Introduction
A patient’s sense of “balance” is a complex, dynamic phenomenon that integrates information from the visual, peripheral vestibular, and somatosensory systems. The vestibular system is comprised of both peripheral sensory organs and central structures within the brainstem, cerebellum, and cerebrum. Chiefly, the peripheral portion consists of the semicircular canal system and otolith organs of the ear. These peripheral components of the vestibular system continuously collect and relay information about motion and position to the central vestibular system. The circuitry of the central vestibular system then integrates these sensory data into the sense of balance and sensory–motor control. Appropriate function is crucial to maintaining the compensatory movements involved with postural control and gaze stabilization in the face of both internally produced and external forces. Damage to either the peripheral and/or central vestibular symptoms can produce debilitating symptoms. Such signs and symptoms may include objective nystagmus, unsteady gait, subjective vertigo, disorientation, postural instability, and imbalance. Given the possibility and symptomatic overlap of both peripheral and central vestibular dysfunction, proper screening and evaluation following identification of vestibular impairments are crucial both to diagnose the causative agent and to tailor intervention. ,
Approximately 35% of Americans aged 40 or older have experienced some form of vestibular dysfunction. This figure rises rapidly with age, with 85% of Americans age 80 or older having evidence of vestibular dysfunction. Among individuals who have suffered a traumatic brain injury, nearly half will experience some form of vestibular dysfunction. Other subpopulations that report high incidences of vestibular dysfunction after head injury include individuals with diabetes mellitus and military veterans. , Patients’ postural instability, imbalance, and gaze instability can have a significant and deleterious impact on quality of life and balance confidence, underscoring the need for proper management.
Diagnosis
As introduced previously, “normal” vestibular function arises from the interplay between the peripheral organs of the inner ear’s vestibular organs, associated nerves, and signal relay centers within the central nervous system. Since damage at any of these constituent components may result in dysfunction, diagnosis of vestibular dysfunction begins by acknowledging that symptoms may manifest from a wide variety of conditions and processes that primarily affect the inner ear and regions of the central nervous system. As such, there is a diverse array of recognized vestibular disorders (i.e., more than 25). These disorders may be discerned via features that can be identified through a patient’s history, physical exam, and diagnostic testing. Analysis of history and the results from physical exams can establish whether further diagnostic testing is required.
Generally, vestibular disorders can be classified as either peripheral or central. The most frequent peripheral vestibular disorders include paroxysmal positional vertigo (BPPV), vestibular neuritis, labyrinthitis, and Ménière’s disease. Common causes of central vestibular dysfunction are more varied and can include demyelinating diseases that affect the vestibular tracts, cerebellum, and brainstem, acute or hemorrhagic ischemic stroke of the vestibular nerve tracts, cerebellum, or brainstem, vertebrobasilar transient ischemic events, and brain injury of the cerebellum and brainstem. Head trauma can result in either peripheral or central dysfunction, thus heightening the importance of correct and precise assessment. Before objective testing is deployed, patient history and a physical exam can begin to narrow the origins of vestibular dysfunction.
History
Clinicians can begin assessing subjective patient symptoms of imbalance through a directed history. Validated survey instruments, such as the Dizziness Handicap Inventory (DHI) and the Veritgo Symptom Scale (VSS), can also assist in itemizing and quantifying vestibular symptoms and their impact. , Scores from these assessments and discussion of patient symptoms, such as gait instability and nausea, can indicate the severity of the patient’s vestibular dysfunction and impact on quality a life. ,
The duration of symptomatic episodes with or without auditory features can be helpful in identifying the type and localization of the physiologic insult ( Table 14.1 ). Acute peripheral vestibular dysfunction is often defined by constant or multiply recurrent and rapid symptom episodes, whereas chronic vestibular dysfunction manifests with less severe or infrequent episodes owing to a process of central compensation in the brain. For example, short bursts of vertigo that last less than a couple of minutes, usually induced by the adoption of certain positions such as lying down, can be suggestive of benign paroxysmal positional vertigo (BPPV). Head trauma is a common catalyst for such brief events such as BPPV or perilymphatic fistula. Longer-duration events that may span hours that occur frequently may indicate Ménière’s disease. In addition, the presence of vertigo alongside “central signs” such as diplopia, weakness, and dysarthria can suggest central nervous system conditions such as multiple sclerosis or acute ischemic stroke. ,
| Disorder | Symptom episode duration | Auditory symptoms | Incidence (per 100,000) | Etiology |
|---|---|---|---|---|
| Benign paroxysmal positional vertigo | Seconds | No | 107 | Peripheral |
| Perilymphatic fistula | Seconds | Yes | 1.5 | Peripheral |
| Vascular ischemia: transient ischemic attack | Seconds to hours | Typically no | 29–61 | Central or peripheral |
| Ménière’s disease | Minutes to hours | Yes | 3.5–513 | Peripheral |
| Syphilis | Hours | Yes | 2.3–16.9 | Peripheral |
| Vertiginous migraine | Hoursddays | Yes | 11,900 | Peripheral |
| Labyrinthine concussion | Days | Yes | Unknown | Peripheral |
| Labyrinthitis | Days | Yes | 3.5 | Peripheral |
| Vascular ischemia: stroke | Days | Typically no | 37 | Central or peripheral |
| Vestibular neuronitis | Days | No | 3.5 | Peripheral |
| Anxiety disorder | Variable | Typically no | 24,900 | Unspecified |
| Acoustic neuroma | Months | Yes | 0.3–1 | Peripheral |
| Cerebellar degeneration | Months | No | 20 | Central |
| Cerebellar tumor | Months | No | 14.1 | Central |
| Multiple sclerosis | Months | No | 309.2 | Central |
| Vestibular ototoxicity | Months | Yes | Unknown | Peripheral |
The patient’s medical history can also aid in a diagnosis. Vascular risk factors including hypertension, diabetes mellitus, and smoking can increase the probability of stroke. Cardiovascular symptoms such as chest pain/angina, sweating, and palpitations may occur in tandem with dysfunction of the vestibuloautonomic pathway; failure to recognize the interplay of these systems can lead to an incorrect diagnosis. Medications including aminoglycosides and chemotherapeutic treatments can result in vestibular toxicity and symptoms of sustained peripheral vestibular dysfunction. Additionally, a history of using seizure medications may result in the patient experiencing symptoms, such as ataxia, which are commonly attributed to pathology of the cerebellum.
Physical examination
In addition to patient history and discussion of symptoms, physical examination can provide complementary insight. The clinician should perform a complete otologic examination, which includes bed side tests such as a tuning fork exam (i.e., Rinne and Weber), the Dix-Hallpike maneuver to assess for positional vertigo and the HINTS examination (horizontal head impulse testing [ H ead I mpulse]; direction-changing nystagmus in eccentric gaze [ N ystagmus]; and vertical skew [ T est of S kew]) to gain the information required for a proper diagnosis. The rationale for these tests and investigations is elaborated in the following.
Due to the proximity between auditory and vestibular systems, hearing loss, either conductive or sensorineural, can coincide with certain vestibular disorders. The clinician can employ the Rinne and Weber tests to quickly screen if either sensorineural or conductive hearing deficits are present. A formal audiogram should follow.
For the Weber test, the clinician oscillates a 512-Hz tuning fork. The oscillating fork is placed on top of the patient’s head in the midline, usually at the forehead, and the patient is asked about the location of the sound. In a patient with normal hearing, the sound is heard in the center of the head or is interpreted as being heard equally in both ears. If the patient has a sensorineural hearing loss, then the perceived sound should lateralize to the normal ear. In the presence of conductive hearing loss, the sound should lateralize to the affected ear.
For the Rinne test, the clinician can further examine whether conductive hearing loss is present. The examiner oscillates a 512-Hz tuning fork, and the patient indicates when the sound is no longer heard. The tuning fork is then repositioned to be adjacent to the auricula, and the patient is again asked if now audible. In a normal test, air conduction (the second tuning fork position) is louder than bone conduction (the first fork position on the mastoid). With conductive loss present, the reverse will be true. Typically, bone conduction is less effective than air conduction. As a result, the patient should hear a louder sound when the fork is placed on the mastoid when a conductive hearing deficit afflicts him or her. Conversely, a patient with sensorineural deficits should have both air and bone conduction loss. The identification of unilateral sensorineural hearing loss helps to define the vestibular dysfunction as possessing a peripheral etiology. For instance, Ménière’s disease manifests with at least a low- to medium-frequency hearing loss and fluctuating aural symptoms such as tinnitus, and sensorineural hearing loss induced by trauma may be associated with a perilymphatic fistula.
In addition to using hearing to identify etiology, assessment of the visual and oculomotor function is prudent.
Bedside vestibular examination
A key component of the bedside vestibular evaluation is the assessment of the vestibuloocular reflex (VOR). Assessing the VOR at the bedside involves observing for the presence of pathologic nystagmus—involuntary “jerky” movements of the eyes—in response to a directed examination that involves specific tasks and patient positioning. as the characteristics of the nystagmus are also important as specific features can suggest a peripheral or central lesion. While a full review of nystagmus and its correlates is beyond the scope of this chapter, peripheral nystagmus is characterized by a horizontal vector, unidirectional, fatiguability, and suppresses with fixation. In contrast, central vestibular dysfunction may manifest as a vertical vector nystagmus, direction changing, and does not suppress with fixation
In the remainder of this section, we review several common bedside examinations that can be helpful in screening for peripheral or central vestibular dysfunction.
Positioning maneuvers
Positioning maneuvers such as the Dix-Hallpike maneuver (DHM) should be deployed to assess for benign paroxysmal positional vertigo—one of the most common causes of peripheral vertigo after a traumatic brain injury. The DHM begins with the patient sitting upright on an exam table with legs stretched out and head facing 45 degrees toward the ear that is being tested. After the clinician leans the patient back into a supine position, the clinician observes the patient’s eyes for the presence of nystagmus. If BPPV is present and affecting the posterior canal, the most common site for BPPV, the clinician may observe torsional and upbeat nystagmus. , The clinician waits for the nystagmus to extinguish prior to testing the opposite ear. Alternatively, the clinician may elect to proceed with the Epley maneuver. The Dix-Hallpike test has an estimated sensitivity of 79% and a specificity of 75%. Testing of each ear enables localization of the disorder.
Head impulse test
The head impulse test (HIT) allows the clinician to gain insight into the patient’s angular vestibuloocular reflex (aVOR) function. The clinician begins the HIT examination by having a sitting patient focus on a target object at midline. As the patient maintains their gaze, the clinician rotates the head approximately 10–15 degrees on the horizontal plane relative to the original position and then returns to the original position via an unpredictable and quick motion. As the clinician performs this maneuver, he or she maintains observation of the patient’s eyes. Typically, the eyes of the patient will track the observed target while the patient’s head is in motion; a positive, abnormal response involves the patient’s eyes “slipping” off of the target following the head thrust, followed by a rapid correction of the eyes back to the target—a response known as a “catch-up” saccade. For detecting vestibular hypofunction, the test has greater sensitivity than specificity. These values are estimated at 82%–100% and 34%–39%, respectively. The test’s sensitivity increases to 71%–84% by modifying the angle of rotation to go to 30 degrees. The use of the HIT at the bedside can aid in screening for a peripheral vestibular dysfunction. In contrast, patients with central lesions tend to have negative results (i.e., no “catch-up” saccade), except for central disorders that also involve the inner ear or eighth cranial nerve pathways. One consideration before performing the HIT test is to consider the possibility of neck trauma. A history of neck trauma may be a contraindication to the HIT test.
Skew deviation
Examination for skew deviation can evaluate for the possibility of a central vestibular lesion. Skew deviation refers to the degree of relative vertical misalignment of the visual axes. The clinician can assess for skew via the alternate cover test while the patient is fixating on a visual target. The patient is instructed to fixate on a stationary target while the examiner covers one of the patient’s eyes. Then, the examiner quickly moves their hand to cover the patient’s other eye. During this process, the examiner is observing the uncovered eye for a corrective movement. ,
Head-shaking nystagmus
The head shake test can be useful for screening for a unilateral vestibular lesion. The examiner beings by tilting the patient’s head 30 degrees downward and oscillates the head for 20–30 revolutions at a gentle velocity of 1–2 Hz. At the end of the oscillation, the examiner observes for the presence or absence of nystagmus. In patients with symmetrical vestibular loss, the test should not elicit nystagmus. Conversely, patients with a unilateral lesion, such as with unilateral vestibular neuritis, typically have nystagmus—usually, the fast phase of the nystagmus is directed away from the lesioned ear. The test has a sensitivity of 46% and a specificity of 75%; in patients with vestibular neuritis, between 85% and 100% display head-shaking nystagmus. The rare presence of pure vertical nystagmus may indicate central etiology, most likely arising from a lateral medullary lesion. ,
Dynamic visual acuity
Vestibular dysfunction may be present in a patient who has degradation in visual acuity with active head movements. The corresponding test, dynamic visual acuity (DVA), involves assessing for changes in acuity before and during oscillatory head movements. The clinician begins by establishing a baseline of visual acuity by having the patient read from a Snellen chart. The examiner clasps the patients head and begins oscillating at a gentle frequency of 1–2 Hz while the patient attempts to read the visual acuity chart. A significant decline in visual acuity suggests a peripheral vestibular loss.
The Romberg
The sharpened, or tandem, Romberg test is a practical test for global balance function. Balance function is dependent on the sensory inputs via vision, somatosensory, and the peripheral vestibular system. Isolation of the peripheral vestibular system can be realized by selectively removing the influence of the visual and somatosensory sensory inputs. The Romberg simulates this isolation by placing an emphasis on the vestibular system. To achieve this result, the patient closes his or her eyes, puts their feet in a tandem arrangement, and crosses their arms. If the patient consistently falls or sways to one side, then there is an indication of a balance dysfunction that may be related to a vestibular deficit.
Objective vestibular testing
In some cases, additional objective vestibular function training may provide additional data to support a diagnosis. A modern battery of studies includes electronystagmography (ENG), videonystagmography (VNG), and rotary chair testing. The increased objectivity of the laboratory testing can enable more impartial and sensitive information, from which patient etiology can be diagnosed.
ENG (or more appropriately VNG in today’s modern vestibular laboratories) comprises noninvasive techniques that assess the vestibular function. During ENG, the patient wears small electrodes placed at various locations along the skin. These electrical sensors monitor eye movement by measuring the corneoretinal potential—a DC potential naturally present between the cornea and the retina. More recently, the development of VNG can conduct the same battery of tests without the use of skin surface electrodes. VNG systems include a pair of goggles with infrared cameras that track and record eye movements during testing.
The modern vestibular test battery consists of several assessments: oculomotor and optokinetic testing, positional testing, caloric testing, and rotational studies.
Oculomotor involves examining the eyes’ ability to track a target as it moves between various locations. Typically, a red light is employed as the target. Optokinetic testing is a variant of target tracking but involves tracking a moving range, typically a field of alternating and contrasting stripes. Abnormalities in oculomotor or optokinetic function may indicate a neurological problem, potentially in the central nervous system or the pathway between the peripheral vestibular system and the brain.
The positional tests assess the presence or absence of nystagmus within different head positions and changes in head position. The patient is instructed to maintain a steady gaze while moving their head and body, such as in the DHM. While the patient is guided through these positions, the electrodes in an ENG or cameras in a VNG goggle measure the velocity, frequency, amplitude, and latency of any nystagmus present.
Caloric testing examines the horizontal semicircular canal of each ear, independently, in addition to offering information on the responsiveness of these pathways and the relative functionality between the left and right. The efficacy of caloric testing arises from how a density change brought about by a temperature differential in the endolymph of the lateral semicircular canal induces nystagmus. Caloric testing can isolate peripheral vestibular dysfunction. ,
Complementing the test battery of ENG/VNG, rotary chair testing can assist in assessing for a bilateral vestibular disorder. Rotary chair testing protocols typically employ a chair capable of rotation in a dark room coupled with VNG goggles to track eye movement. The head is held steady by a security head strap, and a seatbelt secures the body. Lab-specific protocols can vary, but in general three tests are performed including varying the velocity and acceleration of the patient, optokinetic tests, and fixation tests. Using regiments with different chair velocities and acceleration, information regarding the presence or absence of unilateral or bilateral vestibular loss is observed. The optokinetic and fixation tests are helpful in assessing for the presence of central vestibular dysfunction.
Imaging
In some cases where a central process is suspected or needs to be ruled out, magnetic resonance imaging (MRI) of the brain is useful for the identification of central nervous system tumors or masses, cerebrovascular accidents (i.e., stroke), and other soft tissue abnormalities that may account for a patient’s presentation. , Computed tomography (CT) scans provide excellent detail on the bony anatomy of the temporal bone. Abnormalities such as temporal bone fractures can be readily assessed.
Treatment
Treatments for vestibular dysfunction following traumatic brain injury depend on, in part, on the identification of a specific vestibular disorder. As such, the treatment of vestibular dysfunction should address the identified conditions in the given patient.
Most treatment plans should utilize medication for symptomatic management. Medications that mitigate the vegetative symptoms of vestibular dysfunction include antiemetics to reduce nausea, and vestibular suppressants (e.g., benzodiazepines) to minimize the debilitating effects of acute vertiginous events. One potential concern with the sustained use of vestibular suppressants, however, is that their overuse may prolong the period of vestibular compensation.
BPPV is among the most common vestibular disorders after traumatic brain injury. In response, canalith repositioning maneuvers such as the Epley maneuver in the case of posterior canalithiasis are helpful. BPPV arises from the presence of broken calcium carbonate crystals (otoconia) from the utricle in the endolymph of the semicircular canals. Changes in head position can produce the movement of the otoconia in the canals, which leads to vertiginous symptoms. The Epley maneuver aims to resolve BPPV by ushering the otoconia out of the posterior canal and into the vestibule. In the case of BPPV of the right posterior canal, the Epley maneuver begins with the patient rotating their head 45 degrees to the right while sitting upright on the end table. After at least 30 s, the clinician reclines the patient back over the end of the table just lower than the horizontal. After another period of at least 30 s, the patient’s head is to be rotated 90 degrees to the left. After the duration of this position for at least 30 s, the patient adopts a left lateral position with the head facing 135 degrees from supine. Last, the patient should return to a sitting position. Throughout these maneuvers, the examiner observes for the presence or absence of nystagmus. The Epley maneuver can be repeated if necessary. The stated directions should be reversed if BPPV is present in the left ear. The Epley maneuver has a significant probability of success if BPPV is present. Other treatment variants for BPPV include Brandt-Daroff exercise, foster maneuver, half-somersault, and Semont maneuver.
Trauma to the cochlea or vestibular system may be a precipitating factor for Ménière’s disease. Although a full discussion on the treatment for Ménière’s disease is beyond the scope of this chapter, the treatment algorithm typically employs escalating symptom management in response to the frequency and severity of a patient’s symptoms. For example, the prescription of motion sickness and antiemetic medications can help alleviate acute vertiginous symptoms during discrete episodes. Lifestyle changes, such as reducing salt intake to less than two or 3 grams per day, may also help with the frequency and severity of attacks. Patients with Ménière’s disease may also benefit from vestibular rehabilitation for persistent disequilibrium. In addition, audiologist referral for services, including hearing aid fitting, should be done to reduce or eliminate hearing loss and tinnitus.
More invasive surgical options may become necessary for some patients with vestibular hypofunction and unrelenting vestibular symptoms. Broadly speaking, surgical options for peripheral vestibular disorders are classified as either being ablative (i.e., destructive) or nonablative. Such surgical procedures for severe or unrelenting peripheral vestibular symptoms include endolymphatic sac decompression, labyrinthectomy, and vestibular nerve sectioning.
In addition to medication and surgery, many patients suffering from vestibular dysfunction after a traumatic brain injury will benefit from vestibular rehabilitation therapy (VRT) due to the presumed effects on neuroplasticity of brain regions involved with balance (i.e., so-called “central compensation”). Even in extreme cases of compete unilateral vestibular loss, central adaptation can and does occur with the input of intact visual and proprioceptive pathways. Through VRT exercises, the vestibular system compensates for deficits by sensory reweighting. While this compensation occurs progressively in patients not enrolled in a VRT program, VRT may expedite and assist recovery. The primary goals of VRT are to reduce the primary and secondary impairments found in a patient’s diagnosis, such as vertigo, dizziness, gaze instability, and imbalance. Individuals with peripheral vestibular dysfunction are more likely to make a more significant recovery than those with central vestibular dysfunction due to the role of pathological involvement in limiting compensation in the latter.
Patient utilization of VRT depends on a problem-oriented approach with a specialty-trained vestibular physical therapist. A comprehensive initial assessment comprising balance, gait, visual stability, and positional assessments helps determine patients’ vestibular dysfunction functional deficits. In response to this assessment, the therapist prescribes habituation, gaze stabilization, and balance training exercises in an outpatient setting. Habituation exercises focus on reducing vertiginous symptoms brought about by rapid head or body position changes. Gaze stabilization exercises target proper coordination of eye movements to ensure stable vision throughout dynamic head and bodily motion. Balance training exercises work to reduce the patient’s risk of falling and balance confidence. Additionally, VRT should be contextualized in a wider rehabilitation program focused on addressing and reducing the other neurological sequelae that can be present after a traumatic brain injury. ,
Future research
Further work is needed to understand the pathophysiology and optimal treatment programs for patients suffering from vestibular dysfunction after a traumatic brain injury. Other important questions pertain to how vestibular dysfunction presents in diverse patient populations. For example, recent military conflicts have heightened the need to investigate the relationship between traumatic brain injury and vestibular dysfunction. Another line of investigation with limited literature is that of the impact of age on vestibular dysfunction. Among geriatric patient populations, work involving the topic of presbyvertigo—akin to the hearing loss that is attributable to age (presbycusis)—has yet to see significant investigation.
A secondary and important domain for future research involves developing efficacious diagnostic and treatments. Several studies have attempted to use autonomous algorithms, such as machine learning, to process the vast amounts of vestibular laboratory data for accurate diagnostic prediction. Still, more work is needed to improve the sensitivity and specificity of these algorithms. , For treatments, the literature offers a limited perspective on the effectiveness beyond different forms of vestibular rehabilitation therapy, especially in context of significant head trauma. More research is needed to standardize and best target rehabilitation exercises for this specific patient populations.
Conclusion
Vestibular dysfunction after traumatic brain injury is common and requires a comprehensive diagnostic and management approach. Accurate clinical knowledge of specific end-organ sources of vestibular dysfunction is important for proper workup and management. Perhaps most importantly, the diagnostic and treatment journey typically involves collaboration among several specialists including otolaryngology, audiology, neurology, and physical therapy.
References
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