DIZZINESS AND VERTIGO




INTRODUCTION



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Dizziness is an imprecise symptom used to describe a variety of sensations that include vertigo, light-headedness, faintness, and imbalance. When used to describe a sense of spinning or other motion, dizziness is designated as vertigo. Vertigo may be physiologic, occurring during or after a sustained head rotation, or it may be pathologic, due to vestibular dysfunction. The term light-headedness is commonly applied to presyncopal sensations due to brain hypoperfusion but also may refer to 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 a number of potential causes of dizziness. Vascular disorders cause presyncopal dizziness as a result of cardiac dysrhythmia, orthostatic hypotension, medication effects, or other causes. 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. 11, 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 (vertigo or imbalance) 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 (oscillopsia) when the head moves. Other causes of dizziness include nonvestibular 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.




APPROACH TO PATIENT



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APPROACH TO THE PATIENT: Dizziness HISTORY


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 that 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 characteristics is typically unreliable. The history should focus closely on other features, including whether this is the first attack, the duration of this and any prior episodes, provoking factors, and accompanying symptoms.


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 head and body position. Attacks of vestibular migraine 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 migraine and a number of other causes are also possible.


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.

EXAMINATION

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. Nystagmus is most often 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. 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). By contrast, peripheral lesions typically cause unidirectional horizontal nystagmus. Use of Frenzel eyeglasses (self-illuminated goggles with convex lenses that blur the patient’s vision but allow the examiner to see the eyes greatly magnified) can aid in the detection of peripheral vestibular nystagmus, because they reduce the patient’s ability to use visual fixation to suppress nystagmus. Table 12-1 outlines key findings that help distinguish peripheral from central causes of vertigo.


The most useful bedside test of peripheral vestibular function is the head impulse test, in which the vestibuloocular reflex (VOR) is assessed with small-amplitude (~20 degrees) rapid head rotations. While the patient fixates on a target, the head is rotated to the left or right. If the VOR is deficient, the rotation is followed by a catch-up saccade in the opposite direction (e.g., a leftward saccade after a rightward rotation). The head impulse test can identify both unilateral (catch-up saccades after rotations toward the weak side) and bilateral vestibular hypofunction (catch-up saccades after rotations in both directions).


All patients with episodic dizziness, especially if provoked by positional change, should be tested with the Dix-Hallpike maneuver. The patient begins in a sitting position with the head turned 45 degrees; holding the back of the head, the examiner then lowers the patient into a supine position with the head extended backward by about 20 degrees while watching the eyes. Posterior canal BPPV can be diagnosed confidently if transient upbeating-torsional nystagmus is seen. If no nystagmus is observed after 15–20 s, the patient is raised to the sitting position, and the procedure is repeated with the head turned to the other side. Again, Frenzel goggles may improve the sensitivity of the test.


Dynamic visual acuity is a functional test that can be useful in assessing vestibular function. Visual acuity is measured with the head still and when the head is rotated back and forth by the examiner (about 1–2 Hz). A drop in visual acuity during head motion of more than one line on a near card or Snellen chart is abnormal and indicates vestibular dysfunction.

ANCILLARY TESTING

The choice of ancillary tests should be guided by the history and examination findings. Audiometry should be performed whenever a vestibular disorder is suspected. Unilateral sensorineural hearing loss supports a peripheral disorder (e.g., vestibular schwannoma). Predominantly low-frequency hearing loss is characteristic of Ménière’s disease. Electronystagmography or videonystagmography includes recordings of spontaneous nystagmus (if present) and measurement of positional nystagmus. Caloric testing assesses the responses of the two horizontal semicircular canals. The test battery often includes recording of saccades and pursuit to assess central ocular motor function. Neuroimaging is important if a central vestibular disorder is suspected. In addition, patients with unexplained unilateral hearing loss or vestibular hypofunction should undergo magnetic resonance imaging (MRI) of the internal auditory canals, including administration of gadolinium, to rule out a schwannoma.





TABLE 12-1FEATURES OF PERIPHERAL AND CENTRAL VERTIGO
Dec 26, 2018 | Posted by in NEUROLOGY | Comments Off on DIZZINESS AND VERTIGO

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