Office Examination of the Vestibular Patient

2 Office Examination of the Vestibular Patient


Jameson K. Mattingly, Laura Wazen, and Stephen P. Cass


images Introduction


The vestibular physical exam begins with a thorough history, as careful characterization of the patient’s symptoms with knowledge of the various disease entities allows formulation of a differential diagnosis. The physical examination should be thorough and directed at confirming or refuting the potential etiologies of the “dizziness” complaint. Although it is tempting to jump to additional studies, such as imaging and vestibular testing, a significant amount of information can be gleaned from the office examination. The examination should include neurologic (including gait and balance), otologic, and neurotologic examinations, or aspects of each driven by the history. In many instances, a thorough physical exam can help avoid further testing that can be both expensive and uncomfortable to the patient.


images Physical Examination


Functional balance relies upon the interaction of vestibular, visual, and proprioceptive systems, and abnormalities in any one of these can result in the sensation of dizziness, imbalance, or vertigo. A thorough physical examination, then, should include testing of these three elements, by including general otolaryngologic, neurologic, otologic, and neurotologic examinations. Specific attention should be paid to evaluating the oculomotor system in the neurologic examination, as vestibular abnormalities can alter the eye movements in a characteristic way that may provide clues to either central or peripheral etiologies.


The physical examination should begin immediately upon initial interaction with the patient. The examiner should pay close attention to the patient’s gait, use of any assistive devices (e.g., walker or cane) or glasses, and any signs of central neurologic disorders, such as a previous stroke or brain injury.1 Regarding assistive devices, proper use should not be overlooked, and can be assessed by asking the patient to use the device with both walking and turning. If the use appears impaired, the patient may have never been instructed in how to use the device, or they may have a delayed response reaction to prevent falling. Additionally, vital signs should be reviewed, with particular attention to orthostatic blood pressures. A decrease of greater than 20 mm Hg in systolic blood pressure after transitioning from a supine or seated position to standing is consistent with orthostatic hypotension.1


images Neurologic Examination


The neurologic examination of the dizzy patient includes all of the categories of the standard neurologic examination: evaluation of mental status, cranial nerves, motor and sensory systems, coordination and other cerebellar testing, Romberg testing, and assessment of gait.2 The cranial nerve examination should include a thorough evaluation of oculomotor function, including saccades and pursuit, and a search for nystagmus with the eyes open in the light as well as gaze-evoked nystagmus. While examination of eye movements is critical, assessment of all cranial nerves, and motor and sensory function of the extremities, should also be performed. The latter point is critical in evaluating for neuropathy, which can be the etiology of, or contribute to, vestibular symptoms. Neurologic findings, such as ataxia, dysarthria, visual disturbance, and extremity weakness, point toward a central cause of vestibular symptoms.


Romberg testing evaluates the patient’s use of visual, vestibular, and proprioceptive cues to maintain balance. The test should be performed with the feet as close together as possible, and with the hands across the chest. Interpretation of the Romberg test allows the clinician to evaluate the patient’s ability to use the previously mentioned cues to maintain balance. With eyes open (Romberg condition 1), the patient has all three sources of inputs. When the patient performs the test with eyes closed (Romberg condition 2), visual inputs are removed, thus leaving vestibular and somatosensory inputs to maintain balance. Patients who can maintain balance in condition 1, but fall in condition 2, are visually dependent to maintain balance, and thus would be at risk for falls if walking in darkened environments. With eyes open on a foam pad (Romberg condition 3), the patient can use visual and vestibular cues, while somatosensory cues are altered. Patients who fall in this condition are somatosensory dependent, and would be at risk for falls if walking on a compliant or uneven surface, such as grass, sand, gravel, or even very plush carpet. If the patient has sensory deficits, such as peripheral neuropathy, they may not be able to utilize the remaining sensation they have in their feet on surfaces that do not provide hard, stable somatosensory cues. With eyes closed on a foam pad (Romberg condition 4), the use of visual cues has been removed and somatosensory cues have been altered by the cushion, thus leaving vestibular inputs as the remaining set of balance information (Video 2.1). Therefore, falls in this condition suggest a vestibular issue, either peripheral or central.


Gait assessment is a crucial component of evaluating the vestibular patient, and it should encompass multiple key points, including evaluation of the base of support, path sway, ambulation with head turns, and overall assessment of gait quality. Base of support (BOS) is the distance between the two feet when standing or walking, and they should be ~ 4 inches apart.3 The examiner should notice if the patient’s BOS is normal, narrowed, or widened. A narrow BOS can create more instability and risk of falls for the vestibular patient. A widened BOS is commonly seen with patients suffering from bilateral vestibular loss, as it is a compensation used to create more stability.


Assessing path sway determines if the patient is walking straight or veering to one or both sides. Normally, a patient should be able to walk a straight line, staying within a 12-inch path. If sway is present, the direction should be noted, as a patient with unilateral vestibular loss can drift when walking, either pulling toward the strong side or drifting toward the weak side. Ambulation with head turns can help determine if a patient can maintain a steady and straight path when walking and turning the head to the side, looking up and down, and if they are able to maintain their walking pace during the head turn. Patients with vestibular problems may drift in the direction they are looking. Due to dizziness that head motion causes, a patient may avoid turning their head entirely and alternatively look only with their eyes. For example, the patient may turn without first using their head to look in the new direction to prevent head motion-induced symptoms (en bloc). Notice if the head turns cause increased sway, staggering, loss of balance, slowing of gait speed, veering, or dizziness, or if symptoms occur only with head turns in a certain direction. For example, in patients with benign paroxysmal positional vertigo (BPPV), dizziness or imbalance is elicited when the patient tips the head back.


Gait quality should also be assessed; the examiner assesses if the patient has normal step lengths, signs of foot scuffing or decreased heel strike, and the patient’s posture. Foot scuffing may increase the patient’s risk of tripping and falling, and those with peripheral neuropathy may be unaware it is occurring. Scuffing of the feet may be an attempt to increase proprioceptive cues in the absence of appropriate vestibular or visual inputs.


Patients with vestibular disorders often report difficulty with activities associated with postural control. These patients may complain of difficulty maintaining balance when changing positions, such as going from supine to sitting, or sitting to standing. Postural control can be assessed by standardized tests of static stability, such as the Romberg or single-leg stance tests. It can also be assessed by observing dynamic functional activities that require postural control, such as how the person goes from sitting to standing or their ability to walk unsupported. Testing static postural control is often a measure that is utilized in the office evaluation because it is quick, reproducible from one visit to the next, and quantifiable. The measure is usually a reflection of the patient’s ability to maintain a set posture over time without increased sway or loss of balance, and results have been standardized by age group, with most clinicians utilizing 30 seconds as the minimal duration guideline for a normal test during Romberg testing and a minimum of 5 seconds as a normal duration for single-leg stance trials.4,5 During dynamic postural control evaluation, care must be taken to rule out other contributing factors that could affect performance, such as orthopedic issues (e.g., joint pain, muscle weakness, limited flexibility) or neurologic issues (e.g., Parkinson’s disease or neuropathy).


Oculomotor Examination


The oculomotor system should be examined to detect the presence of characteristic eye movement abnormalities suggestive of either central or peripheral vestibular system dysfunction. This is a pivotal portion of the neurologic examination, as ocular findings can help localize the lesion. The bedside eye movement examination should include an assessment of the presence of any nystagmus, alignment and range of movement of the eyes, involuntary saccades, vergence, and pursuit eye movements.2


The presence of nystagmus should be carefully evaluated. The most common nystagmus seen in vestibular abnormalities is jerk nystagmus. Jerk nystagmus has a slow component due to vestibular input signals and a fast component that resets the eye back to the center of the orbit. Although the direction of the slow component is more clinically useful, nystagmus is described in the direction of the fast component due to a greater ease of visualization by the examiner. Characteristics of spontaneous nystagmus of peripheral vestibular origin include the presence of nystagmus with the head still, decreased nystagmus with visual fixation, and increased when fixation is absent, such as with infrared video or Frenzel goggles (Video 2.2).6 Certain characteristics of the nystagmus should also be noted, such as the timing and speed of the components, as these findings can point toward specific diagnoses.


Misalignment of the visual axes, such as with strabismus, may produce complaints similar to those of a vestibular disorder. Misalignment of the visual axis is not an abnormality of the vestibular system per se, but can certainly result in double or blurred vision, or vertiginous sensations that can mimic the presentation of a vestibular disorder. The examiner should begin with a general inspection of the patient’s eyes while both eyes are open and the patient is viewing a single target; the examiner should look for misalignment of the visual axes. Any obvious misalignment of the eyes or any visual disturbances through the full range of eye movements should be noted. More subtle ocular misalignments may be detected using the cover test.2 To perform the cover test, ask the patient to fixate on a distant target, cover one of the patient’s eyes, and look for movement of the uncovered eye. If no movement is detected, remove the cover and place it on the other eye, looking for movement of the uncovered eye. If movement is noted in one eye after covering the other eye, an ocular misalignment is present. Eye movements that occur only after uncovering indicate the presence of an ocular misalignment that is present only when one eye is viewing. The finding may also indicate a restriction or weakness of an extraocular muscle, although it can point to lesions of the vestibular system. However, those with long-standing misalignment may have compensated well and report minimal diplopia.


The finding of vertical misalignment not attributed to ocular muscle palsy suggests the presence of a skew deviation.2 Skew deviation has been reported mostly commonly in association with brainstem or cerebellar lesions, and also can be due to imbalances along peripheral or central pathways that mediate otolith-ocular reflexes.7 Generalized limitation of range of movement may be a sign of a systemic issue, such as myasthenia gravis. Limitation of voluntary vertical gaze may indicate abnormality of the midbrain, including neurodegenerative disorders, such as progressive supranuclear palsy, mass lesions, infarction, hemorrhage, hydrocephalus, or encephalitis.2


Eye movements in an opposite, but coordinated, fashion characterize vergence. These movements are important with movement of a target closer to the viewer (convergence) or further from the viewer (divergence), and are typically slow and smooth. Abnormal oscillation of the eyes during vergence, called convergence spasm, suggests a functional disorder, and should not be confused with bilateral sixth nerve palsy. Nystagmus that is present in primary gaze may change during vergence. For example, congenital nystagmus is typically dampened by convergence, and central vestibular nystagmus may be exaggerated or change direction during convergence.2


Saccades represent rapid changes in eye position from one target to another. Asking the patient to fixate alternately between two stationary targets with the head held still can test these movements. One target, such as the examiner’s nose, should be placed so that the patient can fixate upon it with the eye in primary position, with a second target, such as a finger, positioned to produce an approximate 15° saccade. The examiner should assess the velocity, accuracy, and initiation time of the saccades.8 Slowing of the saccades suggests brainstem dysfunction, such as internuclear ophthalmoplegia, and inaccurate or dysmetric saccades point to cerebellar lesions. Abnormalities in saccadic initiation may be seen in patients with Parkinson’s disease and Huntington’s disease. Extraneous or corrective saccades may be noted during fixation or pursuit. Smooth pursuit is used to track slow objects and relies on the visual cortex. Smooth pursuit can decline with age, sedation, inattention, and changes in visual acuity.1 Square-wave jerks are saccades away from and back to the fixation. Square-wave jerks are seen commonly in older individuals, and may be considered a nonspecific finding. In younger individuals, square-wave jerks are considered abnormal and are most often seen with anxiety or with abnormalities of the cerebellum or brainstem. Ocular flutter and opsoclonus are rapid saccadic to-and-fro movements of the eye without a normal intersaccadic interval in the horizontal plane and multidirectional movement, respectively.2,6 The causes of ocular flutter and opsoclonus include structural lesions of the pons or cerebellum, viral encephalitis, paraneoplastic syndromes, or toxic agents or medications. (Video 2.3, Video 2.4, Video 2.5, Video 2.6, Video 2.7, and Video 2.8)


Otologic Examination


It is valuable to begin with a complete head and neck examination, and then to focus on the otologic portion of the exam. The ear should be examined, preferably using magnification. All obstructing debris should be removed so that complete visualization of the tympanic membrane is possible. The normal landmarks of the tympanic membrane should be identified and attention paid to the status of the middle ear and ossicular chain. If normal landmarks are obscured, infection, middle ear effusion, perforation, or cholesteatoma should be ruled out. The pneumatic otoscope should be used to confirm normal tympanic membrane mobility and to elicit signs or symptoms of vestibular sensitivity to pressure. Pressure-induced eye symptoms, such as nystagmus, may point toward a perilymph fistula or superior semicircular canal dehiscence.


Determining the status of the patient’s hearing can help elicit a peripheral vestibular disorder, as peripheral etiologies are frequently associated with hearing loss and tinnitus. Although not as sophisticated as formal audiometric testing, finger rub or tuning fork examinations can help diagnose a hearing loss, with the latter having the ability to differentiate between conductive and sensorineural losses. The finger rub test is approximately the same as a 30-dB stimulus at 4000 Hz.2 Commonly performed tuning fork exams include the Weber and Rinne tests. The Weber test is performed by placing the tuning fork on the vertex of the head while asking the patient if they hear it midline (normal response) or laterally (pathologic response). The Rinne test is performed by placing the tuning fork over the mastoid, then comparing this to the loudness of the vibrating tines near the external auditory canal. A normal response, or Rinne positive, is air conduction louder than bone conduction, while an abnormal response, or Rinne negative, is bone conduction louder than air conduction. Rinne negative is usually indicative of a conductive hearing loss. For example, a Weber test that lateralizes to an ear that also has a Rinne negative (bone conduction greater than air conduction) may be indicative of a conductive hearing loss. Conductive hearing loss might be associated with otosclerosis, superior semicircular canal dehiscence, cholesteatoma, or fluid within the middle ear space.2 The tuning fork tests can also detect a unilateral sensorineural loss, if, for example, the Rinne test demonstrates air conduction greater than bone conduction bilaterally, but the Weber test lateralizes to the good ear. It is not unusual for vestibular schwannomas or other processes that affect the inner ear to cause sensorineural hearing loss in addition to vestibular symptoms.


The tuning fork can also help point to superior semicircular canal dehiscence. A 128-Hz tuning fork placed on the ankle that is heard by the patient indicates a third-window phenomenon, as in superior semicircular canal dehiscence. This finding may also be associated with additional auditory symptoms (e.g., ear fullness, autophony, or pulsatile tinnitus) in superior semicircular canal dehiscence.9 Despite this, the reliability of the tuning fork is limited, and any abnormal response should be confirmed and further elaborated on by using comprehensive audiometry.


Neurotologic Examination


The neurotologic examination includes several tests that are particularly useful when evaluating patients with dizziness. Tests considered to be essential for a full examination include search for spontaneous nystagmus with eyes open in the dark, post-head-shaking nystagmus, bedside vestibulo-ocular reflex (VOR) tests, including the head thrust/impulse test and dynamic visual acuity, Dix-Hallpike test, and Romberg testing with eyes closed on a foam pad.2 These physical examination tools should be used on all patients presenting with vestibular issues. Many of these tests are facilitated by use of infrared video goggles or Frenzel glasses (Video 2.2). Frenzel glasses enable a reduction of visual fixation while allowing the examiner to view the patient’s illuminated and magnified eyes, while infrared video goggles allow examination of the eyes while they are open in the dark. In this way, vestibular nystagmus not present during visual fixation may be seen. Nystagmus that increases in intensity or that is seen only when the eyes are open in the dark point toward a peripheral etiology.2


A search for spontaneous vestibular nystagmus can be performed with the head upright, and positional nystagmus can be assessed in the supine and head right and left lateral positions. The Dix-Hallpike maneuver is used to elicit BPPV and should be performed on all patients presenting with vestibular issues, even if the symptoms appear to be nonpositional. This test is performed by rotating the patient’s head 30° to 45° to the testing side followed by a rapid placement into a supine position (Fig. 2.1).


The characteristic nystagmus with BPPV has a short latency followed by an upbeat and torsional nystagmus that generally lasts less than 1 minute. A search for post-head-shaking nystagmus (rapid horizontal head movements for 30 seconds followed by an abrupt stop) can also be performed and can help detect unilateral vestibular weakness. Despite its usefulness in detecting asymmetric central function, this test is not reliable for central vestibular abnormalities.2 Nystagmus can also be induced with vibratory stimuli to the skull and neck. Vibration stimulates the labyrinths bilaterally, with the asymmetry in those with unilateral vestibular damage resulting in nystagmus with the slow phase directed toward the side of the lesion.10 Vibratory stimulation is a reliable and easily administered bedside test for asymmetric peripheral vestibular damage.


Apr 3, 2018 | Posted by in OTOLARYNGOLOGY | Comments Off on Office Examination of the Vestibular Patient

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