Overview: The role of the vestibular system

The vestibular system is critical for postural control because it uniquely identifies self-motion of the head as different from motion in the environment. The vestibular system is a mechanical system that creates neural output to create this sense. Fig. 21.1 shows the components of the vestibular mechanism as it sits with the cochlea, the organ of hearing. The vestibular system detects the direct pull of gravity to identify head position during balance activities and maintains vertical alignment of the eyes. This contributes to the head righting or labyrinthine response and activates the ocular tilt triggered by lateral head bend as seen in Fig. 21.2 . Horizontal and vertical accelerations, such as riding in a car or an elevator, are detected by the vestibular otolith mechanism depicted in Fig. 21.3 . The otolith structures provide this input during head movement by identifying the degree and direction of deflection of the hair cells projecting into the macula of the saccule in the vertical plane and macula of the utricle in the horizontal plane. It is the mass of the otoconia that sits on top of the macula and creates the mechanical pull on the hair cells when the head accelerates or tilts. The vestibular system calibrates the speed of head movement or degree of tilt in relation to the input from the nerve cells that project from the otoliths.

Components of the Vestibular System and Cochlea With Distribution of Neural Connections.

(A) Membranous labyrinth refers to the structure of the vestibular and cochlear mechanism. (B) Plane of reference for the canals and otliths. (C) Cross section of the ampulla within the semicircular canal. (D) Cross section of the macula of the otoliths. (E) The structure and activation pattern of the nerves within the semicircular canals and otliths.

(From Felten DL, O’Banion K, Maida M. Sensory Systems. In: Netter’s Atlas of Neuroscience ; 3rd ed. Elsevier; 2016.)

Patterns of excitation and inhibition for the left utricle and saccule when the head is upright (A) , tilted with the left ear 30 degrees down (B) , and tilted with the right ear 30 degrees down (C) . The utricle is seen from above and the saccule from the left side.

(From Haines DE. Fundamental Neuroscience for Basic and Clinical Applications. 3rd ed. Philadelphia: Churchill Livingstone; 2006.)

The Otoliths Register Linear Acceleration and Static Tilt of the Head.

(From Hain TC, Ramaswany TS, Hillman MA. Anatomy and physiology of the normal vestibular system. In: Herdman SJ, editor. Vestibular Rehabilitation. 3rd ed. Philadelphia: FA Davis; 2007.)

The vestibular spinal reflex (VSR) creates the response from the otolithic structures of the vestibular mechanism to the muscles to provide postural control through the activation of the vestibulospinal tracts. The medial vestibulospinal tract (MVST) descends only to the axial cervical musculature. The coordination of head movements and the integration of head and eye movements are activated through the medical tracts. The lateral vestibulospinal tract (LVST) descends to the muscles of the trunk, providing orientation for body position in space to support upright balance activities and gait. Together these tracts provide efficient head righting. Activation will cause ipsilateral increased tone in extensors with reciprocal inhibition of reciprocal inhibition of flexors. Someone with an acute vestibular disorder that affects the VSR will often increase weight shift to the side of the lesion. It is important to remember that vestibular nuclei are connected to other sensory and motor systems involved with balance. The connection to the cerebral cortex is associated with spatial orientation. Both top down and bottom up referencing (see later) are used to create the necessary integration for balance. The inferior vestibular nuclei connect to the reticular activating system, which is the cause for the nausea and anxiety often associated with disruption within the vestibular system.

Angular and linear acceleration of the head are detected through the semicircular canals that are part of the labyrinth on each side. When the head moves or changes position, there is movement of endolymph fluid within the canal that moves in the opposite direction of the head movement. The ampulla, which appears as a bump in the canal, houses the cupula containing a group of hair cells; the kinocilia are the longer hair cells, and the stereocilia are shorter hair cells. The hair cells are deflected as the endolymph pressure increases or decreases, reflecting the speed and direction of the head motion. When the stereocilia move toward the kinocilium, the canal is excited, and when the pressure moves the kinocilium toward the stereocilia, the canal is inhibited. In the posterior canal and anterior canal the stereocilia are closest to the otolith, whereas in the horizontal canal the kinocilium is closest to the otolith. This relationship will determine the how the nervous system will react to changes in head position and rotation of the canal. The canals are aligned to provide information about head position and angular acceleration in all planes of movement. For example, the posterior canal on one side is in relative alignment with the anterior canal on the opposite side. This allows for redundant information to be provided by the canals through a push–pull relationship.

To maintain a stable gaze during head movement, the eyes respond through the vestibulo-ocular reflex (VOR). This is achieved as the excitation signal is activated as described previously in the direction of head turn. For example, in a right head turn, the movement of the fluid in the semicircular canal is in the opposite direction, or toward the left. The endolymph presses the kinocilium of the right horizontal canal toward the otolith (excitation), and the endolymph in the left horizontal canal pulls the kinocilium away from the otolith (inhibition). The excitation moves through the vestibular nerve to the level of the oculomotor nuclei activating the medial rectus muscle of the ipsilateral eye and the lateral rectus of the contralateral eye. This pulls the eye in the opposite direction as the head turn. At the same time, the medial rectus of the contralateral eye is inhibited along with the lateral rectus of the ipsilateral eye, which allows the eyes to move without resistance. In a properly functioning system, the eyes move at the same time and at a speed exactly opposite the head, providing a gain of 1:1 (eye movement speed reflects head movement speed). The relationship between eye movement and head movement can be seen in Fig. 21.4 .

Vestibuloocular Reflex.

When the head is turned to the right, inertia causes the fluid in the horizontal semicircular canals to lag behind the head movement. This bends the cupula in the right semicircular canal in a direction that increases firing in the right vestibular nerve. The cupula in the left semicircular canal bends in a direction that decreases the tonic activity in the left vestibular nerve. Neurons whose activity level increases with this movement are indicated in solid lines. Neurons whose activity level decreases are indicated in dotted lines. For simplicity, the connections of the left vestibular nuclei are not shown. Via connections between the vestibular nuclei and the nuclei of cranial nerves III and VI, both eyes move in the direction opposite to the head turn.

(From Felten DL, O’Banion K, Maida M. Sensory Systems. In: Netter’s Atlas of Neuroscience ; 3rd ed. Elsevier; 2016.)

When the signals from the labyrinth mechanisms are not equal and opposite, usually when there is damage to one side anywhere along the pathway, nystagmus results. Nystagmus is nonvoluntary, rhythmic oscillation of the eyes, with movement in one direction clearly faster than movement in the other direction. Nystagmus reflects the abnormal VOR response when the system is not calibrated. The eye movements represent the slow drift of the eye with a fast catch up saccade returning the eye to the original position. This is due to the unopposed neural activity in the intact vestibular pathways. The slow phase represents the vestibular insult, and the fast phase is the central reset. Nystagmus is labeled by the fast phase. In a patient with a peripheral vestibular disorder, horizontal nystagmus will intensify with the gaze toward the fast phase; this is known as Alexander’s Law. Disruption of the vestibular system resulting in nystagmus causes an immediate sensation of blurriness of vision or the sense the room is moving, known as vertigo. Vertigo is a specific type of dizziness that reflects the vestibular system involvement. Vertigo can cause imbalance as it disrupts the visual reference for head position.

Abnormal eye movements can also reflect the vestibular system function as it passes through the cerebellum, where the Purkinje cells provide inhibitory control of the vestibular nuclei. The flocculonodular lobe and medial zone of the cerebellum will affect postural control and eye movements. For example, dysfunction in the flocculus will cause abnormal smooth pursuits, abnormal VOR suppression, and nystagmus patterns, which include downbeat, gaze-evoked, and rebound. Central positioning and periodic alternating nystagmus (PAN) patterns are seen in nodulus lesions. Saccadic movement, or the ability to move the eyes quickly between targets, is controlled in the vermis so a lesion can cause hypometric eye movements. Disruption of function in the fastigial nucleus can cause hypermetric eye motion. The cerebellum also has a role in motor skill adaptation and error correction. Disease processes, such as multiple sclerosis, which can progress to disruption of cerebellar pathways, can cause nystagmus and loss of postural control. Strokes that affect the cerebellum can cause persistent dizziness as well as imbalance, even when the vestibular testing is normal and there is no concomitant hemiplegia.

The hippocampus is linked to the functionality of the vestibular system and contains “place cells” that create an inner map of our environment. These cells work together with connections in the entorhinal and thalamic areas to assist us in way finding, or spatial orientation. These cells become dysfunctional with peripheral vestibular lesions. The evolutionary gravity sensing function of the otoliths may be connected to both spatial and cognitive functions. There is a further connection to the striatal component of the basal ganglia, which has an additional impact on both spatial orientation and cognition. This may be the reason that diseases affecting the basal ganglia, such as Parkinson disease, have components that may overlap. There appears to be a connection to vestibular dysfunction related to atrophy of the hippocampus and changes in the posterior parietal–temporal, medial temporal, and cingulate regions seen in people with Alzheimer disease, mostly in the subset known to have spatial disorders that lead to wandering.

The vestibular projections to the cortex pass through other parts of the brain. The thalamus works as part of the sensory relay system. It has a connection with the vestibular cortex and the reticular formation, so it affects arousal and conscious awareness of the body to provide the determination of self-movement compared to environmental movement as described in the opening paragraph. Vestibular connections to the cortex provide spatial orientation and perceived vertical. The roles of the vestibular cortical areas, such as the parieto-insular vestibular cortex, are the focus of research directed toward changing firing patterns in the brain to address concerns as mal de debarquement noted later in this chapter. The connections to the autonomic nervous system, such as the locus coeruleus, amygdala, and parabrachial nucleus, provide the link to symptoms of stress and panic, activation of the fight or flight response, emotional memories, and the malaise that includes nausea. This is another area of active research (see Fig. 21.5 ).

Potential Location of Lesions That May Affect the Vestibular System.

(From Felten DL, O’Banion K, Maida M. Sensory Systems. In: Netter’s Atlas of Neuroscience ; 3rd ed. Elsevier; 2016.)

It is very important to remember that the vestibular system never works in complete isolation; it is always integrated with the somatosensory system or the visual system. Vestibular rehabilitation as an intervention is always dependent on sensory integration. The vestibular and somatosensory systems preferentially operate at different velocities of postural sway because of differences in sensory thresholds and sensitivities. It is believed that misinterpretation of multisensory inputs during postural sway may underlie the imbalance associated with either vestibular or somatosensory impairments. The term “sensory reweighting switch” describes the unconscious shift from a surface reference using somatosensory input to a gravitational reference that relies on the vestibular system information. This can be described as a switch from a “body on support” to a “body in space” orientation.

Top down postural control

Vestibular inputs are critical to determine whether the body is moving on a fixed surface or if the surface is moving. The perception of verticality used to orient to gravity, when the support surface is perceived to be unstable, is provided by the vestibular system. Vestibular inputs are used to recognize the changes in angle of the support surface. ^, The vestibular system provides a top-down reference for the head and trunk stability in line with gravity, while the leg segment is coordinated to maintain surface reference. It is important to remember that at the same time the vestibular system is activated in this moving surface condition, the somatosensory system is still providing feedback about the relationship to the surface. Resulting patterns of muscle activation reflect vestibular and somatosensory integration to maintain continuous upright postural control.

Studies performed on rotating surfaces demonstrate how the use of vestibular, visual, and somatosensory reference differs under conditions that mimic environmental situations. At very slow speeds, somatosensory reference is the primary reference used. As a surface rotates greater than 6 degrees of tilt and increases velocity (range of 2 to 8 degrees per second) there is more focus of the sensory systems away from the somatosensory reference toward the vestibular and visual references. Correct visual information can compensate for loss of vestibular information. However, when the eyes are closed, individuals with vestibular deficits will typically lose balance as the surface tilts at 4 degrees per second. Patients with missing or maladapted vestibular function lack the awareness of angle changes and demonstrate abnormal firing patterns in the muscles of the lower leg, aligning their bodies with respect to the surface instead of gravity, which is described as active postural destabilization. Instead of changing the ankle angle to adjust to the tilt, the torque around the ankle remains locked with excessive reference to the surface. The head and trunk follow the direction of the surface tilt. This concept can be seen in Fig. 21.6 . As the surface tilt angle exceeds 8 degrees, the individual who cannot activate gravitational reference or adjust the ankle angle will be unable to maintain balance without visual input. ^, When the surface is uneven, compliant, or narrow, the vestibular system will provide adequate information on head position, even if vision is occluded.

In anterior tilt of the platform, the head and trunk follow the reference of the platform rather than maintaining a gravity-neutral position. This is reported as surface reference.

(Courtesy Perry Dynamics, Decatur, IL.)

Bottom up reference for postural control

As stated previously, the somatosensory system can determine the orientation of the head compared to the surface tilt through cutaneous, proprioceptive, pressure, and stretch receptors of the muscles and joints, primarily related to pressure through the balls of the feet.

The somatosensory system is necessary to interpret vestibular information. It contributes significantly to balance when the surface is stable or moving slowly (at less than 4 degrees per second). At the other end of the spectrum, in very fast oscillations, the muscle spindles provide stabilizing information that can contribute to head and trunk stability. Patients with vestibular deficits typically rely primarily on their ankle strategy during typical activities by keeping the head aligned with the body. This can be seen in a patient who demonstrates rotation “en bloc”; the head will stay aligned with the body while turning. This can be seen in Fig. 21.7 during a lateral tilt where the trunk will follow the direction of the platform.

(A) The patient references her trunk to the platform, shifting weight downhill to the downhill leg. (B) The patient has referenced her trunk and head to gravity, resulting in improved postural control.

(Courtesy Perry Dynamics, Decatur, IL.)

The vestibulospinal system also activates the neck muscles in response to head motion. When the vestibular system function is missing or inaccurate, there is abnormal muscle activation in the muscles of the neck. This is usually seen as excessive co-contraction of both flexors and extensors. Abnormal firing of the sternocleidomastoid (SCM) with restriction of rotation of the head is often seen in both acute and chronic settings. The suboccipital muscles can develop a pattern of overuse that can contribute to headache. See cervical spine function and dysfunction in concussion in Chapter 23 .

Having even the slightest touch reference, so that the somatosensory system can orient the trunk through upper extremity joint position sense, is another way to substitute somatosensation for vestibular reference. The position of the head and trunk can be determined by this touch even when the vestibular system function lacks normal function and the eyes are closed. Because the arm stabilizes the trunk more than the legs do, reaching for a stable surface is a common way to maintain balance when challenged. The therapist must recognize when the patient is using this touch reference to substitute for gravity orientation.

When the brain is not able to use somatosensation to identify the relationship between appropriate body segments and the surface, the patient often will report feeling lightheaded or has the sense of floating. When somatosensory inputs from the neck are reduced, absent, or distorted, it affects the stability and mobility of the individual spinal segments. Co-contraction of the SCM, levator scapulae, upper trapezius, and superficial neck extensors may indicate abnormal sensory feedback, altered afferents, and recruitment patterns, which are ineffective. Nociception from cervical segments can create “noise” in the postural control system contributing to dysmetric postural responses and nausea. Impaired cervical afferents will cause changes in cadence and length of stride when neck motion is introduced to gait. This should be considered in planning interventions for patients who are sent for vestibular rehabilitation. ^,

Gait dysfunction

Chapter 20 on Balance describes automatic postural responses and describes balance testing in detail. It is important to understand the role of the vestibular system in movement disorders related to balance. These consequences can have an impact on the gait patterns related to vestibular dysfunction.

Vestibular system losses can result in motor responses that are larger than necessary for the task, which can predispose a patient to falling. This can be seen in the gait cycle when the body center of mass moves faster and farther than the individual can control. This movement appears similar to that of the patient with cerebellar dysfunction, and indeed may represent the loss of vestibular input to the Purkinje cells in the cerebellum that would normally modulate vestibular pathways. ^, The gait pattern reflected by vestibular dysfunction, or lack of integration, often involves flat-foot gait with minimal heel strike and abnormal foot placement requiring larger than normal trunk adjustment. To control the position of the trunk, the base of support is widened. Speed of gait is another indication of vestibular function from the perspective that patients with bilateral loss or uncompensated vestibular loss demonstrate a slower self-selected speed. Typically, there is increased double limb stance time and decreased stability at heel strike. Vestibular control of position for the upper body and head appears to be separated from the lower body in gait in a similar pattern as noted during perturbed stance. Head and trunk stability normally remain constant throughout the phases of gait, and vestibular inputs appear to be most critical during initiation of gait, toe off, and heel strike. Vestibular information contributes to the planned foot trajectory and placement of the foot to prevent disequilibrium. It is interesting to note that during steady state gait—and even more so with running—vestibular contribution appears to diminish in importance. This may be because movement in running is highly automatic and the trajectory remains steady.

When the vestibular system does not accurately inform the patient about the speed and direction of head movement, visual cues are used to determine movement speed and direction of gait in relation to nonmoving objects. However, in environments with a lot of motion, or when someone approaches in the opposite direction, determining speed and direction of self-movement becomes more difficult. Patients often report dizziness and imbalance in a crowd. Walking with head turns becomes even more challenging as the vestibular system is activated and the somatosensory and visual systems are disadvantaged. Head turns included in the Functional Gait Assessment provide a way to identify this impairment. Because head movement can cause visual disturbances and dizziness, the patient with a vestibular disorder will significantly limit head movement while walking. When visual cues are used predominantly for balance, the patient will try to keep the body in line with vertical and horizontal visual targets. This will decrease the small, natural movements typically made during the gait cycle. A change in visual environments can trigger imbalance in the patient with visual dependency. Walking into a darkened room, especially if the surface is uneven (e.g., in a theater where the surface is sloping), can often trigger a fall or stumble. Patients with permanent vestibular loss should be educated about these potentially high-risk environments and taught compensatory strategies to ensure safe mobility. Patients with potentially recoverable vestibular function should be trained to walk with eye and head movements, trunk rotation, and arm swing.

Vestibular contributions to stability during transitions from sit-to-stand, initiation of gait, and abnormal foot placement can be identified during standard tests such as the Timed Up and Go, the Tinetti, and Dynamic Gait Index. Scores are adversely affected when vestibular system functions are diminished. The Functional Gait Assessment has been developed specifically for use in patients with vestibular disorders (see Table 20.1 in Balance chapter).

Recovery of function: Adaptation versus substitution

During most daily functions, the vestibular system creates little awareness or sensation that it has been activated. When it is stimulated beyond the typical level (e.g., during a fast spin or when a roller coaster suddenly drops), it creates a strong sensation of uneasiness or dizziness. This is often accompanied by nausea, sweating, and feeling out of control. Often the balance system is also affected for a short time, causing an unsteady gait. The dizziness that occurs in the normal individual when the vestibular system is overstimulated can mimic the feeling of dizziness that occurs when the brain encounters sudden changes or losses of input from the vestibular system.

Acute disorders of the vestibular system can cause devastating lack of visual stability, loss of balance, and inaccurate sense of movement. As stated previously, there is an initial loss of trunk and gaze stability with vestibular dysfunction. Central nervous system (CNS) adaptation is critical to recovery of function. During recovery, the visual or somatosensory systems may be used excessively to counteract the loss of information from the vestibular system.

In the patient with an acute unilateral vestibular disorder, the brain identifies this abnormal state, recognizing that the perceived motion from the visual system is not congruent with the feedback provided by the somatosensory system. If there is stable visual input available, the brain will begin to use the stable visual input to assist the CNS recalibration. There is usually adequate central adaptation to stop the spontaneous nystagmus in a lighted environment within 3 days. The spontaneous nystagmus may continue to be active in a dark room, and even for weeks after the insult there may still be a sensation that the head is rotating when the eyes are closed.

CNS adaptation represents the highest level of recovery in the patient with a vestibular dysfunction, and therefore as much adaptation as possible should be facilitated to improve functional outcomes. ^, Although some patients with vestibular lesions appear to be well-compensated, they often require increased attention to perform daily activities. This increased demand for attention appears to extend beyond postural control and may be associated with sensory integration resolving multiple sensory signals for spatial orientation. Vestibular adaptation programs should challenge the patient at the limit of his or her ability. Patients often choose to do the easiest exercise and avoid the more difficult exercises if they are not educated about the need to trigger the symptoms. Conversely, if the challenge is too far above the ability of the patient, the CNS will fail to adapt. Comorbid dysfunction can also affect functional recovery, especially if it affects the visual or somatosensory inputs. Disorders that effect the autonomic nervous system can significantly impede recovery. Trauma, either physical or psychological, can cause maladaptive responses that are inconsistent with typical recovery. Conditions such as concussion and persistent postural-perception dizziness (PPPD) are prime examples of this concept and are discussed later in the chapter.

Clinicians are exposed to patients at many different levels of adaptation in clinical settings. It is critical to understand the level of adaptation and potential for recovery for each patient. For example, tests such as video nystagmography (VNG) will identify an existing impairment; the level of physiological adaptation is identified by nystagmus in room light or tests such as the head impulse test. Functional adaptation is determined through activities such as dynamic visual acuity (DVA), loss of balance during gait with head turns, tandem gait, and walk with sudden stops. Dependency patterns are identified by observing the change in status when vision or somatosensation is removed, for example, by using the sensory organization test, namely Clinical Test of Sensory Organization and Balance, or moving platforms. Functional scales (e.g., the Functional Gait Index) can help the knowledgeable clinician identify which impairments may be having the greatest impact on the activity limitation of the patient. Successful intervention is achieved by accurate analysis of both the missing and available components of the system—facilitating adaptation, avoiding excessive sensory substitution, and determining appropriate compensatory strategies when necessary. Home exercise programs must be created to optimize the recovery process while keeping the patient safe. The patient should clearly understand the purpose for each exercise and the progression to higher-level activities. Guided home-based vestibular rehabilitation programs will likely become more widely used with enhanced education and increased adherence.

Importance of taking the history

The term “dizziness or dysequilibrium” can mean something different to each person who describes the experience. For the therapist, this description is the first opportunity to begin the differential diagnosis to determine the appropriate impairments to focus on during the evaluation process. The onset or circumstance that created the dizziness can give a clue to the cause. In patients with long-term dizziness, it is important to determine the most recent concern, or the reason that brought the patient in for this evaluation. The intensity of symptoms and what makes them better or worse can guide both the evaluation and intervention. A true spin, or vertigo, indicates an asymmetry of neural activity from the vestibular system that occurred rapidly. This most often represents a lesion below the pons or cerebellum, such as vestibular neuritis, or a disruption of blood flow in the basilar or vertebral artery. Lightheadedness can indicate problems with maintaining postural tension of blood pressure, lesions deeper into the CNS that likely involve somatosensation, peripheral somatosensory loss such as diabetic neuropathy, or the inaccurate somatosensory input after whiplash or concussion. When dizziness is accompanied by dysphagia, dysarthria, diplopia, and dysmetria, this can be a red flag for brain stem lesions or those that may involve the cerebellar or cerebral cortex.

Dizziness can be reported as panic, heart palpitations, tingling in the face or hands, or feeling out of touch with the environment. This may be associated with PPPD or may be the phenomenon of posttraumatic stress. Autonomic nervous system dysregulation can cause dizziness that can be orthostasis, exercise induced, and related to other factors such headache and gastrointestinal symptoms. In these cases, the underlying disorder needs to be diagnosed and managed properly as noted later in the chapter.

The temporal course of the symptoms can assist diagnosis. Slow onset of dizziness especially with progressive imbalance can indicate a mass effect, perhaps an acoustic schwannoma or infratentorial meningioma. Determining the timing of the symptoms when there is a sudden onset can determine the cause. When it is described in seconds, one might think first of benign paroxysmal positional vertigo (BPPV), but when it is hours or days, a migraine or Meniere disease is suspected. A report of continuous dizziness with exacerbations will lead toward a diagnosis of possible fistula, perhaps superior canal dehiscence, mal de debarquement, or other causes of inhibited adaptation. Provocation with head motion gives additional clues to the diagnosis. Motion-provoked symptoms may indicate inadequate adaptation. Head position dizziness can be related to BPPV if symptoms are brief, or central dysfunction if symptoms persist. Maladapted patients can describe constant and vague symptoms. Comorbid complaints of hearing loss, tinnitus, and fullness in the ear are indications of conditions that involve the cochlea. These conditions will be described in detail at the end of this chapter.

Determining the adaptation status through examination that guides intervention

There are many known ways to identify acute vestibular lesions. To determine the level of adaptation using visual cues, look for nystagmus in room light with the patient looking at a stable object. Nystagmus from peripheral vestibular lesions is easily inhibited with visual fixation. Nystagmus caused by central lesions of the brain stem or cerebellum is not inhibited with visual fixation. Blocking visual fixation to look for spontaneous nystagmus is achieved with the use of infrared goggles or Frenzel lenses.

Videonystagmography (VNG) captures eye movements related to vestibular dysfunction using video goggles or electrodes surrounding the orbit (electronystagmography). Oculomotor testing is included in this test to determine the status of saccades and smooth pursuits as well as eye speed and optokinetic response. It is critical to determine the baseline oculomotor functions because, as noted previously, this can be an independent cause of dizziness. Nystagmus patterns are determined to be spontaneous, positional, with head motion, or during the Dix Hallpike positioning. The vestibular component of the VNG is the caloric test, the use of warm and cold air to manipulate the fluid in the horizontal canal to isolate the ear and indicate the relative function on one side compared to the other. Central disorders will produce nystagmus patterns that are different than those related to a peripheral lesion. The caloric portion of this test is reported as a relative percentage of reduced vestibular response in the affected ear.

Vestibular-evoked myogenic potentials (VEMP) is based on the principle that the saccule of the otolith is sensitive to sound and responds in a similar fashion to clicking sounds as it does to tilt. A click produced in the ear stimulates the saccule that in turn inhibits the synchronous discharges of muscles in the SCM on the same side. It is thought that this reflex allowed the head to turn toward the sound of a predator. Abnormal hearing can interfere with the ability to perform the test as will dysfunction in the SCM muscle.

The rate of firing or tone of the SCM is inhibited during the recorded sounds, and this change is captured using surface electromyography (SEMG). Surface electromyography the response in one ear can be compared to the response on the other side in the same person. VEMPs are abnormal when they are very asymmetrical such that one side is more than two times as large as the other, low in amplitude, or absent. An abnormal VEMP can represent an ipsilateral lesion in the saccule, the inferior vestibular nerve, the lateral vestibular nucleus, or the MVST. The inferior component of the vestibular nerve can be preserved in a neuritis, and the VEMP can be normal even with loss of superior innervation of the horizontal canal. Intervention in this case would be determined with enhanced use of head righting and the adaptation of VOR.

Subjective visual vertical (SVV) is used to test the degree of ocular torsion present in unilateral lesions. The SVV is tested in absolute darkness or an environment that prevents visual reference to the vertical. The patient is asked to orient a rod to gravity, and the degree of off-axis tilt represents the torsion of the eye, or skew deviation, which is common in acute unilateral lesions. When looking at skew it is important to realize that the vestibular system skew is a nonparalytic ocular misalignment due to utricle-ocular motor pathway asymmetry. This should not be confused with a paralytic skew that represents a nerve palsy or intranuclear ophthalmoplegia (INO). This can be tested with a Maddox rod, or the Cover-Uncover and Alternate Cover tests can help determine a con-concomitant or nonconcomitant dysfunction. Medullary and medial longitudinal fasciculus lesions need to be ruled out as well when a skew is identified.

Sensation of motion at rest

The tonic firing of the vestibular system, when the head is in a neutral nonmoving state, is symmetrical, at approximately 90 spikes per second recorded in the canal and otolithic systems. When there is disruption of signal from only one side of the vestibular pathway, it will change the relative input into the CNS resulting in a perception of the head rotating even if the head is not actually moving.

To determine the degree to which the patient has adapted using somatosensory cues, ask them to sit still on a stable surface with eyes closed. If there is a sensation of motion, the somatosensory system and vestibular system are still out of synch. If the sensation is that of rotation, it is likely that the CNS has not adapted to the unequal signals caused by vestibular system lesion.

Enhanced input through stable joint surfaces can facilitate the CNS recalibration early in the adaptation process. This appears to be most effective through mechanical pressure through the top of the head or as shown in Fig. 21.8 with the use of weights on the shoulders to increase the vertical reference of the spine in a neutral position with vision occluded. In the very acute patient, this may need to be started in the supine position. This allows the vestibular system to calibrate using somatosensory input as a reference. This activity, known as settling, is a good way to allow the patient to manage symptoms when they have been exacerbated by activity. Using the weight or pressure for several minutes at a time can control symptoms. The use of settling is reduced as the system adapts during movement—the final goal of the intervention. If the use of weights increases the sensation of movement with a report of being lightheaded, the clinician should suspect abnormal central sensory weighting of somatosensory inputs. Slow progressive introduction of weights may be necessary to achieve decreased sensation of movement. Closer examination of the musculoskeletal system may be necessary. Joint position sense and neck torsion smooth pursuits should be examined and treated as well. It is a critical first step in the rehabilitation process to achieve accurate CNS recalibration with the head at rest before initiating intervention that requires movement of the head.

The use of 5-pound weights on each shoulder to increase the somatosensory reference allows the vestibular system to recalibrate to the body reference. Eyes are closed so that the head position is not referenced by vision.

Dynamic visual acuity

DVA can be tested with manual head turns using a Snellen chart, with the patient reading the smallest line that is possible when the head is still, then the therapist passively rotates the head at 2 Hz and the patient attempts to read the same line. When acuity drops more than three lines, the patient will be unable to maintain visual acuity during typical daily activity. Quantified DVA can be recorded as the logarithm of minimal angle of resolution (LogMAR). As seen in Fig. 21.9 this can be tested and quantified by use of equipment such as inVision (NeuroCom Int.). Gaze stability also can be quantified using the same equipment, but the measure is one of function, reporting the head speed that can be obtained while maintaining gaze stability. This is a good way to clarify the amount of deceleration that is necessary for the patient to maintain proper vision.

Quantified Dynamic Visual Acuity Is Possible With Systems Such as in Vision.

(Courtesy NeuroCom International, Clackamas, OR.)

In the clinical examination, the VOR is reported as abnormal only if there is loss of gaze stability that leads to blurring of target object with head movement at 2 Hz to 3 Hz.

If the vestibular ocular reflex is not functioning efficiently and it does not drive the eyes to the correct position for a stable gaze, the result is known as vestibular driven oscillopsia, causing visual targets to appear to move as the head moves. This disorder has significant functional implications: the individual will try to limit the head motions that cause gaze instability, walk with increased base of support to enhance somatosensation, and increase the use of hand holds or use wall walking (touching the wall to stay upright while walking). Gait speeds slow while trunk and head remain locked in relation to each other during turns. This can often be observed during the initial evaluation.

VOR adaptation requires movement of images on the retina, or retinal slip. Therefore intervention begins with head movement at the speed that allows stable vision. ^, Adaptation of the VOR is accomplished by having the patient move the head while trying to maintain gaze stabilization, keeping a stationary object in clear focus. As the system adapts, the speed of head movement increases, with the goal of achieving head movement at 2 Hz without the object blurring. Initially, the patient can focus on the thumb or a business card held at arm’s length. The activity is progressed to a higher level of difficulty by adding background visual stimulus such as a television set or a visually complex environment. Gaze stabilization with head turns while standing on an uneven surface or while walking creates a higher-level challenge. Many patients have avoided head movement, so simply turning the head may initially trigger dizziness. As stated previously, dizziness with head motion should not be confused with abnormal VOR; in VOR dysfunction, the visual image blurs as the head moves.

Visual dependency

Patients may experience discomfort when their eyes are closed or may find it impossible to walk down an incline in a visually challenging environment without the need to hold on to a railing. Patients with visual dependency often report excessive fatigue after activity because of the strain of using vision for postural stability. When these patients are in situations with excessive visual stimulation, reports of dizziness increase. The subtle eye movements associated with viewing a computer monitor cause more fatigue for the individual with vestibular disorder when they display visual dependency. These individuals also often avoid crowds as in a mall, grocery store, or airport. Attending religious services, which are often characterized by low lighting, visual stimulation, and the need to stand with eyes closed or read a hymnal while singing, can create challenges to the vestibular system and can reduce an individual’s participation.

Destabilization can occur when the peripheral visual references appear to move as a component of physiological diplopia. When the eyes are tracking something moving in the central gaze field, the background or peripheral visual field will appear to move in the opposite direction. During diagonal smooth pursuit tracking, for example, the patient with visual dependence will orient the head and trunk to the perceived movement in the room creating postural adjustment patterns as if the room is tilting. The patient is pulled off balance when they align themselves with the apparent visual motion. This can also be tested when a patient is standing on a compliant surface or on a single leg, tracking a target moving in a figure of eight. Head and trunk sway match the apparent visual field movement instead of actual gravity vertical in the patient who is visually dependent. This test can be used in a clinical battery to determine degree of visual dependence to compensate for missing the gravity reference. Patients can be taught to perform this and other activities at home to increase the use of the vestibular system function as seen in Fig. 21.10 . Tossing a ball in the air and following it with the eyes while standing on a compliant surface, or while walking, will allow for balance without visual fixation as seen in Fig. 21.11 .

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

Contemporary issues and theories of motor control, motor learning, and neuroplasticity Medical and developmental challenges of infants in neonatal intensive care: Management and follow-up considerations Neuromuscular diseases Brain tumors Aging, dementia, and disorders of cognition Electrophysiological testing and electrical stimulation in neurological rehabilitation

Stay updated, free articles. Join our Telegram channel

Join