges with that from the vestibular organs and enhances their effect, that is, stimulating the right vestibular nuclei positively and the left negatively. Via the vestibulo-spinal tract the tonic signal to the extensor muscles on the right is increased, which has the effect of counteracting the increased body mass on this side during the turn. At the same time there is a corollary increase of tonus to the left flexor muscles.

Vestibular System Research Paper

When the function of one vestibular labyrinth (right or left) is suddenly reduced due to an accident, an infection, or an operation the person feels a tendency to fall to the injured, or diseased, side. However, this symptom lasts only for a number of days, even in those cases where the function of the diseased side does not recover. The reason for this recovery and for the similar reduction of other symptoms lies with the powerful self-reparatory capability, or adaptability, of the vestibular system. A major therapeutic approach to vestibular deficits is based on self-training. In the first weeks after the sudden loss of vestibular function the patient undergoes training involving general natural body movements; in the following weeks specific training of impaired functions and symptoms is necessary.

The phenomenon of height vertigo can also be explained within the context of sensory mismatch or conflict. This ‘physiological vertigo syndrome’ (Brandt 1991) occurs when a person stands on the top of a high tower or on the brink of a cliff. In every normal person a certain degree of random body sway can be measured during upright stance. This body sway is regulated by the multisensory convergence in the vestibular nuclei. In this context spatial vision plays a major role, particularly the perceptual relationship between foreground to background. While standing on the edge of a high tower or cliff the relative motion of the background—now located many metres distant in comparison to normal—is perceived visually as much greater. This discrepancy in visual perception destabilises the regulatory mechanism for postural stability and body sway increases. On continued exposure this ‘positive feedback’ can lead to serious instability. How this fundamentally physiological response is processed cognitively and psychologically can vary enormously among individuals, in some people leading to severe height anxiety with vegetative symptoms. Such physiological instability can be counteracted immediately by stepping back from the brink so that the discrepancy is resolved by viewing a normal foreground at foot level, or by providing more contact to the ground by grasping a handle or rail, sitting down or kneeling. Extreme forms of height vertigo can be cured by behavioural therapy.

Goethe treated his height vertigo by repeatedly climbing up the tower of Strasburg’s Gothic cathedral and standing on exposed platforms (similar to contemporary ‘flooding’ therapy). Another kind of training of height anxiety is shown in Alfred Hitchcock’s film Psycho.

6. Stabilization Of The Visual Field During Locomotion

The stabilization of eye position in the head during locomotion is supported by the so-called vestibuloocular reflex. Afferent nerve fibres project from the ipsilateral superior and the contralateral medial nuclei upwards via the medial longitudinal fasciculus (MLF) to the oculomotor nuclei, which in turn govern the input to the motor neurons driving the eye muscles (Fig. 6). This reflex is described here briefly since it plays a major role in the diagnosis of vestibular disorders.

Vestibular System Research Paper

Again taking the example of a rotation to the right, the surrounding visual field rotates too the left. If the eyes were to remain fixed in the head during this rotation, the image of the surroundings would slip on the retina, causing a blurring of perception until the head was stationary. This would obviously deteriorate spatial orientation. A major purpose of the vestibuloocular reflex is to rotate the eyes compensatorily to the head movement, thus retaining a focussed image on the retina. Under normal conditions the vestibuloocular reflex facilitates compensatory eye movement equivalent to the concomitant head movement, regardless about which axis the head is rotated. In this manner, head movement in three-dimensional space is compensated for by appropriate reflex eye movement. However, the mechanical range of eye rotation is limited anatomically by the extraocular muscle and optical nerve structures. Thus, during a full headand body-rotation, eye position is compensatory, but is regularly reset by means of a quick phase in the anticompensatory direction. This leads to a sawtooth pattern of eye movement, known as ‘nystagmus,’ during full body rotation. The nystagmus eye movement pattern is defined by the sawtooth pattern consisting of the vestibularly induced slow phase and the quick reset movement (Fig. 6). Such nystagmus patterns of eye movement are elicited by natural movements or by unilateral or bilateral stimulation of the vestibular organs. A similar pattern, known as optokinetic nystagmus, can also be elicited by rotation or translation of the visual field while the subject is held stationary.

Optokinetic nystagmus can be seen easily when a person looks out of a train’s window or out of the side window of a car. The moving optical pattern causes a slow deviation of the eye in the direction opposite to the train’s motion with a fast phase in the direction of the train’s motion.

Since the visual system is hierarchically superior to the vestibular system, visual fixation of a target point suppresses these nystagmus responses. A practical consequence is the fact that we are able to read during active or passive motion, although this may lead to a sensory mismatch which may cause motion sickness in sensitive individuals. On the other hand we have to prevent fixation in order to be able to measure nystagmus. This is done usually by means of thick lenses in a goggle (Frenzel glasses), by electric or magnetic nystagmography or by videoimaging of the eyes in infrared light.

Observation and measurement of eye movements represents an important inroad for the examination of the function and dysfunction of the vestibular system, and therefore provides an important diagnostic tool for the clinician who has to deal with patients suffering from dizziness)

7. Typical Vestibular Disturbances

7.1 Peripheral Disturbances

(a) Sudden unilateral loss of function of the vestibular organ.

Pathophysiology: unknown, virus infections of Scarpae’s ganglion, disturbed blood supply, trophic disorders of the cupula in the ampullae of the semicircular canals (Helling et al. 2001, 2000) are discussed.

Symptoms: heavy turning sensations in the first days, the symptoms decline gradually.

(b) Meniere’s disease.

Pathophysiology: osmotic disturbance within the two components of inner ear fluids, leading to a hydrops of the endolymphatic space and a sudden poisoning of nerve fibers with potassium.

Symptoms: sudden attacks of severe vertigo and vomiting in combination with low tone hearing loss and tinnitus in the affected ear.

(c) Benign paroxysmal positioning vertigo (BPPN).

Pathophysiology: aberrated otoconia from the otolith organs lying in the vertical semicircular canal initiating a unphysiologically endolyph wave.

Symptoms: heavy torsional sensation, which lasts for 10 to 20 seconds after performing a fast body motion.

(d) Acoustic neuroma.

Pathophysiology: benign tumor growing in the vestibular part of the eight cranial nerve in the inner auditory canal.

Symptoms: unilateral, slowly intensifying loss of vestibular and acoustic function. While the vestibular defect usually is well compensated and asymptomatic, the acoustic defect brings the patient to the doctor.

(e) Psychogenic (phobic) vertigo.

Vertigo is a frequent symptom of psychiatric illness (Brandt 1991). Alternatively, a transient labyrinthine dysfunction may initiate development of neurosis in which anxiety, panic attacks and depression are most common, and which typically preserves subjective vertigo and postural imbalance (Brandt 1991).

7.2 Central Vestibular Disorders

A lot of central disorders induce vertigo or postural instability. Most common disorders are mentioned (for details see Brandt 1991)

(a) Basilar artery migraine

(b) Vestibular epilepsy

(c) Down- or upbeat vertigo syndromes

(d) Central positional vertigo

(e) Posttraumatic vertigo (central or peripheral)

(f) Familial vertigo

(g) Drug vertigo (central or peripheral).

Bibliography:

  1. Baloh R W, Halmagyi G M 1996 Disorders of the Vestibular System. Oxford University Press, Oxford, UK
  2. Brandt T 1991 Vertigo. Springer, New York
  3. Brodal 1981 Neurological Anatomy in Relation to Clinical Medicine. Oxford University Press, New York
  4. Goebel J A 2001 Practical Management of the Dizzy Patient. Lippincott, Williams, Wilkins, Philadelphia
  5. Helling K, Clarke A H, Watanabe N, Scherer H Investigation on the morphology of the cupula in semicircular canal ampulla. HNO 48: 822–7
  6. Helling K, Watanabe N, Jijawa H, Mizuno Y, Watanabe S, Scherer H in press Altered cupular mechanics—A cause for peripheral vestibular disorders? Acta Otolaryngology
  7. Scherer H 1997 Das Gleichgewicht.. Springer, New York
  8. Scherer H, Helling K, Hausmann S, Clarke A H 1997 On the origin of interindividual susceptibility to motion sickness. Acta Otolaryngology 117: 149–53
  9. Sharpe J A, Barber H O 1993 Vestibulo-ocular reflex and vertigo. Raven, New York
  10. Volkmann D, Behrens H M, Sievers A 1986 Development and gravity sensing of cress roots under Microgravity. Naturwis-senschaften 73: 438–44
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