Abstract
So common is vertigo that diverse healthcare professionals, from audiologists to orthopedic surgeons, will eventually encounter it in their patients, if not in themselves. So treatable are vestibular disorders that it is an immense advantage to know how to assess the vestibular system. This review summarizes the history and physical examination that will help diagnose common vestibular disorders presenting with vertigo.
© 2019 S. Karger AG, Basel
The History: What to Ask
Is there a hallucination of movement? Vertigo is a false sense of movement [1] that might be spinning, rocking, swaying or bouncing, caused by disorders affecting the vestibular end-organs, their peripheral or central connections. Some vestibular disorders can present with lightheadedness or “brain fog,” but these symptoms could also arise from orthostatic hypotension, anemia, hypoglycemia, thyroid disease, B12 deficiency, anxiety or depression and merit a broader search. If it is vertigo, is this the first presentation? A first attack of acute spontaneous vertigo, lasting about 24 h or longer, merits careful consideration of the common causes of “acute vestibular syndrome” (vestibular neuritis and stroke) whereas recurrent vertigo is more likely to represent an innocuous cause. Episodes of recurrent vertigo increasing in frequency and severity (crescendo vertigo) also merit careful consideration of transient ischemic attacks. Is the vertigo spontaneous or triggered? Can it happen when sitting perfectly still, in the absence of a trigger or is it only brought on by a change in head position: bending down, arching back to instill eye drops or turning over in bed? Spontaneous vertigo occurs at rest and will, of course, worsen with head movement. Positional vertigo that is absent at rest and triggered by head movement is likely to represent benign positional vertigo (BPV). Other vertigo triggers such as a strong perfume or a compelling visual stimulus might point to vestibular migraine (VM), while symptoms brought on by entering a supermarket or crowded public place may represent psychophysiological vertigo. How long does each episode last? Brief spells of vertigo lasting seconds to minutes may represent BPV, VM or vestibular paroxysmia whereas vertigo lasting hours could be VM or Ménière’s disease (MD) [2, 3]. Continuous vertigo lasting days may be encountered in VM, vestibular neuritis or stroke [2–5]. Is there hearing loss, tinnitus or aural fullness? Aural symptoms that are time locked with episodic spontaneous vertigo are commonly encountered in MD [3]. When aural symptoms accompany acute vestibular syndrome, labyrinthine ischemia must be considered [6]. Is there a current, past or a family history of migraine headaches or aura or even motion sensitivity? Some patients may have difficulty recognizing that their “ordinary headaches” which are moderate to severe, sometimes unilateral, throbbing and associated with nausea, photophobia or phonophobia, could represent migraines. Are there non-vestibular neurological symptoms? Speech disturbances, limb weakness, clumsiness and symptoms referable to the remaining cranial nerves could indicate central vertigo. Once a careful history is taken, if the diagnosis is not already apparent, it will at least be narrowed down to one of the following syndromes: episodic positional vertigo, episodic spontaneous vertigo or acute vestibular syndrome (Table 1).
The Examination: What to Look For
The history will lead you to the most important aspect of the neuro-otological examination. Recurrent positional vertigo needs a careful search for benign paroxysmal positional nystagmus, while in a patient with acute vestibular syndrome, it is a priority to prove or disprove vestibular neuritis.
General Inspection
First check if the patient has a head tilt, which is ipsilesional to a peripheral vestibular loss [4, 7]. Is there a Horner’s syndrome, which could be indicative of a lesion affecting the descending sympathetic pathways such as a brainstem infarction (Fig. 1a)? Vertical misalignment of the eyes in the absence of an extraocular muscle palsy (skew deviation) can occur in peripheral and central vestibular loss, but is thought to occur more commonly in the latter. Ocular tilt reaction (OTR) refers to the triad of skew deviation, head tilt (toward the hypotropic eye), and ocular counter-roll (Fig. 1b). These 3 findings are attributed to a unilateral lesion of the “graviceptive pathways” arising from the utricle [7]. A vestibular or lower brainstem lesion causes an ipsiversive OTR whereas an upper brainstem lesion causes a contraversive OTR. To check for skew deviation, alternate cover test should be performed; when each eye is covered in turn, a corrective vertical saccade occurs in the uncovered eye, bringing the hypotropic (down) eye upwards or the hypertropic (up) eye downwards. Otoscopy is performed to evaluate the tympanic membrane directly and rule out active ear disease (infection or cholesteatoma) as a cause of vertigo.
Oculomotor Examination: Spontaneous and Gaze-Evoked Nystagmus
With the patient sitting up, look for spontaneous nystagmus in the primary position, leftward and rightward gaze (15 degrees to either side). In a brightly lit room, spontaneous nystagmus may not be visible until visual fixation is removed. Use optical frenzels, video frenzels or a pair of inexpensive take-away Frenzels [8] to remove fixation. To record the absence of spontaneous nystagmus without removing visual fixation is as meaningful as commenting on the state of the tympanic membranes without an otoscope. Typical peripheral nystagmus is seen in vestibular neuritis, the paretic phase of Ménière’s disease or after an acute surgical resection of the vestibular nerve and is horizontal torsional, beating away from the lesion. It enhances when visual fixation is removed (Fig. 2; online suppl. Video 1; for all online suppl. material, see www.karger.com/doi/10.1159/000490267) and when looking in the direction of the fast-phase of the nystagmus (“Alexander’s Law”) and is unidirectional (i.e., beating in the same direction in the primary position, leftward and rightward gaze; Fig. 3; online suppl. Video 2). Central vestibular disorders could present with spontaneous vertical, torsional or horizontal nystagmus. Cerebellar nystagmus, unlike peripheral nystagmus is bidirectional (i.e., left beating on left gaze and right beating on right gaze; Fig. 3; online suppl. Video 3). It is vexing that many central causes of vertigo, including stroke, can present with “typical peripheral nystagmus” because they could affect the vestibular nucleus or nerve root entry zone [5].
Table 1. Common vertigo syndromes, their differential diagnoses, findings on history and examination that could help their separation