Chapter 19: Dizziness and Vertigo

Dizziness is an imprecise symptom used to describe a variety of common sensations that include vertigo, light-headedness, faintness, and imbalance. Vertigo refers to a sense of spinning or other motion that may be physiological, occurring during or after a sustained head rotation, or pathological, due to vestibular dysfunction. The term light-headedness is classically applied to presyncopal sensations resulting from brain hypoperfusion but as used by patients has little specificity, as it may also refer to other symptoms such as disequilibrium and imbalance. A challenge to diagnosis is that patients often have difficulty distinguishing among these various symptoms, and the words they choose do not reliably indicate the underlying etiology.

There are many causes of dizziness. Vestibular dizziness (vertigo or imbalance) may be due to peripheral disorders that affect the labyrinths or vestibular nerves, or it may result from disruption of central vestibular pathways. It may be paroxysmal or due to a fixed unilateral or bilateral vestibular deficit. Acute unilateral lesions cause vertigo due to a sudden imbalance in vestibular inputs from the two labyrinths. Bilateral lesions cause imbalance and instability of vision when the head moves (oscillopsia) due to loss of normal vestibular reflexes.

Presyncopal dizziness occurs when cardiac dysrhythmia, orthostatic hypotension, medication effects, or another cause leads to brain hypoperfusion. Such presyncopal sensations vary in duration; they may increase in severity until loss of consciousness occurs, or they may resolve before loss of consciousness if the cerebral ischemia is corrected. Faintness and syncope, which are discussed in detail in Chap. 18, should always be considered when one is evaluating patients with brief episodes of dizziness or dizziness that occurs with upright posture. Other causes of dizziness include non-vestibular imbalance and gait disorders (e.g., loss of proprioception from sensory neuropathy, parkinsonism), and anxiety.

When evaluating patients with dizziness, questions to consider include the following: (1) Is it dangerous (e.g., arrhythmia, transient ischemic attack/stroke)? (2) Is it vestibular? (3) If vestibular, is it peripheral or central? A careful history and examination often provide sufficient information to answer these questions and determine whether additional studies or referral to a specialist is necessary.

Treatment of vestibular symptoms should be driven by the underlying diagnosis. Simply treating dizziness with vestibular suppressant medications is often not helpful and may make the symptoms worse and prolong recovery. The diagnostic and specific treatment approaches for the most commonly encountered vestibular disorders are discussed below.

An acute unilateral vestibular lesion causes constant vertigo, nausea, vomiting, oscillopsia (motion of the visual scene), and imbalance. These symptoms are due to a sudden asymmetry of inputs from the two labyrinths or in their central connections, simulating a continuous rotation of the head. Unlike BPPV, continuous vertigo persists even when the head remains still.

When a patient presents with an acute vestibular syndrome, the most important question is whether the lesion is central (e.g., a cerebellar or brainstem infarct or hemorrhage), which may be life-threatening, or peripheral, affecting the vestibular nerve or labyrinth (vestibular neuritis). Attention should be given to any symptoms or signs that point to central dysfunction (diplopia, weakness or numbness, dysarthria). The pattern of spontaneous nystagmus, if present, may be helpful (Table 19-1). If the head impulse test is normal, an acute peripheral vestibular lesion is unlikely. A central lesion cannot always be excluded with certainty based on symptoms and examination alone; thus, older patients with vascular risk factors who present with an acute vestibular syndrome should be evaluated for the possibility of stroke even when there are no specific findings that indicate a central lesion.

Most patients with vestibular neuritis recover spontaneously, but glucocorticoids can improve outcome if administered within 3 days of symptom onset. Antiviral medications are of no proven benefit and are not typically given unless there is evidence to suggest herpes zoster oticus (Ramsay Hunt syndrome). Vestibular suppressant medications may reduce acute symptoms but should be avoided after the first several days because they may impede central compensation and recovery. Patients should be encouraged to resume a normal level of activity as soon as possible, and directed vestibular rehabilitation therapy may accelerate improvement.

BPPV is a common cause of recurrent vertigo. Episodes are brief (<1 min and typically 15–20 s) and are always provoked by changes in head position relative to gravity, such as lying down, rolling over in bed, rising from a supine position, and extending the head to look upward. The attacks are caused by free-floating otoconia (calcium carbonate crystals) that have been dislodged from the utricular macula and have moved into one of the semicircular canals, usually the posterior canal. When head position changes, gravity causes the otoconia to move within the canal, producing vertigo and nystagmus. With posterior canal BPPV, the nystagmus beats upward and torsionally (the upper poles of the eyes beat toward the affected lower ear). Less commonly, the otoconia enter the horizontal canal, resulting in a horizontal nystagmus when the patient is lying with either ear down. Superior (also called anterior) canal involvement is rare. BPPV is treated with repositioning maneuvers that use gravity to remove the otoconia from the semicircular canal. For posterior canal BPPV, the Epley maneuver (Fig. 19-1) is the most commonly used procedure. For more refractory cases of BPPV, patients can be taught a variant of this maneuver that they can perform alone at home. A demonstration of the Epley maneuver is available online (http://www.dizziness-and-balance.com/disorders/bppv/bppv.html).

Vestibular migraine is a very common yet underdiagnosed cause of episodic vertigo. Vertigo sometimes precedes a typical migraine headache but more often occurs without headache or with only a mild headache. Some patients who have had frequent migraine headaches in the past present later in life with vestibular migraine as the predominant problem. In vestibular migraine, the duration of vertigo may be from minutes to hours, and some migraineurs also experience more prolonged periods of disequilibrium (lasting days to weeks). Motion sensitivity and sensitivity to visual motion (e.g., movies) are common. Even in the absence of headache, other migraine features may be present, such as photophobia, phonophobia, or a visual aura. Although data from controlled studies are generally lacking, vestibular migraine typically is treated with medications that are used for prophylaxis of migraine headaches (Chap. 422). Antiemetics may be helpful to relieve symptoms at the time of an attack.

Attacks of Ménière’s disease consist of vertigo and hearing loss, as well as pain, pressure, and/or fullness in the affected ear. The low-frequency hearing loss and aural symptoms are key features that distinguish Ménière’s disease from other peripheral vestibulopathies and from vestibular migraine. Audiometry at the time of an attack shows a characteristic asymmetric low-frequency hearing loss; hearing commonly improves between attacks, although permanent hearing loss may eventually occur. Ménière’s disease is thought to be due to excess fluid (endolymph) in the inner ear; hence the term endolymphatic hydrops. Patients suspected of having Ménière’s disease should be referred to an otolaryngologist for further evaluation. Diuretics and sodium restriction are typically the initial treatments. If attacks persist, injections of glucocorticoids or gentamicin into the middle ear may be considered. Non-ablative surgical options include decompression and shunting of the endolymphatic sac. Full ablative procedures (vestibular nerve section, labyrinthectomy) are seldom required.

Vestibular schwannomas (sometimes termed acoustic neuromas) and other tumors at the cerebellopontine angle cause slowly progressive unilateral sensorineural hearing loss and vestibular hypofunction. These patients typically do not have vertigo, because the gradual vestibular deficit is compensated centrally as it develops. The diagnosis often is not made until there is sufficient hearing loss to be noticed. The vestibular examination will show a deficient response to the head impulse test when the head is rotated toward the affected side, but nystagmus will not be prominent. As noted above, patients with unexplained unilateral sensorineural hearing loss or vestibular hypofunction require MRI of the internal auditory canals to look for a schwannoma.

Patients with bilateral loss of vestibular function also typically do not have vertigo, because vestibular function is lost on both sides simultaneously, and there is no asymmetry of vestibular input. Symptoms include loss of balance, particularly in the dark, where vestibular input is most critical, and oscillopsia during head movement, such as while walking or riding in a car. Bilateral vestibular hypofunction may be (1) idiopathic and progressive, (2) part of a neurodegenerative disorder, or (3) iatrogenic, due to medication ototoxicity (most commonly gentamicin or other aminoglycoside antibiotics). Other causes include bilateral vestibular schwannomas (neurofibromatosis type 2), autoimmune disease, superficial siderosis, and meningeal-based infection or tumor. It also may occur in patients with peripheral polyneuropathy; in these patients, both vestibular loss and impaired proprioception may contribute to poor balance. Finally, unilateral processes such as vestibular neuritis and Ménière’s disease may involve both ears sequentially, resulting in bilateral vestibulopathy.

Examination findings include diminished dynamic visual acuity (see above) due to loss of stable vision when the head is moving, abnormal head impulse responses in both directions, and a Romberg sign. Responses to caloric testing are reduced. Patients with bilateral vestibular hypofunction should be referred for vestibular rehabilitation therapy. Vestibular suppressant medications should not be used, as they will increase the imbalance. Evaluation by a neurologist is important not only to confirm the diagnosis but also to consider any other associated neurologic abnormalities that may clarify the etiology.

Central lesions causing vertigo typically involve vestibular pathways in the brainstem and/or cerebellum. They may be due to discrete lesions, such as from ischemic or hemorrhagic stroke (Chaps. 419, 420, 421) demyelination (Chap. 436), or tumors (Chap. 86), or they may be due to neurodegenerative conditions that include the vestibulocerebellum (Chaps. 423, 424, 425, 426). Subacute cerebellar degeneration may be due to immune, including paraneoplastic, processes (Chaps. 90 and 431). Table 19-1 outlines important features of the history and examination that help to identify central vestibular disorders. Acute central vertigo is a medical emergency, due to the possibility of life-threatening stroke or hemorrhage. All patients with suspected central vestibular disorders should undergo brain MRI, and the patient should be referred for full neurologic evaluation.

Psychological factors play an important role in chronic dizziness. First, dizziness may be a somatic manifestation of a psychiatric condition such as major depression, anxiety, or panic disorder (Chap. 443). Second, patients may develop anxiety and autonomic symptoms as a consequence or comorbidity of an independent vestibular disorder. One particular form of this has been termed variously phobic postural vertigo, psychophysiologic vertigo, or chronic subjective dizziness, but is now referred to as persistent postural-perceptual dizziness (PPPD). These patients have a chronic feeling (3 months or longer) of fluctuating dizziness and disequilibrium that is present at rest but worse while standing. There is an increased sensitivity to self-motion and visual motion (e.g., watching movies), and a particular intensification of symptoms when moving through complex visual environments such as supermarkets. Although there may be a past history of an acute vestibular disorder (e.g., vestibular neuritis), the neurootologic examination and vestibular testing are normal or indicative of a compensated vestibular deficit, indicating that the ongoing subjective dizziness cannot be explained by a primary vestibular pathology. Anxiety disorders are particularly common in patients with chronic dizziness; when present, they contribute substantially to the morbidity. Treatment approaches for PPPD include pharmacological therapy with selective serotonin reuptake inhibitors (SSRIs), cognitive-behavioral psychotherapy, and vestibular rehabilitation. Vestibular suppressant medications generally should be avoided.