The approach to the patient with dizziness and/or vertigo requires a careful history. Vertigo, which is the illusion of movement, is highly suggestive of a peripheral vestibular disorder. After a thorough history, the physician should be able to narrow the suspected condition to a peripheral vestibular disorder, central vestibular disorder, or nonvestibular cause. Common peripheral vestibular diseases include benign positional paroxysmal vertigo, vestibular neuronitis, labyrinthitis, superior canal dehiscence and Ménière’s disease. Common central vestibular disorders include vestibular migraine, and posterior circulation (vertebrobasilar) ischemia. Nonvestibular dizziness could be due to medications, cardiac diseases, or psychogenic causes. The physical examination should include otoscopy and cranial nerve testing as well as selected cerebellar testing. Audiometry and videonystagmography are important tests, while MRI and CT may also provide helpful information. Common medications used to treat vertigo include antihistamines and benzodiazepines. Vestibular rehabilitation therapy can be useful in many peripheral and central vestibular disorders.

The approach to the dizzy patient requires a very careful history and physical examination.¹ The goal of the history is to narrow the diagnosis into one of 3 categories – peripheral vertigo, central vertigo, or a likely nonvestibular cause. As the term “dizziness” and/or “vertigo” may denote different symptoms to each patient, it is often helpful to have the patient describe their symptoms without using these terms. Vertigo is the illusion of movement, which may apply to either the patient or his/her surroundings. It is highly suggestive of a peripheral vestibular cause. Symptoms of dizziness, lightheadedness, and imbalance are much less nonspecific and may or may not be due to a peripheral vestibular cause. Many physicians group these latter terms under the heading “disequilibrium.”

Many times, the single most useful localizing symptom in evaluating a patient with vertigo is a unilateral otologic complaint. Aural fullness, aural pressure, tinnitus, hearing loss, or auditory distortion usually indicates a peripheral lesion. The onset and duration of the episodes are also important to elicit, as these help point to the diagnosis. Vertigo with neurological symptoms such as headache, diplopia, slurred speech, or extremity weakness is highly likely to point to a central vestibular cause. Other general medical conditions may present with a complaint of dizziness but in fact represent metabolic or cardiovascular disturbances. Syncope, which is defined as fainting or passing out is likely reflex related (vasovagal syncope) or due to cerebrovascular diseases or cardiac disease.

It is also important to note the effect of the dizziness and vertigo symptoms on the patient’s quality of life. Those who operate complex equipment or work at heights have a much greater need to have a well-functioning balance system. The Dizziness Handicap Inventory is a useful tool to document the impact of dizziness/vertigo and the degree that it impairs the patient’s daily activities.²

Factors that precipitate or mitigate the vertigo are also important to elicit. Vertigo induced by head movements such as rolling over in bed is typical of benign paroxysmal positional vertigo. This should be distinguished from vertigo that occurs when going from a lying position to a sitting or standing position, which is typical of orthostatic hypotension. Recurring episodic vertigo with otologic symptoms of fluctuating tinnitus and hearing loss suggest a recurring labyrinthine dysfunction or Ménière’s disease. An isolated episode of intense vertigo with or without hearing loss represents labyrinthitis or vestibular neuronitis, respectively. Also, a headache history is important to obtain, as up to 30–50% of patients with migraine have vertigo.^3,4

The physical examination is important but may in fact be normal if the patient is currently between vertigo spells. Cranial nerve testing, otoscopy, and cerebellar testing should be performed as well as assessment for spontaneous nystagmus and Dix–Hallpike test. Audiometric testing, videonystagmography, and magnetic resonance imaging have a role in selected patients.

Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of peripheral vertigo,⁵ and is characterized by short attacks of vertigo lasting several seconds associated with changes in head position. Patients typically describe vertigo when rolling in bed or when looking up or down. It is the result of stimulation of the posterior semicircular canal ampulla by calcium carbonate crystals, known as otoconia. Causes include trauma or labyrinthitis, or it can occur spontaneously. The Dix–Hallpike test is used to confirm the diagnosis. In this test, the physician is to the side of the patient. The patient’s head is turned toward the examiner with the head tilted gently back. The patient is then reclined and the eyes are examined for rotatory nystagmus. Both sides are tested. If the Dix–Hallpike test is positive, the patient is treated with particle repositioning maneuvers, the most common of which are called Epley maneuvers. The Epley maneuver is similar to the Dix–Hallpike test but slightly modified. For right BPPV, the physician would turn the patient’s head to the right with the neck slightly extended, then lay the patient back. The rotatory nystagmus would then be seen and would likely dissipate after 3–5 seconds. The physician then turns the patient’s head all the way to the left, again waits for 3–5 seconds, then has the patient roll on their side to the left, again for 3–5 seconds. Then the patient is allowed to sit up. Several treatments can be performed, and if successful, the patient would generally have a significant reduction in their nystagmus when the Dix–Hallpike test is repeated. The maneuvers are generally effective; however, recurrences can occur in approximately 1/3 of patients.⁶ In such cases, another series of repeat Epley maneuvers are indicated.

Acute vestibular neuronitis is characterized by the acute onset of vertigo usually accompanied by nausea and vomiting. It is the second most common cause of peripheral vertigo.⁵ The presenting symptoms are often severe enough to cause patients to visit the emergency room for fear of a possible stroke. Patients with acute vestibular neuronitis lack associated otological symptoms such as acute hearing loss or tinnitus as well as other neurological symptoms. The cause is believed to be due to reactivation of herpes simplex virus in the vestibular ganglion.⁷ If the patient is seen initially soon after onset, the physical examination would show spontaneous horizontal torsional nystagmus that beats away from the side of the lesion and the patient would usually fall toward the side of the lesion. Head impulse testing is usually abnormal, indicating a peripheral vestibular lesion.⁸

Recovery occurs over several days, with vertigo improving but imbalance may occur for weeks or even months. Vestibular sedatives such as meclizine, diazepam, or zofran (ondansetron) have a limited role mainly in decreasing acute vestibular symptoms. Long-term use of these medications may delay or prolong recovery. Vestibular rehabilitation therapy may be helpful in patients with a prolonged or delayed recovery.

Labyrinthitis is characterized by the acute onset of vertigo with associated otological symptoms including hearing loss, tinnitus, and possibly ear fullness. It is also believed to be due to a viral etiology.⁹ As many of these patients may initially present with an acute sudden sensorineural hearing loss (SSNHL), the disorder is often classified under this category. SSNHL is more common in the elderly with an incidence of 77 in 100,000 in patients older than 65 years of age and only 11 in 100,000 in patients less than 18 years of age.¹⁰ The vertigo is of similar onset and duration to vestibular neuronitis. Audiometric testing is necessary to confirm the diagnosis. Patients with SSNHL have a loss of hearing of 30 dB or more in 3 contiguous frequencies. Treatment generally includes oral steroid therapy in a dosage or 1 mg/kg tapering over 10–14 days with intratympanic steroid therapy reserved for refractory cases or those in whom oral steroid therapy is contraindicated. Antiviral therapy has not been shown to be beneficial.¹¹ Patients should also undergo magnetic resonance imaging of the brain and internal auditory canals with gadolinium especially in cases with limited recovery to assess for retrocochlear pathology such as vestibular schwannoma.

Dehiscence of the bony labyrinth is most commonly found in the superior semicircular canal, but can also occur in the posterior semicircular canal or horizontal semicircular canal. Such patients may present with vertigo and/or disequilibrium. Figure 26-1 is a drawing of a cross section of the human ear showing the position of the balance canals in relation to the middle ear and middle cranial fossa dura.

A common cause of dehiscence of the horizontal canal is a cholesteatoma. A cholesteatoma is a benign but locally aggressive tumor that usually begins as an ingrowth or retraction of the tympanic membrane from the middle ear into the mastoid cavity (Figure 26-2). Patients who have a cholesteatoma usually have ear canal drainage that is chronic and foul smelling. As the disease progresses, it can cause hearing loss by involvement/erosion of the ossicular chain and/or the labyrinth. As the labyrinth includes the semicircular canals, vestibule, and cochlea, an erosion can result in sensorineural hearing loss and a positive fistula sign (vertigo with pressure insufflation of the ear). Treatment of cholesteatoma is surgical.

Superior semicircular canal dehiscence syndrome (SSCD) was first described by Minor in 2000.¹² He described a series of 17 patients who presented with vertigo and/or oscillopsia induced by sounds or pressure changes, pulsatile tinnitus and conductive hearing loss. Thirteen of these patients had chronic disequilibrium. Diagnosis was confirmed on computed tomography of the temporal bone. He performed surgical plugging or resurfacing of the canal in 5 of these patients with improvement in their symptoms.

Since then, SSCD has been shown to present with various otological symptoms including conductive hearing loss, sensorineural hearing loss, mixed hearing loss, autophony, and tinnitus.¹³ It is possible that increased intracranial pressure may have a role in this disorder as the disease is more common in patients with an increased body mass index.¹⁴

The belief that the inner ear could be a cause of vertigo was first appreciated and described by Prosper Ménière in 1861, who described a series of patients with episodic vertigo and hearing loss.¹⁵Ménière’s disease is now defined as a symptom complex of unknown cause characterized by recurrent episodic vertigo, aural fullness and/or pressure, fluctuating hearing loss, and ipsilateral tinnitus. It usually occurs in patients in middle age with an incidence of 190 per 100,000 with a female to male prevalence of 1.89 to 1. The disorder is relatively rare in children but more common in the elderly.¹⁶

Ménière’s disease and vestibular migraine are the two most common causes of recurring episodic vertigo, and some patients may indeed have components of both disorders. Statistically, vestibular migraine is much more common than Ménière’s disease, as it affects approximately 1% of the population and is seen in 10% of patients seen in dizzy clinics.¹⁷ Patients with aural symptoms who also have headache, photophobia, phonophobia, auras, or motion sickness are better classified as having vestibular migraine than Ménière’s disease.^18,19

Again, the history is key in differentiating these two disorders. While vestibular migraine can have otological symptoms such as hearing loss, tinnitus, and aural fullness, the hearing may be normal or mild to moderate and is unlikely to be severe or progressive.²⁰ Also important is that the vertigo spells may not be associated with or accompanied by a headache in approximately 30% of patients with vestibular migraine.¹⁸ Another reason why it is important to clarify these two disorders is that the treatment of each is significantly different. Some patients with Ménière’s disease who fail medical therapy may be candidates for surgical therapy. The following vignette study of a Ménière’s patient will hopefully further elucidate these points.