Dizziness is a common, vexing symptom, and epidemiologic data indicate that more than 20% of adults experience dizziness within a given year. The diagnosis is frequently challenging, in part because patients use the term to refer to a variety of different sensations, including feelings of faintness, spinning, and other illusions of motion, imbalance, and anxiety. Other descriptive words, such as light-headedness, are equally ambiguous, referring in some cases to a presyncopal sensation due to hypoperfusion of the brain and in others to disequilibrium and imbalance. Patients often have difficulty distinguishing among these various symptoms, and the words they choose do not describe the underlying etiology reliably.
Vascular disorders cause presyncopal dizziness as a result of cardiac dysrhythmia, orthostatic hypotension, medication effects, or another cause. 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. 20, should always be considered when one is evaluating patients with brief episodes of dizziness or dizziness that occurs with upright posture.
Vestibular causes of dizziness may be due to peripheral lesions that affect the labyrinths or vestibular nerves or to involvement of the central vestibular pathways. They 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). Other causes of dizziness include nonvestibular imbalance and gait disorders (e.g., loss of proprioception from sensory neuropathy, parkinsonism) and anxiety.
In 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? and (3) if vestibular, is it peripheral or central? A careful history and examination often provide enough information to answer these questions and determine whether additional studies or referral to a specialist is necessary.
Approach to the Patient: Dizziness
When a patient presents with dizziness, the first step is to delineate more precisely the nature of the symptom. In the case of vestibular disorders, the physical symptoms depend on whether the lesion is unilateral or bilateral and whether it is acute or chronic and progressive. Vertigo, an illusion of self or environmental motion, implies asymmetry of vestibular inputs from the two labyrinths or in their central pathways and is usually acute. Symmetric bilateral vestibular hypofunction causes imbalance but no vertigo. Because of the ambiguity in patients' descriptions of their symptoms, diagnosis based simply on symptom character is typically unreliable. The history should focus closely on other features, including whether dizziness is paroxysmal or has occurred only once, the duration of each episode, any provoking factors, and the symptoms that accompany the dizziness.
Causes of dizziness can be divided into episodes that last for seconds, minutes, hours, or days. Common causes of brief dizziness (seconds) include benign paroxysmal positional vertigo (BPPV) and orthostatic hypotension, both of which typically are provoked by changes in position. Attacks of migrainous vertigo and Ménière's disease often last hours. When episodes are of intermediate duration (minutes), transient ischemic attacks of the posterior circulation should be considered, although these episodes also could be due to migraine or a number of other causes.
Symptoms that accompany vertigo may be helpful in distinguishing peripheral vestibular lesions from central causes. Unilateral hearing loss and other aural symptoms (ear pain, pressure, fullness) typically point to a peripheral cause. Because the auditory pathways quickly become bilateral upon entering the brainstem, central lesions are unlikely to cause unilateral hearing loss (unless the lesion lies near the root entry zone of the auditory nerve). Symptoms such as double vision, numbness, and limb ataxia suggest a brainstem or cerebellar lesion.
Because dizziness and imbalance can be a manifestation of a variety of neurologic disorders, the neurologic examination is important in the evaluation of these patients. Particular focus should be given to assessment of eye movements, vestibular function, and hearing. The range of eye movements and whether they are equal in each eye should be observed. Peripheral eye movement disorders (e.g., cranial neuropathies, eye muscle weakness) are usually disconjugate (different in the two eyes). One should check pursuit (the ability to follow a smoothly moving target) and saccades (the ability to look back and forth accurately between two targets). Poor pursuit or inaccurate (dysmetric) saccades usually indicates central pathology, often involving the cerebellum. Finally, one should look for spontaneous nystagmus, an involuntary back-and-forth movement of the eyes. Most often nystagmus is of the jerk type, in which a slow drift (slow phase) in one direction alternates with a rapid saccadic movement (quick phase or fast phase) in the opposite direction that resets the position of the eyes in the orbits. Table 21-1 lists features that help distinguish peripheral vestibular nystagmus from central nystagmus. Except in the case of acute vestibulopathy (e.g., vestibular neuritis), if primary position nystagmus is easily seen in the light, it is probably due to a central cause. Two forms of nystagmus that are characteristic of lesions of the cerebellar pathways are vertical nystagmus with downward fast phases (downbeat nystagmus) and horizontal nystagmus that changes direction with gaze (gaze-evoked nystagmus).
Table 21-1 Features of Peripheral and Central Vertigo
| Save Table
Table 21-1 Features of Peripheral and Central Vertigo
|Sign or Symptom||Peripheral (Labyrinth or Vestibular Nerve)||Central (Brainstem or Cerebellum)|
|Direction of associated nystagmus||Unidirectional; fast phase opposite lesiona||Bidirectional (direction-changing) or unidirectional|
|Purely horizontal nystagmus without torsional component||Uncommon||May be present|
|Purely vertical or purely torsional nystagmus||Never presentb||May be present...|
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