Dizziness and Vertigo

Matthew S. Siket

Jonathan A. Edlow

THE CLINICAL CHALLENGE

Dizziness poses a conundrum for patients and health care providers. First, it is a common and nonspecific symptom accounting for over 4.3 million emergency department (ED) visits annually in the United States.¹ Although the vast majority of patients with dizziness are experiencing a benign process, approximately 15% of patients have a dangerous and potentially life-threatening underlying cause. Differentiating the dangerous from benign causes can be challenging, especially because more than half of all patients in the ED report having experienced the subjective sensation of dizziness within the preceding week.²

The term “dizziness” means different things to different people. Classic teaching used the diagnostic paradigm that separates dizziness into “lightheadedness” or “vertigo” or “disequilibrium.” The value of this approach has been challenged and is currently being reassessed: In one study, patients were presented with a series of options to describe the “type” of dizziness experienced, and then reasked the same question with the same choices, but in a different sequence 6 minutes later. Concordance was less than 50%.³ In the real world, not all patients with vestibular dysfunction report vertigo, and not all patients with cardiovascular dysfunction report lightheadedness. Relying on symptom description to guide the differential considerations is a setup for diagnostic error.

As an alternative, patients are much more consistent in reporting the timing and triggers of their symptoms. As part of a history and review of systems, providers should elucidate the context of the symptoms to individualize the differential diagnosis.

Did the symptoms begin abruptly?
Has the dizziness been persistent or episodic?
Were there any precipitating triggers to provoke the dizziness?
Were there associated symptoms such as focal neurologic deficits, palpitations, shortness of breath, ear pain, or tinnitus?

These are all reasonable questions to ask to gain a better understanding of precisely what the patient experienced and hone in on the underlying cause.

We recommend using the ATTEST mnemonic as a helpful way to systematically approach the chief complaint of dizziness and avoid misdiagnosis.⁴^,⁵ ATTEST stands for Associated symptoms, Timing, Triggers, Examination Signs, and Testing (Figure 10.1, Table 10.1). This approach focuses on key components of the history and examination to distinguish four different vestibular syndromes:

Acute spontaneous vestibular syndrome (A_SVS)
Acute triggered vestibular syndrome (A_TVS)
Episodic spontaneous vestibular syndrome (E_SVS)
Episodic triggered vestibular syndrome (E_TVS)

Figure 10.1: Diagnostic approach to the acutely dizzy patient. AVS, acute vestibular syndrome; BPPV, benign paroxysmal positional vertigo; CPPV, central paroxysmal positional vertigo; s-EVS spontaneous episodic vestibular syndrome; t-EVS, triggered episodic vestibular syndrome; TIA, transient ischemic attack.

TABLE 10.1 The ATTEST Mnemonic

Associated symptoms

Timing

Triggers

Exam

Signs

Testing

Each of these distinct vestibular syndromes is discussed in greater detail later in this chapter in Approach/The Focused Examination section.

ANATOMY AND PATHOPHYSIOLOGY

The sensation of dizziness typically occurs either after a loss of postural tone causing decreased cerebral perfusion, or dysfunction of the vestibular system. Having a basic knowledge of vestibular neurologic physiology provides a foundation on which a general diagnostic framework can be built.

The peripheral vestibular system includes the labyrinths and hair cells of each inner ear (Figures 10.2 and 10.3). Each labyrinth is composed of the cochlea (which controls hearing), the anterior, lateral, and posterior semicircular canals (SCCs) (which sense rotational motion), and the utricle and saccule (which sense linear motion). These structures are connected to one another and filled with endolymph fluid. Hair cells within the utricle and saccule sense movement of endolymph and displace the cupula, which triggers an electrical impulse via the vestibular nerve to the brainstem, causing the sensation of motion. The three paired SCCs, and each utricle and saccule collectively comprise each individual’s vestibular apparatus, which is subject to dysregulation through a number of mechanisms (otolithic, inflammatory, infectious, traumatic, etc.). Vestibular apparatus dysfunction is typically unilateral, such as in vestibular neuritis, labyrinthitis, benign paroxysmal positional vertigo (BPPV), Meniere disease, and perilymphatic fistulas, each presented in more detail in Table 10.2.

Figure 10.2: The anatomy of the inner ear. The eighth cranial nerve includes the cochlear nerve and the superior and inferior vestibular nerves, and it traverses the internal auditory canal with the facial nerve and labyrinthine artery. The semicircular canals, utricle, and saccule are innervated by the vestibular nerves, whereas the cochlea is supplied by the cochlear nerve. Courtesy of Dr. Jonathan A. Edlow and © Marie Rossettie, CMI.

The central vestibular system originates in the vestibular nuclei of the pons and upper medulla, which receive afferent input from the vestibular apparatus via the vestibular nerves (Figure 10.4). They relay connections to the cerebellum, oculomotor system, cerebral cortex, and spinal cord, orchestrating balance via intricate control of trunk and oppositional muscles, eye movements, and position sense. Both ablative (such as stroke) and irritative (such as migraine) phenomena can produce symptoms of central dizziness and vertigo, as outlined in Table 10.3.

Figure 10.3: Vascular anatomy of the inner ear. The anterior inferior cerebellar artery (AICA) branches from the basilar artery and feeds the labyrinthine artery, which supplies the cochlea and vestibular apparatus. Courtesy of Dr. Jonathan A. Edlow and © Marie Rossettie, CMI.

TABLE 10.2 Partial List of Peripheral Vestibular Disorders

Condition	Mechanism	Classic Presentation
BPPV	Canalolithiasis caused by otolithic debris within the SCCs (85% posterior)	Brief, but intense, episodes of dizziness and vertigo triggered by head turning associated with nausea and vomiting. Upward torsional nystagmus during episodes is pathognomonic
Vestibular neuritis	Unilateral vestibular hypofunction, usually from an inflammatory process of the vestibular nerve afferent signals	Acute-onset and sustained dizziness and vertigo without a trigger. May be postinfectious and is associated with horizontal and unidirectional nystagmus with the fast phase beating toward the unaffected ear
Labyrinthitis	Similar to vestibular neuritis, but affecting the cochlear nerve afferents as well	Similar to, but less common than, vestibular neuritis with associated hearing loss
Meniere disease	Overproduction or under-resorption of endolymph in the cochlea causing hydrops	Spontaneous episodic dizziness and vertigo, with a sensation of aural fullness as well as hearing loss and tinnitus
Perilymphatic fistula	Leakage of perilymphatic fluid into the middle ear, usually following a trauma	Subacute dizziness and vertigo with hearing loss or sensitivity, and aural fullness typically following head or barotrauma
BBPV, benign paroxysmal positional vertigo; SCC, semicircular canal.
Data from Jahn K. Vertigo and dizziness in children. Handb Clin Neurol. 2016;137:353-363. doi: 10.1016/B978-0-444-63437-5.00025-X

Figure 10.4: Vestibular anatomy and physiology. Hair cells in the utricle (A) sense linear motion such as gravitational force (B). The semicircular canals, specifically the cupola in the ampulla (C), sense rotational acceleration, such as being on a merry-go-round (D). Courtesy of Dr. Jonathan A. Edlow and © Marie Rossettie, CMI.

TABLE 10.3 Partial List of Central Vestibular Disorders

Condition	Mechanism	Classic Presentation
Posterior circulation ischemia	Focal cerebral hypoperfusion from an occlusion (from an embolus or from atherosclerosis) or dissection along the vertebrobasilar circulation	Spontaneous and abrupt-onset dizziness, usually with additional focal neurologic deficits. May be transient (transient ischemic attack)
Vestibular migraine	Excitation along the trigeminovascular pathway	Episodic with or without an associated aura and/or headache

Posterior circulation stroke predominantly affects the cerebellum and brainstem and, although it is an infrequent cause of dizziness, it is among the most commonly misdiagnosed stroke syndromes.³ Most will have measurable neurologic deficits, but of all patients with posterior stroke, approximately 10% had isolated dizziness on presentation. Among strokes affecting the cerebellum, dizziness was reported in 73% of cases.⁶ Occlusion of the anterior inferior cerebellar artery (AICA) mimics labyrinthitis and causes vestibular dysfunction and hearing loss, whereas posterior inferior cerebellar artery (PICA) infarction resembles vestibular neuritis. Differentiating dangerous central lesions from benign peripheral causes is diagnostically challenging, but critically important because missed cerebellar strokes portend a high risk of long-term morbidity and mortality (˜40%).

Special consideration should be given to toxic exposures and to acute and chronic medication, drug, or alcohol effects. Dizziness is a common symptom of carbon monoxide toxicity, which can also cause hearing loss due to damage to the cochlea, vestibular nerve, and central auditory pathways. Alcohol intoxication may alter endolymph density, causing dizziness and gait instability, whereas vestibular toxicity can be caused by chronic alcohol abuse, antiepileptic drugs, aminoglycoside antibiotics, and some chemotherapeutic agents.

PREHOSPITAL CONCERNS

Reliably differentiating benign from dangerous causes of dizziness and vertigo can be difficult from the field. Individuals experiencing debilitating dizziness seeking medical care should not attempt to drive themselves. Prehospital providers should do their best to determine the likelihood of posterior circulation stroke by knowing the warning signs and symptoms, following local emergency medical service (EMS) protocols, using validated stroke recognition/severity grading tools, and adhering to destination determination protocols. A finger-stick glucose test is easy to perform and generally indicated, and if stroke is suspected, obtaining a confirmed time last known well (LKW) is very important in screening eligibility for stroke reperfusion therapies. If able, an electrocardiogram (ECG) is often useful to screen for cardiac dysrhythmias in addition to a full set of vital signs. If the patient is ambulatory, an assessment of gait stability is very helpful as well.

APPROACH/THE FOCUSED EXAMINATION

Use ATTEST to help guide the history of present illness and review of systems and resist the urge to anchor your patient into either a “lightheadedness” or “vertigo” track. Spend a few moments reviewing associated symptoms to get a better sense as to whether the cause appears to be neurovestibular or cardiac in etiology or from an underlying medical cause. Commonly relevant associated symptoms are listed in Table 10.4.

Interpret historic data in conjunction with the patient’s vital signs to determine whether a general medical cause should be pursued. Note that some patients with an underlying medical cause of their dizziness (such as hypotension) may have a central neurologic process as well, or have a stroke mimicking a general illness, so it is best to still perform a targeted neurologic examination in these patients. Next, determine the timing of symptoms and any precipitating triggers to differentiate A_SVS, A_TVS, E_SVS, and E_TVS, further described in Table 10.5.

TABLE 10.4 Partial List of Associated Symptoms Relevant in Dizziness

Infectious	Fever, chills, dysuria, cough, sinus congestion
Gastrointestinal	Abdominal pain, black or bloody stools, profuse diarrhea, heavy nonsteroidal anti-inflammatory use
Traumatic	Head or neck injury, whiplash, recent cervical manipulation
Reproductive	Lower abdominal pain, vaginal bleeding, positive pregnancy test
Medication related	New antihypertensive or other medication with dizziness as a side effect, potentially ototoxic medication use
Cardiovascular	Chest pain, palpitations, shortness of breath, dyspnea on exertion, orthopnea, syncope
Aortic	Chest/back/abdominal/flank pain, discrepant pulses, known aortic aneurysm
Neurologic	Visual loss, diplopia, ataxia, unilateral weakness, speech disturbance, loss of coordination, seizure

Acute Spontaneous Vestibular Syndrome

A_SVS should be considered in patients with abrupt-onset and persistent dizziness without a precipitating trigger that remains present during the time of evaluation. Some patients may have difficulty assessing whether symptoms have abated, because they may still feel nauseous or generally unwell. The key is to ascertain whether the patient is still experiencing the full extent of their dizziness at the time of the evaluation. If so, the patient should be presumed to have A_SVS and the ensuing physical examination should be targeted to differentiate central from peripheral causes. Nystagmus is one of the best tests to help discern central from peripheral causes and is an appropriate first test in the physical examination. We recommend testing for nystagmus first because it is easy for the patient, and if it is absent, it makes vestibular neuritis and labyrinthitis very unlikely diagnoses (it is almost always present in the first 2-3 days), and, furthermore, it informs using the Head Impulse Test (HIT), which has only been validated in patients with acute vestibular syndrome (AVS) with nystagmus.

Patients with peripheral A_SVS from vestibular neuritis or labyrinthitis should have a characteristic horizontal and unidirectional nystagmus. Nystagmus has a slow phase (when the eyes slowly move toward the side of the pathology) and a fast phase (when the eyes quickly jerk back). This is noted on neutral gaze (with patient staring straight ahead) and becomes more pronounced when the eyes look in the direction of the fast phase. When looking to the opposite side, unidirectional nystagmus should become less pronounced or extinguish altogether. Alternatively, if the fast phase of the nystagmus changes and begins beating in the other direction (eg, beats to the right when looking to the right and to the left when looking to the left), then that is bidirectional or direction-changing nystagmus and is concerning for a central cause, such as stroke.

To perform this test, simply have the patient open their eyes and look forward. Wearing Frenzel goggles will magnify the patient’s eyes and overcome fixation (which can suppress nystagmus) through an illuminating light. However, these are seldom available in the ED, and are not necessary to detect the presence and type of nystagmus, which is usually easy to see. The direction of the fast phase of nystagmus points toward the unaffected ear in peripheral A_SVS. Approximately 50% of cerebellar strokes do not cause nystagmus, so if no nystagmus is seen in a patient who otherwise seems to have an ASVS, stroke is still a possible diagnosis. Patients with vertical, pendular, torsional, or direction-changing nystagmus have a central cause.

Nystagmus testing is one of the three components of the HINTS examination, which is a battery of three tests including the Head Impulse Test, Nystagmus, and Test of Skew. The HINTS examination was shown to outperform early diffusion-weighted magnetic resonance imaging (MRI), which is widely regarded as the gold standard for stroke diagnosis.⁷ It should be noted that the HINTS examination was developed and validated by neuro-otologists, and performed only on patients with A_SVS with nystagmus, which is present in only half of patients with cerebellar stroke.⁸ Although it is believed that emergency clinicians can accurately perform and interpret this examination, widespread adoption in EDs is low.⁹ Furthermore, a recent meta-analysis found that HINTS, as performed by emergency physicians, lacked adequate diagnostic sensitivity.¹⁰ HINTS
should be performed in conjunction with a more complete neurologic examination including a targeted assessment of the posterior circulation (cranial nerves, assessment for dysmetria, dysdiadochokinesia, and gait).

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