Dizziness and Vertigo

Epidemiology

Dizziness is an extremely common yet complex neurologic symptom that reflects a disturbance of normal balance perception and spatial orientation. Patients use the term dizziness to describe a variety of experiences, including sensations of motion, weakness, lightheadedness, unsteadiness, emotional upset, and depression. Dizziness has historically been categorized in a symptom-based approach into one of four categories though the validity of this categorization has recently been called into question. The historical categories include vertigo, which is an illusion of motion and typically described as the room spinning; near syncope, which is a sensation of feeling faint or lightheaded; disequilibrium, which is a sense of unsteadiness when walking; and nonspecific dizziness, which is generally thought to be related to a polysensory disorder with an anxiety component.

Acute vestibular syndrome (AVS) is used to describe a clinical condition in which dizziness develops acutely, is constant, persists longer than a day, and is accompanied by nausea or vomiting, unsteady gait, nystagmus, and intolerance to head motion. The major differential diagnosis in acute vestibular syndrome is vestibular neuritis versus posterior circulation stroke. Some recommend subdividing this into acute vestibular syndrome with nystagmus and acute vestibular syndrome without nystagmus because the diagnostic approach differs between them.

Approximately 4% of ED visits are from dizziness, and strokes are the underlying cause in approximately 5% of those visits. Although common causes of dizziness (e.g., benign paroxysmal positional vertigo [BPPV] and vestibular neuritis) can often be readily diagnosed via history and specific diagnostic tests, a precise diagnosis is not always possible even after imaging and neurology consultation. Thus the challenge for the emergency clinician is to identify the patient with a dangerous underlying disorder from the many others who have benign causes.

Pathophysiology

The maintenance of equilibrium and awareness of the body in relationship to its surroundings depend on the interaction of the visual, proprioceptive, and vestibular systems. Input from these three systems is connected to the cerebellum by way of the vestibular nuclei in the brainstem. Any disease that causes a mismatch of information from any two of these three systems may give rise to symptoms of vertigo.

The vestibular apparatus helps maintain head position and stabilize head movement. It is housed in the inner ear, or labyrinth, which lies embedded in the petrous portion of the temporal bone. The vestibular apparatus consists of three semicircular canals and two otolithic structures (the utricle and the saccule). The semicircular canals and the utricle are connected to each other and contain endolymph. The semicircular canals provide information about movement and angular momentum, whereas the utricle (via otoliths, which are calcium carbonate particles attached to hair cells) provides information about head tilt and vertical linear acceleration.

The semicircular canals are paired (left and right ears) structures that normally respond to motion in a symmetrical manner. With inner ear disease, the resting discharge or the discharge stimulated by motion can be altered in one ear. This alteration produces asymmetric responses and results in the perception of vertigo. For example, freely moving otoliths that are inappropriately located within the semicircular canals, as in BPPV, can produce positional vertigo even when the head is currently still if the head had been recently moved. This is because the recent head movement causes the otoliths to move under the influence of gravity and inappropriately signal the brain.

Impulses leave the vestibular apparatus by the vestibular part of the acoustic nerve (cranial nerve [CN] VIII), enter the brainstem just below the pons and anterior to the cerebellum, and proceed to the four vestibular nuclei of the brainstem and to the cerebellum. From there, impulses travel along two pathways that contribute to the clinical manifestations of vertigo: (1) the medial longitudinal fasciculus (MLF) and (2) the vestibulospinal tract, which connect to the motor neurons that supply the muscles of the extremities. In individuals with healthy vestibular systems, these connections allow the eyes to compensate for body movement in different directions and to maintain a visual axis that is stable with respect to the environment. However, patients with a defective vestibular apparatus may experience false steps or other body movements, which is different from true ataxia, because they attempt to correct for an imagined change in position. Connections between the vestibular nuclei and the autonomic system account for the perspiration, nausea, and vomiting that commonly accompany an attack of vertigo. Connections between the vestibular nuclei and the cerebellum account for the modulating influence of this organ on motor activity.

Nystagmus occurs when the synchronized vestibular information becomes unbalanced. Typically, it results from unilateral vestibular disease, which causes asymmetric stimulation of the medial and lateral rectus muscles of the eye. This unopposed activity causes a slow movement of the eyes toward the side of the stimulus, regardless of the direction of deviation of the eyes. The cerebral cortex then corrects for these eye movements and rapidly brings the eyes back to the midline, only to have the process repeated. By convention, the direction of nystagmus is denoted by the direction of the fast “cortical” component.

Vertebrobasilar insufficiency (VBI) describes a temporary set of symptoms due to ischemia in the posterior circulation of the brain, which supplies the medulla, pons, midbrain, and cerebellum. Major arteries of the posterior circulation include the posterior inferior cerebellar artery (PICA), which is a branch of the vertebral artery, and the anterior inferior cerebellar artery (AICA), which is a branch of the basilar artery.

Table 15.1 lists the pathophysiology for selected causes of peripheral vertigo.

Differential Considerations

The differential diagnosis for peripheral and central vertigo is summarized in Box 15.1 . More detailed information is given on selected causes in Table 15.2 . Peripheral disorders are generally benign, whereas central disorders usually have serious consequences. Table 15.3 summarizes the different characteristics of peripheral and central vertigo.

The symptom-based approach to categorizing dizziness into four categories (vertigo, near syncope, disequilibrium, and nonspecific dizziness) has been criticized as being imprecise, and new categorization systems have been recently proposed. One system uses three general categories: (1) acute severe dizziness (e.g., vestibular neuritis, stroke), (2) recurrent attacks of dizziness (e.g., Ménière disease, TIA), and (3) recurrent positional dizziness (e.g., BPPV, cerebellar tumor, multiple sclerosis). Another system uses a “timing and triggers” approach, resulting in three categories: (1) acute vestibular syndrome (e.g., vestibular neuritis, cerebellar stroke), (2) spontaneous episodic vestibular syndrome (e.g., Ménière disease, VBI), and (3) triggered episodic vestibular syndrome (e.g., BPPV). Neither of these approaches has been prospectively validated or systematically studied as a diagnostic paradigm, but they may provide a superior way to differentiate among the many causes of dizziness and vertigo.