Vestibular Disorders: Pearls and Pitfalls

Woo Young Choi, MD, PhD, FRCPC; Daniel R. Gold, DO


Semin Neurol. 2019;39(6):761-774. 

In This Article

Taking the History

Background and Definitions

Common vestibular disorders such as benign paroxysmal positional vertigo (BPPV) and vestibular neuritis are frequently misdiagnosed,[1,2] and their management tends to be variable and nonevidence based.[3,4] Correctly diagnosing peripheral vestibular disorders is important because they are common and evidence-based treatments improve outcomes.[5–8] Also, correctly diagnosing central vestibular disorders, such as strokes and transient ischemic attacks (TIAs), are of paramount importance because posterior circulation strokes commonly present with acute dizziness or vertigo, and the consequences of missing a posterior fossa stroke can be devastating.[9,10]

Patients with vestibular conditions typically present with symptoms of vertigo, dizziness, oscillopsia, or unsteadiness. Although the terms and descriptors used by patients are often vague, imprecise and even misleading,[11] international consensus on the definitions of the symptom types have been published and are described below.[12,13]

Vertigo is defined as a sensation of self-motion or of motion of the external environment when none is occurring, or a distorted sensation of self or external motion during an otherwise normal head movement. Vertigo generally, but not always, indicates a vestibular imbalance caused by processes affecting the semicircular canal (SCC) afferents in the labyrinth, the eighth cranial nerve (CN), or vestibular connections through the brainstem or cerebellum prior to reaching the ocular motor nuclei. Vertigo can be divided into spinning or nonspinning (the latter comprising swaying, tilting, bobbing, bouncing, or sliding),[12,14,15] and these types may help to distinguish whether symptoms originate in the SCC (anterior, horizontal, and posterior canals) or otolithic (utricle and saccule) pathways, respectively. However, it is important to understand that patients with orthostatic hypotension, cardiac arrhythmias, or other non-vestibular conditions may also experience vertigo.[16] While a patient's description of their symptoms is of some importance, the description alone lacks specific diagnostic value in most cases.

Dizziness is the sensation of disturbed or impaired spatial orientation without a false or distorted sense of motion.[12,14,15] Dizziness may be experienced in vestibular or nonvestibular conditions. Oscillopsia is a specific term defined as a false (visual) sense of environmental motion. For simplicity, it can be further divided into "sitting" or "walking" oscillopsia. In "sitting" oscillopsia, the visual world moves independent of head movement–for example, the visual symptoms accompanying nystagmus or saccadic intrusions/oscillations. In "walking" oscillopsia, the visual world moves during head movements–for example, oscillopsia while walking that occurs with bilateral vestibular loss (most common) or when vestibular function is preserved but suppression of the vestibular–ocular reflex is impaired (less common). As oscillopsia is a visual sensation, it should abate with the eyes closed. However, closing the eyes will not eliminate vestibular symptoms such as dizziness or vertigo. In some cases, oscillopsia and other vestibular symptoms may both be present; for example, in acute vestibular neuritis, closing the eyes will eliminate the symptom of oscillopsia associated with nystagmus, but the feeling of vertigo will persist. Simply put, oscillopsia is a visual sensation (absent with eyes closed), while vertigo is a balance sensation (still present with eyes closed). Other definitions to be aware of include unsteadiness, which is the feeling of instability while seated, standing, or walking, without a directional preference;[12,15] presyncope, which is the sensation of impending loss of consciousness; and syncope, which is a transient loss of consciousness related to global cerebral hypoperfusion.

Pitfalls: Traditional Approach to Dizziness

In the traditional approach to dizziness, the most important distinguishing feature was the symptom type. Symptoms were classified according to vertigo (the illusion of spinning or other false motion), presyncope (a feeling of impending faint), disequilibrium (unsteadiness when walking), or nonspecific dizziness (other balance-related sensation not fitting the prior three categories, such as lightheadedness, wooziness, and giddiness).[17] The advantage of this approach is that it can quickly narrow the differential diagnosis and guide diagnostic testing, with vertigo suggesting vestibular causes, presyncope implying cardiovascular causes, unsteadiness prompting a search for neurologic causes, and nonspecific dizziness inferring psychiatric or metabolic causes. This symptom-type approach has been often frequently endorsed, and frontline physicians consider the type of dizziness to be very important.[18] However, several studies show that the type of vestibular symptom is not reliably reported by patients and does not validly discriminate among different causes of dizziness.[11,19] A symptom-type approach by itself can easily lead a clinician to pursue the wrong diagnosis with inappropriate diagnostic testing and should be avoided.

Recently, a novel evidence-based approach to taking the vestibular history has been proposed, which emphasizes timing and triggers rather than the patient's qualitative description of the symptom.[14,20]

Pearls: Triage-TiTrATE-test Method

Historical elements that should be emphasized when evaluating a patient with vestibular symptoms include the distinction between new or recurrent attacks, symptom onset, triggers, associated symptoms, and duration of spells.[14,20] The triage-TiTrATE (timing, triggers, and targeted examinations)-test method offers a convenient mnemonic to organize this approach.[14]

Triage (Triage-TiTrATE-test). This step is intended to quickly identify the most dangerous and nonvestibular conditions through history (e.g., chest pain, shortness of breath, symptoms typical of panic attacks, new medications, or recent dose adjustments); vital signs (e.g., hypertensive emergency, hypotension, and bradycardia); and basic, targeted ancillary testing (e.g., EKG, blood glucose level, and anticonvulsant serum levels).[21] Of note, medication side effects are common causes of constant dizziness or vertigo and can be associated with specific ocular motor abnormalities.[22] For example, anticonvulsant toxicity can cause vestibular symptoms and gaze-evoked nystagmus, and lithium can cause downbeat nystagmus.

Timing (Triage-TiTrATE-test). The following factors are critically important to correctly diagnose a vestibular condition: (1) how did the symptoms begin (i.e., did they evolve over seconds, minutes, hours, days, or more)?; (2) is this an acute and prolonged first event (monophasic), or are the symptoms episodic (with discrete attacks) or chronic (constant for weeks-months)?; and (3) what is the duration of symptoms (especially important for episodic conditions)?

Triggers (Triage-TiTrATE-test). Correctly identifying the triggers of vestibular symptoms can significantly narrow the differential diagnosis. Positional triggers are very common, where symptoms come on immediately after a head movement (e.g., BPPV). In other cases, the symptoms may be time-locked to a head movement (e.g., unilateral or bilateral vestibulo–ocular reflex [VOR] deficit). Notably, vestibular migraine (VM) patients often possess symptoms that are time-locked to head movements (sometimes referred to as head motion intolerance), although the VOR is normal. Symptoms can be visually induced by a complex or busy visual environment in VM, persistent postural perceptual dizziness, and other vestibular conditions that lead to overreliance on visual inputs with resultant "visual vertigo."[23] Triggers can be sound induced (Tullio's phenomenon),[24] for example, in superior canal dehiscence syndrome (SCDS).[25] The Valsalva maneuver may induce symptoms and signs (nystagmus) with a cervicomedullary lesion (e.g., Arnold–Chiari) or in SCDS.[26] An important and common postural cause of dizziness is orthostatic hypotension, which can be historically differentiated from BPPV by the presence of symptoms following rolling over in bed or going from seated to lying in bed in the latter condition. In many cases, there is no discernible trigger, which can also be diagnostically meaningful (e.g., TIA).

Targeted Examination (Triage-TiTrATE-test). The proper examination should be designed to test hypotheses raised by the history. For example, the HINTS exam (head impulse, nystagmus, and test of skew) should be performed in the setting of an acute vestibular syndrome (see below), while the Dix–Hallpike (DH) maneuver is performed when BPPV is suspected.

Test (Triage-TiTrATE-test). Depending on the history and tailored exam, the most appropriate diagnostic testing is ordered Box 1.