Dizziness and Vertigo

Chapter 19


Dizziness and Vertigo




Perspective


Dizziness is an extremely common yet complex neurologic symptom that reflects a disturbance of normal balance perception and spatial orientation. An estimated 7.5 million patients with dizziness are seen each year in ambulatory care settings.1 Dizziness is also one of the most common principal complaints in the emergency department (ED) and is responsible for 2.5% of all ED visits.2 Among patients older than 60 years, 20% have experienced dizziness severe enough to affect their daily activity.3


“Dizziness” is an imprecise descriptor. Patients use the term to describe a variety of experiences, including sensations of motion, weakness, lightheadedness, unsteadiness, and depression. Even clinical experts do not uniformly agree to precise definitions, with some defining it broadly and others more narrowly. Dizziness is historically categorized into one of four categories based on symptom quality: vertigo (illusion of motion, often spinning), near syncope (feeling of impending faint), disequilibrium (loss of equilibrium when walking), and nonspecific dizziness.4


Dizziness can be caused by a myriad diseases. In older persons it is associated with a variety of cardiovascular, neurosensory, and psychiatric conditions and with the use of multiple medications.5 The challenge for the emergency physician is to sift out the rare 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. The eyes, muscles, joints, and otic labyrinths continuously supply information to the brain about the position of the body. Visual impulses, mediated through the higher brain centers, provide information about body position in space. Impulses from proprioceptors of the joints and muscles supply data about the relative positions of the parts of the body. Impulses from the neck are of special importance in relating the position of the head to the rest of the body. The sense organs of the visual, vestibular, and proprioceptive systems are connected to the cerebellum by way of the vestibular nuclei in the brainstem. Any disease that interrupts the integration 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. Here it is vulnerable to trauma, blood-borne toxins, and infections in nearby structures, including the middle ear and meninges. 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) provides information about the orientation of the body with respect to gravity.


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 asymmetrical responses and results in the perception of vertigo. For example, freely moving otoliths that are inappropriately located within the semicircular canals, as in benign paroxysmal positional vertigo (BPPV), can produce positional vertigo as the otoliths move under the influence of gravity.


Impulses leave the vestibular apparatus by the vestibular part of the acoustic nerve (cranial nerve 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: the medial longitudinal fasciculus (MLF) and the vestibulospinal tract. 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.


Nystagmus occurs when the synchronized vestibular information becomes unbalanced. Typically, it results from unilateral vestibular disease, which causes asymmetrical 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. Nystagmus caused by vestibular disease tends to be unidirectional and horizontorotary. If the nystagmus is vertical, a central lesion (either brainstem or cerebral) is usually the cause.


The vestibular nuclei send information to the lateral vestibulospinal tract, where they connect with motor neurons that supply the muscles of the extremities. This explains the phenomenon of false steps or other body movements made by people with a defective vestibular apparatus who are attempting 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.



Diagnostic Approach



Differential Considerations


It is often helpful to have dizzy patients describe the sensation they are experiencing without using the word dizzy. When this is done, one can generally categorize the dizziness into one of four categories: vertigo, near syncope, disequilibrium, and nonspecific dizziness. Vertigo is an illusion of motion, classically described as the room spinning. Some further subdivide this into objective vertigo (external environment is spinning) and subjective vertigo (spinning of self). Near syncope is usually described as feeling faint or lightheaded. Disequilibrium is usually described as an unsteady gait. Nonspecific dizziness is generally thought to be related to anxiety. The validity of this symptom-oriented method of categorizing dizziness has been recently challenged.6 For some patients, dizziness is simply a metaphor for malaise, representing a variety of causes, such as anemia, viral illness, or depression. The primary focus of this chapter is to provide a framework to differentiate vertigo from other types of dizziness and to identify potentially life-threatening causes of these symptoms.


If the patient has true vertigo, the clinician should determine whether the cause is a peripheral lesion, such as from the vestibular system, or a central process, such as cerebrovascular disease or a neoplasm. In most cases, peripheral disorders are benign, whereas central disorders have more serious consequences. Occasionally, as in the case of a cerebellar hemorrhage, immediate therapeutic intervention is indicated. Acute suppurative labyrinthitis is the only cause of peripheral vertigo that requires urgent intervention. Box 19-1 lists causes of vertigo and identifies the peripheral, central, and systemic diagnoses. Table 19-1 summarizes the different characteristics of peripheral and central vertigo.





Pivotal Findings



History


The medical history is used to determine if true vertigo exists. Although usually described as the environment spinning, any sensation of disorientation in space or sensation of motion can qualify as vertigo. Some nausea, vomiting, pallor, and perspiration accompany almost all but the mildest forms of vertigo. A sensation of imbalance often accompanies vertigo, and this can be extremely difficult to distinguish from true instability until after the patient’s symptoms have been reduced by treatment. True instability, disequilibrium, or ataxia indicates a higher likelihood of a central process.7 Because the labyrinth has no effect on the level of consciousness, the patient should not have an associated change in mentation or syncope.


The time of onset and the duration of vertigo are important clues to the cause. Episodic vertigo that is severe, lasts up to several hours, and has symptom-free intervals between episodes suggests a peripheral labyrinth disorder. Vertigo produced primarily by a change in position also suggests a peripheral disorder, usually BPPV.


The presence of auditory symptoms suggests a peripheral cause of the vertigo, as in middle and inner ear problems. The ear with abnormal hearing is usually on the side of end-organ disturbance. Although vertigo can occur with acoustic neuroma, it is usually a progressive unilateral hearing loss, typically of several months’ duration, that prompts the patient with acoustic neuroma to seek medical attention. Hearing loss, vertigo, and tinnitus form the characteristic triad of Ménière’s disease.


Head injury can cause vertigo occasionally from intracerebral injury and more commonly from labyrinth concussion. Neck injury can cause vertigo from vertebral artery dissection, resulting in posterior circulation ischemia.8


Vestibular neuritis and labyrinthitis are very similar, though in labyrinthitis hearing is affected. Patients often develop continuous vertigo that can be worsened by movement and may take several months to fully resolve.


Are there associated neurologic symptoms? The patient or family members should be questioned about the time of onset of ataxia or gait disturbances. Ataxia of recent and relatively sudden onset suggests cerebellar hemorrhage or infarction in the distribution of the posterior inferior cerebellar artery or the superior cerebellar artery. Ataxia that is slowly progressive suggests chronic cerebellar disorders. True ataxia may be difficult to discern from the unsteadiness that occurs when a patient with significant vertigo attempts to walk, though other findings such as nystagmus and dysmetria can often help narrow the differential diagnosis. The symptom of imbalance raises the likelihood of TIA and stroke. Isolated vertigo can be the only initial symptom of cerebellar and other posterior circulation bleeds, transient ischemic attacks (TIAs), and infarction.9,10 One study showed that emergency physicians often did not make the correct diagnosis in patients with validated strokes or TIAs whose presenting symptom was only vertigo.7 Identifying these individuals is a significant and important challenge for clinicians taking care of vertiginous patients. The vast majority of patients with isolated dizziness do not have TIA or stroke, but the risk of not identifying the few who do is significant for ultimate patient outcomes. Stroke has been seen in 3.2% of patients with dizziness syndrome, but only 0.7% of those with isolated dizziness had a stroke.7 A recent study also showed that fewer than 1 in 500 patients discharged with a diagnosis of dizziness or vertigo experienced a major vascular event in the month after discharge.11


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Jul 26, 2016 | Posted by in ANESTHESIA | Comments Off on Dizziness and Vertigo

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