IMPORTANT NOTE: JAAPA CME activities consist of 2 articles. To obtain credit, you must also read
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KEY POINTS
■ A history that includes the right questions can shorten the workup for dizziness and provide key clues to the diagnosis. The first steps are to determine if the patient truly has vertigo and whether it is peripheral or central.
■ The physical examination should focus on the head and neck and on the neurologic and cardiovascular systems. Tests of vestibular function are also important. Neuroimaging is valuable when a central cause of vertigo is suspected.
■ Vestibular suppressants and antiemetic drugs are first-line choices for managing acute vertigo. A combination of an antihistamine and an antiemetic is commonly prescribed.
■ Other helpful interventions include salt restriction, use of a mild diuretic, and vestibular habituation or rehabilitation. Support groups can also be helpful in letting patients know they are not alone.
One of the most frequently encountered patient complaints is vertigo or disequilibrium. Reasonably, the evaluation of this complaint often creates anxiety in the clinician because of both the seemingly endless differential diagnosis and the question as to whether the patient has true vertigo at all. This article reviews the basic components of the evaluation—a comprehensive history and physical examination—and provides additional pearls that can help to determine the diagnosis. With a thorough yet purposeful evaluation, the cause of the patient's symptoms can be uncovered and treatment options can be more efficiently utilized.
PATHOPHYSIOLOGY
Most advances in treating vestibular disorders have come from a thorough understanding of the physiology of the inner ear. The labyrinth is an inner ear neurosensory organ made up of two components: the semicircular canals used for balance and the cochlea used for hearing.1 Typically, vertigo is caused by an imbalance of sensory inputs into the two vestibular nuclei from overactivity or underactivity of either or both sides of the labyrinth.1 Any disturbance of the labyrinth, visual-vestibular interaction centers in the brain stem and cerebellum, and sensory pathways to or from the thalamus can result in vertigo.1 One of the most common types of peripheral vertigo is benign paroxysmal positional vertigo (BPPV) which is caused by displacement of calcium carbonate crystals, called otoconia, from the utricle into the semicircular canals. Typically, patients with BPPV will be able to reproduce their symptoms by lying down or moving the head because these trapped otoconia continue to move within the semicircular canals during position change (Figure 1).
EPIDEMIOLOGY
Vestibular disorders are frequently encountered not just by neuro-otologists but also by emergency department (ED) and primary care providers. According to a 2008 study, dizziness and/or vertigo had a prevalence and incidence of 22.9% and 3.1%, respectively, over a 12-month interval.2 The study revealed a male-to-female ratio of 1:2.7; and vertigo was diagnosed almost three times more frequently in the elderly based on the age groups studied (18-39 years, 40-59 years, and 60-79 years).2 These data demonstrate how important it is for generalist clinicians to understand how to evaluate vertigo.
Apart from the challenge it presents to clinicians, vertigo also has an enormous impact on the lives of those afflicted. Compared with nonvestibular dizziness, vestibular vertigo was more frequently followed by medical consultation, sick leave, interruption of daily activities, and avoidance of leaving the house.2 Additionally, vestibular vertigo accounted for 29% of the dizziness/vertigo complaints seen by a physician.2 Interestingly, although 70% of vertigo sufferers consulted a physician, more than half the participants with clear-cut vestibular vertigo received a diagnosis of a nonvestibular disorder, often leading to a costly workup.2
THE CHALLENGES OF VERTIGO
Although understanding vertigo from a personal and epidemiologic perspective is important, clinicians also should understand the difficulties associated with evaluating this complaint. Vertiginous patients often have trouble detailing their symptoms, and some hesitate to describe exactly what they experience for fear of being perceived as foolish. Furthermore, clinicians, especially in the ED, are consumed with ruling out central causes of dizziness, which can lead to overuse of imaging and avoidance of necessary first steps in formulating a diagnosis. Another issue is the negative connotation associated with the complaint of vertigo. Providers tend to couple the complaint with lengthy histories and physical examinations, thereby leading to unnecessary referral to specialists.
Providers have an obligation to guide patients toward giving an accurate history, which in turn greatly helps the diagnostic process. A study conducted at the Mayo Clinic assessed patients' description of the quality of dizziness using four types of questions: open-ended, multi-response, single-choice, and directed.3 The researchers found that open-ended descriptions were frequently vague and that of 218 patients who did not identify vertigo, spinning, or motion on the first three questions, 70% confirmed spinning or motion sensation on directed questioning. The authors deemed that descriptions of dizziness are unclear and inconsistent and concluded that alternative approaches that emphasize timing and triggers should be further explored. Furthermore, they suggested that clinicians should rely less strictly on symptom quality to direct diagnosis and more on timing and triggers. The description of symptom quality is often misleading and can lead to inaccuracies.3
HISTORY AND EXAMINATION
Clinicians are frequently told that the history alone can often lead to an accurate diagnosis, and this is especially true when evaluating a dizzy patient. A history that includes the right questions can shorten the evaluation, as it provides key clues to the diagnosis (Figure 2).
The first step in the history is to define vertigo and then determine if the patient truly has it. Vertigo is an illusion or hallucination of movement, usually rotational, either of oneself or the environment.4 In a prospective cohort study, Hanley and O'Dowd determined if their subjects had true vertigo by asking, "When you have dizzy spells, do you feel light-headed or do you see the world spin around you?"4 This question is commonly used and is easily understood by patients. Patients who see the world spin around them have true vertigo. The duration of symptoms can also provide important clues, as detailed in Table 1.
The next step is to distinguish peripheral from central vertigo. Peripheral vertigo usually has a more sudden onset and is associated with a rotational sensation.5 Patients often have mild to moderate imbalance, can have nausea and vomiting, and usually experience auditory symptoms such as hearing loss and tinnitus. Central vertigo tends to persist for a longer period of time (hours to weeks). Often the imbalance inhibits the patient from walking or standing still, and auditory complaints are rare5 (Table 2).
Other important questions are whether anything provokes the patient's sensation of vertigo and if there are associated symptoms. For example, vertigo brought on by positional changes, bending at the waist, or hyperextending the neck is often BPPV.5 Associated symptoms such as hearing loss, tinnitus, aural fullness, nausea, and vomiting usually indicate a peripheral cause of vertigo, such as Meniere disease.6 Other symptoms such as visual disturbances, dysarthria, and headaches are more often associated with central causes of vertigo.6 Recent viral infection may precede vestibular neuronitis or labyrinthitis; a history of anxiety may suggest hyperventilation as a cause of vertigo.5 A good social and medication history is also important, as aminoglycosides, diuretics, antidepressants, alcohol, and antipsychotics can
all cause vertigo.1
A focused physical examination is the next step. The head and neck examination should include use of an otoscope; if a pneumatic-otoscope is available, insufflating air is useful in detecting middle ear disease by checking mobility of the tympanic membrane. Specific noteworthy abnormalities of the tympanic membrane include vesicles seen in herpes zoster oticus, fluid behind the tympanic membrane, or white debris behind the tympanic membrane seen in cholesteatoma.
After the auricle, canal, and tympanic membrane are examined, testing for Hennebert sign can be performed by pushing on the tragus and external auditory meatus of the affected side to induce vertigo or nystagmus.5 A positive result indicates perilymphatic fistula, which is a breach between the middle and inner ear often caused by trauma or excessive straining.5
A tuning fork should be included in the examination of all vertiginous patients, even in the ED. The clinician should look for signs of sensorineural or conductive hearing loss and use the Weber test, which should be midline if normal, and the Rinne test, which should show air conduction greater than bone conduction if within normal limits.
The neurologic examination should include special attention to cranial nerve testing. With peripheral vertigo, nystagmus is most often a combination of horizontal and torsional, lessens or disappears when the patient focuses the gaze, and is usually triggered by a provoking factor. Spontaneous horizontal nystagmus with or without rotary nystagmus is consistent with vestibular neuronitis. Central vertigo will manifest as nystagmus that is purely horizontal, vertical, or rotational and does not lessen when the patient has a focused gaze. Vertical nystagmus is 80% sensitive for vestibular nuclear or cerebellar vermis lesions.5 Balance should be evaluated by checking normal gait, tandem gait, heel and toe walking, and balance in a stationary position. Patients with peripheral vertigo have impaired balance but are still able to walk, whereas patients with central vertigo have more severe imbalance limiting their ability even to stand on their own.5 Patients should perform limb coordination tests—that is, finger-to-nose, heel-to-shin, and rapid alternating movement testing.
Lastly, a cardiovascular examination should look for orthostatic changes in BP, evidence of volume loss such as in dehydration, or cardiac arrhythmias.
EVALUATING VESTIBULAR FUNCTION
The clinical utility of vestibular function signs is unclear as few studies have been done; however, they can be helpful adjuncts in reaching a diagnosis. Positional tests, such as the Dix-Hallpike maneuver, are best suited for patients who are asymptomatic at rest in order to reproduce their vertigo and nystagmus on clinical examination.
The Dix-Hallpike maneuver is thought to be the most valuable clinical vestibular test, with a positive predictive value of 83.3% and a negative predictive value of 52%.1 To perform this test, the examiner stands at the patient's head 45 degrees to the right to align the right posterior semicircular canal with the sagittal plane of the body (Figure 3).
The examiner then moves the patient, whose eyes are open, from the seated to the supine, right ear down position and extends the neck slightly so that the chin is pointed slightly upward. The latency, duration, and direction of the nystagmus, if present, should be noted. This maneuver should be performed bilaterally and is thought to be diagnostic for BPPV. Signs of a positive Dix-Hallpike test result include nystagmus with a latent of onset (usually 5-10 seconds), rotational nystagmus, fatigable nystagmus where multiple repetitions of the test will progressively decrease the eye beating, or reversal of nystagmus when the patient is sat upward.
The Romberg test is used to assess the integrity of peripheral proprioception, cerebellar function, and vestibular function.1 The patient places both feet close together and attempts to maintain balance. The result is positive when a patient cannot maintain balance with the eyes closed.
The Fukuda-Unterberger test is used to detect vestibular hypofunction. The patient is asked to march in place with eyes closed and arms outstretched. The result is positive if the patient deviates from midline, approximately 30 degrees or more, usually toward the side with the lower vestibular activity.1
The vestibulo-ocular reflex (VOR) test is performed by placing the head in a midline position and instructing the patient to maintain visual fixation on the examiner's nose. The examiner thrusts the patient's head quickly to one side, and if a refixation saccade back to the nose is seen, canal paresis is present on the side to which the head was turned. The test should be done on both sides. When studied in ED populations, a positive head impulse test result was 100% sensitive for a peripheral disorder.7 A negative result was found in 91% to 96% of patients with cerebellar infarction.7
LABORATORY TESTING AND IMAGING
In general, laboratory testing should be reserved for patients with vertigo of unknown etiology (when the physical examination has excluded common causes of vertigo). Laboratory testing may include blood counts and measures of electrolytes, glucose, and thyroid function, among other tests.5 In general, however, laboratory testing is not helpful in most cases of vertigo.
Neuroimaging can be of great value, however, especially when signs and symptoms point to a central cause of vestibular dysfunction. In general, MRI is the study of choice to detect acute cerebellar ischemia and can detect acute and chronic hemorrhage as well.8 Additionally, MRI with gadolinium contrast is used to diagnose vestibular schwannoma. MRI is warranted in patients with asymmetric hearing loss, vertical nystagmus, sudden onset of symptoms, focal neurologic deficits, or nonresponse to acute treatment given for peripheral vertigo. Routine MRI in the evaluation of dizziness is not recommended because abnormalities such as cerebral atrophy and white matter lesions are common in patients with and without vertigo.9
New technologies are gradually increasing the efficacy of the bedside examination of vertiginous patients by otolaryngologists. Electronystagmography (ENG) is done by placing electrodes around the patient's eyes, in both a horizontal and vertical axis, to record the corneal-retinal potential differences. The test measures eye movements in response to visual or vestibular stimuli and can be utilized to confirm diagnosis of BPPV, vestibular neuritis, or Meniere disease; it is usually the first objective vestibular test performed in patients with imbalance issues.
Caloric testing is performed by infusing warm or cold water into the ear. When the patient's head is tilted at 30 degrees and warm water is infused, the normal response is nystagmus toward the ear infused with water. When cold water is infused, the normal response is nystagmus away from the water-infused ear. Lack of response to warm or cold water on one side suggests disease on that side, usually peripheral lesions. Proper precaution should be taken prior to testing to rule out cerumen interference and/or tympanic membrane perforation.
Finally, clinical measurements of vestibular function can be obtained from myogenic potentials in response to air-conducted sound or bone-conducted vibration recorded by electromyogram (EMG) electrodes over contracted sternocleidomastoid muscles, called cervical vestibular evoked myogenic potentials (cVEMP). This test is performed with a loud sound delivered to one ear while muscular activity is recorded in the ipsilateral sternocleidomastoid muscle and is especially useful for detecting superior semicircular canal dehiscence syndrome, which will manifest as a VEMP with a reduced threshold.10
DIFFERENTIAL DIAGNOSIS
Peripheral causes of vertigo In benign paroxysmal positional vertigo, patients experience intense vertigo with head movement toward the affected ear and when looking upward, usually lasting for seconds.6 For this reason, the Dix-Hallpike maneuver is usually accurate in reproducing symptoms and causing nystagmus. BPPV is a clinical diagnosis and is usually idiopathic, but it can occur after head trauma or in association with other ear disorders, such as vestibular neuritis or labyrinthitis.11 Patients will usually report that reclining in bed, arising quickly, or even looking up provoke symptoms.11 The clinician should explain that although acute symptom relief may be achieved, the condition can become chronic.
Vestibular neuritis is characterized by intense vertigo lasting for a few days followed by disequilibrium and imbalance lasting for days to weeks.6 The unsteadiness is often incapacitating and is associated with nausea and vomiting. The condition is thought to be caused by inflammation due to a viral infection or vascular occlusion. Unlike with labyrinthitis, patients neither report nor have evidence of hearing loss.6 Results of cranial nerve, sensory-motor, and mental status tests are normal.
Labyrinthitis typically develops over a period of minutes to hours and may be associated with systemic, ear, or meningeal infection. Patients can have signs and symptoms of hearing loss unilaterally and may also give a history of a recent upper respiratory tract infection.12 If a patient has evidence of hearing loss on clinical examination, a formal audiogram is warranted.
Meniere disease is characterized by fluctuating low-frequency hearing loss on audiometric testing, episodic vertigo, aural fullness, and tinnitus.6 A distinctive feature is duration of vertigo, which typically lasts for hours and rarely lasts for more than a day.6 When episodes occur, they are usually severe and can cause nausea and vomiting.6 The cause is not completely understood, but theories suggest that viral infection, allergies, genetic factors, or trauma may cause excessive endolymph production or decreased absorption, which may elevate endolymph pressure.6 The increase in pressure can also cause a fluctuation of hearing loss, which can become severe.
Central causes of vertigoMigrainous vertigo, also known as migraine-associated dizziness, has a high prevalence in the general population and deserves appropriate consideration when formulating a differential diagnosis. Affected patients often have a bimodal distribution of duration of vertigo or disequilibrium, with most experiencing symptoms that last minutes to hours or all day and longer.13 The dizziness experienced is usually variable in relation to the headache.13 The migraine can also manifest with and without aura. Patients often need diagnostic tests, such as audiometry and MRI, to rule out competing diagnoses.13 Formal diagnostic criteria for migrainous vertigo have been proposed and include recurrent episodes of vertigo, a formal migraine diagnosis by International Headache Society criteria, a migraine symptom during the attack (headache, photophobia, or aura), and exclusion of other causes.14 The category of probable migrainous vertigo is used for patients with some elements in the presentation to suggest migraine but no other identifiable cause.14
Vestibular schwannoma, also known as acoustic neuroma, is a benign tumor of the cerebellopontine angle of the Schwann cell sheath of either the vestibular or cochlear nerve. An overwhelming number of affected patients seek medical attention because of unilateral hearing loss, either sudden or fluctuating. Others may present with dizziness or gait disturbance and, less commonly, vertigo.6 Additionally, patients may complain of aural fullness, headache, and/or facial numbness.
Cerebellar infarction usually manifests with sudden onset of symptoms and reaches maximal intensity at once. Cerebellar infarction is present in 3% of patients presenting with vertigo; and of these, only 10% lack focal neurologic deficits.14 Risk factors for cerebellar infarction include hypertension, coronary artery disease, diabetes, previous transient ischemic attack (TIA)/stroke, tobacco use, hypercholesterolemia, atrial fibrillation, and alcohol consumption.15 In addition to a complaint of dizziness, patients will present with severe ataxia evident as inability to walk without support and direction-changing nystagmus, also called multidirectional nystagmus or gaze-evoked nystagmus.14 In one population-based study, stroke/TIA was diagnosed in 3.2% (53 of 1,666) of patients with dizziness when only 0.7% (9 of 1,297) of those with isolated dizziness symptoms had had a stroke/TIA.15 The proportion of cerebrovascular events in patients presenting with dizziness, vertigo, or imbalance is very low, and isolated dizziness, vertigo, or imbalance strongly predicts a noncerebrovascular cause.15
Psychogenic dizziness is important to consider in patients whose vertigo does not fall into one particular category and in instances where other causes of vertigo have been excluded. In a study by Staab and Ruckenstein, 60% of patients who were referred for chronic dizziness of uncertain cause had a primary or secondary anxiety disorder.16
OVERVIEW OF MANAGEMENT
The scope of possible treatments for vertigo is broad and dependent on diagnosis; a comprehensive discussion is therefore outside the scope of this article. This section focuses on some helpful interventions for certain patients
in the acute phase of vertigo.
Vestibular suppressants and antiemetic drugs are considered the mainstay of acute vertigo treatment. Because there is no single effective medication for vertigo, a combination of an antihistamine and an antiemetic is commonly prescribed. Long-term use is not recommended.
Dietary changes have proven helpful in patients suspected of having Meniere disease. Salt restriction (1-2 grams of salt per day) and use of a mild diuretic, such as hydrochlorothiazide-triamterene (Dyazide, Maxzide, generics), is occasionally advised.17 This regimen may also reduce the frequency of attacks and slow down progression of hearing loss.17
Vestibular habituation or rehabilitation is a mainstay of nonpharmacologic treatment. In the 1940s, Cawthorne and Cooksey suggested that encouraging vertiginous patients to move their heads repeatedly to elicit vertigo would eventually alleviate it.18 These movements, today known as the Cawthorne-Cooksey exercises, consist of a series of eye, head, sitting, and standing movements that patients can do in the privacy of their homes under proper supervision. A study by Cohen and colleagues showed that after 6 weeks of repetitive head movements, subjects with chronic peripheral vestibular impairments improved on measures of balance, functional performance, and vertigo.18
Patients should know that there usually is not one treatment in particular that works for each person. They should also understand that vertigo is a symptom that sometimes requires evaluation over an extended period of time until an underlying etiology is found. Support groups can also be helpful in letting patients know they are not alone.
Finally, the clinician should refer the patient to a specialist when appropriate. If medication therapy has failed or an operable cause of vertigo is discovered, a timely referral can save a patient from a variety of adverse outcomes such as permanent hearing loss, frequent falls, or enlargement of potential tumor. JAAPA
Monica Furman practices in otolaryngology at NYU Medical Center in New York City and is a graduate of the Pace University-Lenox Hill Hospital PA program.
Denise Rizzolo is an assistant clinical professor at Pace University and an associate professor in the Seton Hall University PA program. The authors have indicated no relationships to disclose relating to the content of this article.
IMPORTANT NOTE: JAAPA CME activities consist of 2 articles. To obtain credit, you must also read
Using the new ACR criteria for early diagnosis of rheumatoid arthritis; the post-test will include questions related to both articles. AAPA Fellow members should complete and submit the post-test on the AAPA Web site by going to
www.aapa.org and searching for keyword
JAAPA post-tests. All others may complete and submit the post-test online at no charge at
www.mycme.com. To obtain 1 hour of AAPA Category I CME credit, PAs must receive a score of 70% or better on each test taken.
REFERENCES
1. Kuo C-H, Pang L, Chang R. Vertigo: part 1—assessment in general practice. Aus Fam Physician. 2008;37(5):341-347.
2. Neuhauser HK, Lempert T. Vertigo: epidemiologic aspects. Semin Neurol. 2009;29(5):473-481.
3. Newman-Toker DE, Cannon LM, Stofferahn ME, et al. Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting. Mayo Clin Proc. 2007;82(11):1329-1340.
4. Hanley K, O'Dowd T. Symptoms of vertigo in general practice: a prospective study of diagnosis. Br J Gen Pract. 2002;52(483):809-812.
5. Labuguen RL. Initial evaluation of vertigo. Am Fam Physician. 2006;73(2):244-251, 254.
6. Kutz JW Jr. The dizzy patient. Med Clin N Am. 2010;94(5):989-1002.
7. Newman-Toker DE, Kattah JC, Alvernia JE, et al. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008;70(24 pt 2):2378-2385.
8. Chalela JA, Kidwell CS, Nenwich LM, et al. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007;369(9558):293-298.
9. Colledge N, Lewis S, Mead G, et al. Magnetic resonance brain imaging in people with dizziness:
a comparison with non-dizzy people. J Neurol Neurosurg Psychiatry. 2002;72(5):587-589.
10. Iwasaki S, Smulders YE, Burgess AM, et al. Ocular vestibular evoked myogenic potentials to bone conducted vibration of the midline forehead at Fz in healthy subjects. Clin Neurophysiol. 2008;119(9):2135-2147.
11. White J, Savvides P, Cherian N, Oas J. Canalith repositioning for benign paroxysmal positional vertigo. Otol Neurotol. 2005;26(4):704-710.
12. Baloh RW. Clinical practice: vestibular neuritis. N Engl J Med. 2003;348(11):1027-1032.
13. Reploeg MD, Goebel JA. Migraine-associated dizziness: patient characteristics and management options. Otol Neurotol. 2002;23(3):364-371.
14. Nelson JA, Virre E. The clinical differentiation of cerebellar infarction from common vertigo syndromes. West J Emerg Med. 2009;10(4):273-277.
15. Kerber KA, Brown DL, Lisabeth LD, et al. Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population-based study. Stroke. 2006;37(10):
2484-2487.
16. Staab JP, Ruckenstein MJ. Expanding the differential diagnosis of chronic dizziness. Arch Otolaryngol Head Neck Surg. 2007;133(2):170-176.
17. Hain TC, Yacovino D. Pharmacologic treatment of persons with dizziness. Neurol Clin. 2005;
23(3):831-853.
18. Cohen HS, Kimball KT. Increased independence and decreased vertigo after vestibular rehabilitation. Otolaryngol Head Neck Surg. 2003;128(1):60-70.
IMPORTANT NOTE: JAAPA CME activities consist of 2 articles. To obtain credit, you must also read
Using the new ACR criteria for early diagnosis of rheumatoid arthritis; the post-test will include questions related to both articles. AAPA Fellow members should complete and submit the post-test on the AAPA Web site by going to
www.aapa.org and searching for keyword
JAAPA post-tests. All others may complete and submit the post-test online at no charge at
www.mycme.com. To obtain 1 hour of AAPA Category I CME credit, PAs must receive a score of 70% or better on each test taken.