Adult vestibular dysfunction following head injury: diagnosis and management

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. ^,

Table 14.1

Common peripheral and central disorders, symptom duration, and association with auditory features (i.e., hearing loss, tinnitus).

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.

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