DIZZINESS AND VERTIGO

DIZZINESS AND VERTIGO

  1. 1
    Current Diagnosis
    • Benign paroxysmal positional vertigo
      • Repeated, brief episodes lasting less than 1 minute
      • Triggered by changes in head position
      • Positive Dix-Hallpike maneuver
    • Vestibular neuritis
      • Single, severe, constant episode lasting days
      • Subacute onset
      • Positive head impulse test
      • Nystagmus is unilateral, horizontal, and spontaneous
    • Vestibular migraine
      • Recurrent episodes lasting hours
      • Associated with migraine headache
      • Responds to traditional migraine treatment
    • Ménière’s disease
      • Recurrent episodes of vertigo lasting hours
      • May have unilateral hearing loss, tinnitus, or ear fullness
    • Red flags for stroke include:
      • Sudden onset
      • Risk factors for stroke
      • Nystagmus with a central pattern
      • Negative head-thrust test
      • Additional neurologic signs
      • Inability to walk
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  2. 2
    Current Therapy
    • Benign paroxysmal positional vertigo
      • The canalith repositioning procedure (Epley maneuver) is the most effective treatment
      • Vestibular rehabilitation is effective
      • Consider observation with close follow-up if a patient will not tolerate the canalith repositioning procedure or if symptoms are mild
      • Avoid symptomatic medications
    • Vestibular neuritis
      • Brief symptomatic care with benzodiazepines, antiemetics, and antihistamines
      • Early vestibular rehabilitation speeds recovery
      • Use of corticosteroids is controversial

    The “dizzy” patient is often a frustrating phenomenon in clinical medicine. However, after a careful history and physical examination, most patients can be diagnosed and serious causes excluded.

    Peripheral causes of vertigo are usually benign, and include vestibular neuritis and benign paroxysmal positional vertigo (BPPV). Life- threatening central causes include stroke, vertebrobasilar, insufficiency, demyelinating disease, and an intracranial mass. The first step in evaluating vertigo is differentiating among the four types of dizziness: near syncope or light-headedness, disequilibrium, psychogenic dizziness, and true vertigo. True vertigo is a false sense of motion, and patients typically report that “the room is spinning.” This chapter will focus on the two most common causes of episodic vertigo: BPPV and vestibular neuritis.

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  3. 3
    Epidemiology

    Vertigo is a common office complaint. In fact, 7.5 million Americans are evaluated for dizziness in ambulatory care settings each year, and approximately 50% of these cases are vertigo. In primary care office setting, BPPV and vestibular neuritis account for the majority of vertigo diagnoses, followed by vestibular migraine, Ménière’s disease and vascular causes. BPPV is the most common vestibular disorder across the lifespan.

     

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  4. 4
    Risk Factors

    BPPV is seven times more likely in individuals over age 60, and it is also more common in women. A history of prior head trauma and other vestibular disorders places patients at risk for BPPV. There are no identified risk factors for vestibular neuritis.

     

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  5. 5
    Pathophysiology

    BPPV is thought to occur when calcium carbonate debris (otoconia) are dislodged and float freely in the semicircular canals of the inner ear. The posterior canal is most often involved. During head movement, loose otoconia move in the canal and cause a continued sense of motion for a few seconds until they settle. The pathophysiology of vestibular neuritis is uncertain. Evidence supports a viral infection, most likely HSV-1, which causes inflammation of the eighth cranial nerve. When hearing loss accompanies vertigo, the condition is called acute labrynthitis.

     

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  6. 6
    Clinical Manifestations

    The history and physical examination are fundamental in the evaluation of vertigo. Key questions include the frequency and duration of attacks, triggers such as positional or pressure changes, prior head trauma, associated neurologic symptoms, hearing loss, and headache. A personal history of diabetes, hypertension, and hyperlipidemia are risk factors for stroke. BPPV, stroke, and migraine can have a familial preponderance, and a family history of these disorders should be elicited. Many medications, including anticonvulsants and antihypertensives, cause dizziness.

    BPPV causes brief, recurrent episodes that last less than 1 minute and are brought on by changes in head movement or position. Nausea and vomiting may be associated. Vestibular neuritis usually has a subacute onset over several hours, peaks in intensity for 1 to 2 days, and then gradually subsides over the next few weeks. Symptoms of vertigo are constant, and nausea and vomiting can be severe during the first few days. Patients with vestibular neuritis may have difficulty standing and veer toward the affected side. Although changes in position worsen the vertigo in vestibular neuritis, vertigo is always present at baseline. In BPPV, patients are normal between attacks.

    General physical examination should include a thorough cardiovascular, ear, nose, throat, and neurologic examination. The neurologic examination can differentiate between benign (peripheral) and life-threatening (central) causes based on the ability to walk, type of nystagmus, results of the head-thrust test, and presence of associated neurologic signs (Table 1).

    Table 1

    Differentiating Peripheral and Central Causes of Vertigo

     

    Abbreviation: BPPV = benign paroxysmal positional  vertigo.

    Patients with vestibular neuritis may have difficulty walking, but the inability to walk is a red flag for a central lesion. Nystagmus is unidirectional (always beats in the same direction) and horizontal in vestibular neuritis, and is suppressed by visual fixation. Having a patient focus on an object in the room will stop the nystagmus, which reappears if a blank sheet of paper is placed a few inches in front of the patient’s face. Nystagmus in central causes is not suppressed by visual fixation, and may be direction-changing (nystagmus beats to the right when the patient looks right, and beats to the left when the patient looks left) or pure vertical. The head impulse test (Figure 1) is positive in peripheral causes like vestibular neuritis. The examiner holds the patient’s head while the patient fixes her eyes on the examiner’s nose, and then the examiner quickly moves the patient’s head 10 degrees to the right and left. If a saccade (the eyes look away and then re-fixate on the examiner’s nose) is found, this indicates a peripheral lesion on the side that the head is turned towards. Central lesions will not cause saccades and the head impulse test will be normal. HINTS (Head Impulse test, Nystagmus, Test of Skew) combines three physical examination findings which has been found to have a 97% sensitivity and 99% specificity for diagnosis, which is a central cause of vertigo in the acute setting. If any of the tests indicate a central cause, including a positive head impulse test, nystagmus that is bidirectional, purely vertical or purely torsional, and vertical eye misalignment, then the HINTS test is considered positive.

    FIGURE 1    Head impulse test. Top panel shows a positive  head-thrust test. The examiner moves the patient’s head quickly 10 degrees to the side, in this case to the patient’s left. A catch-up saccade is observed when the patient looks away and then refixes on the visual target, indicating a peripheral lesion on the left. Lower figure shows a normal head-thrust test. The patient maintains visual fixation during head movement. (Adapted from Seemungal BM, Bronstein AM. A practical approach to acute vertigo. Pract Neurol 2008; 8:211–21.)

    The Dix-Hallpike maneuver is diagnostic of posterior canal BPPV (Figure 2). The patient should be warned that nausea and vomiting may occur. After the patient is placed in the head-hanging position, there is a 5- to 20-second latency period before the nystagmus and symptoms appear. Both the nystagmus and vertigo will increase in severity and then resolve within 60 seconds. The nystagmus observed is up-beating and torsional. The maneuver should be repeated with the head held to the opposite side. The side that elicits the symptoms and nystagmus diagnoses BPPV in the ipsilateral ear. If both sides elicit symptoms, the patient may have bilateral BPPV. If the test is negative and BPPV is strongly suspected, the patient should lie supine and the examiner can turn the head to each side (supine roll test). This maneuver will cause symptoms and nystagmus in patients with horizontal canal BPPV.

    FIGURE 2    Treatment maneuver for posterior canal  benign paroxysmal positional vertigo affecting the right ear. To treat the left ear, the procedure is reversed. The drawing of the labyrinth in the center shows the position of the particle as it moves around the posterior semicircular canal (PSC) and into the utricle (UT). The patient is seated upright, with head facing the examiner, who is standing  on the right. A, The patient is rapidly moved to head-hanging right position (Dix-Hallpike test). This position is maintained until the nystagmus ceases. B, The examiner moves to the head of the table, repositioning hands as shown. C, The head is rotated quickly to the left with right ear upward. This position is maintained for 30 seconds. D, The patient rolls onto the left side while the examiner rapidly rotates the head leftward until the nose is directed toward the floor. This position is then held for 30 seconds. E, The patient is rapidly lifted into the sitting position, now facing left. The entire sequence should be repeated until no nystagmus can be elicited. After the maneuver, the patient is instructed to avoid head-hanging positions to prevent the particles from reentering  the posterior canal. (Reprinted with permission from Rakel RE. Conn’s Current Therapy 1995. Philadelphia, WB Saunders, 1995, p 839.)

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  7. 7
    Diagnosis

    BPPV and vestibular neuritis are diagnosed clinically. Further diagnostic testing is indicated if the diagnosis is uncertain or a central cause is suspected. Audiometry may be abnormal in Ménière’s disease. MRI is the best imaging test for central lesions because it includes the posterior fossa and is most sensitive for stroke. Vestibular function testing is useful if the diagnosis is unclear or in cases of refractory vertigo. Vestibular function testing includes several different specialized tests that evaluate the ocular and vestibular response to position changes and caloric stimulation. Video- oculographic recordings of nystagmus can magnify the eye and allow for repeated viewings for further study. Some patients with BPPV may have additional vestibular disorders causing vertigo that vestibular function testing can elucidate.

    Differential Diagnosis

    Ménière’s disease is suspected in patients with the triad of tinnitus, fluctuating hearing loss, and vertigo. Episodes usually last hours, are disabling, and are recurrent over years. Migrainous vertigo features episodes lasting hours to days in patients with other migraine symptoms such as headache, photophobia, phonophobia, or aura.

    Central lesions such as stroke, vertebrobasilar insufficiency, or intracranial mass are most concerning. Red flags for stroke include sudden onset, risk factors for stroke, associated neurologic signs, inability to walk, negative head-thrust test, severe associated headache, and characteristic nystagmus. Posttraumatic vertigo may occur in patients after head trauma who present with vertigo, tinnitus, and headache. A perilymphatic fistula is rare, but may be suspected in a patient with episodic vertigo after head trauma, heavy lifting, or barotrauma. Pressure changes with sneezing or coughing trigger vertigo attacks. Postural hypotension should be ruled out in all patients. An acoustic neuroma presents with slowly progressive, unilateral sensorineural hearing loss and tinnitus. Many patients may have an unsteady gait, but true vertigo is rare.

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  8. 8
    Treatment

    Posterior canal BPPV is best treated with the canalith repositioning procedure, also known as the Epley maneuver (Figure 2). Studies have shown the procedure is safe and effective with an odds ratio of 4.2 (95% CI. 2.3-11.4) for symptom resolution. Patients should be warned that nausea or vomiting may occur during the procedure, and may be pre-treated with an antiemetic medication. The procedure can be repeated if unsuccessful. Posttreatment activity restrictions are unnecessary. Horizontal canal BPPV can be treated with the barbeque roll maneuver. Vestibular rehabilitation is another valuable treatment for BPPV, but it is less effective than the canalith repositioning procedure. It enhances central compensation for peripheral deficits and leads to faster symptom recovery than observation alone, though most patients will improve spontaneously after 4 to 6 weeks.

    Observation is an option if symptoms are mild or if a patient will not tolerate the canalith repositioning procedure or vestibular rehabilitation. However, observation is associated with higher recurrence rates than the canalith repositioning procedure. Vestibular- suppressant medications such as antihistamines and benzodiazepines are discouraged because they interfere with central compensation and increase the risk for falling. Surgery is rarely needed for BPPV, but may be helpful in refractory cases.

    Vestibular neuritis is primarily treated with rest, vestibular suppressant medications, and vestibular rehabilitation. Patients may initially be admitted if symptoms, such as nausea and vomiting, are severe or if stroke is suspected. Treatment with antihistamines (dimenhydrinate [Dramamine]1 50 mg every 6 hours), antiemetics (promethazine [Phenergan]1 25 mg every 6 hours) or benzodiazepines (lorazepam [Ativan]1 1 to 2 mg every 4 hours) may be used to treat severe symptoms. However, these should not be continued for more than 2 to 3 days because they inhibit central compensation. The use of corticosteroids is controversial. Although studies show that

    vestibular-function testing improves more quickly in patients treated with corticosteroids, there is conflicting evidence that corticosteroids hasten the recovery of clinical signs and symptoms of vestibular neuritis. A 2011 Cochrane review concluded that there is insufficient evidence to recommend corticosteroids for the treatment of vestibular neuritis. Finally, antiviral medications have not been proven effective for vestibular neuritis.

    For patients with vestibular neuritis, vestibular rehabilitation should be started as soon as symptoms improve and a patient can tolerate the exercises. Exercises include balance and gait training as well as coordination of head and eye movements. Vestibular rehabilitation hastens recovery and improves balance, gait, and vision by increasing central compensation for vestibular dysfunction.

    Exercises may be home-based for compliant patients with mild symptoms, whereas formal referral may be more beneficial for patients with severe symptoms, or for the elderly.

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  9. 9
    MONITORING

    Patients diagnosed with BPPV should be reassessed in 1 month regardless of treatment. Failure to improve warrants further evaluation for other etiologies, including central causes. Similarly, patients with vestibular neuritis should slowly improve over several weeks, and failure to do so suggests alternative diagnoses.

     

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  10. 10
    Complications

    Patients with BPPV are at increased risk for falls. Thirty percent of elderly patients with BPPV have multiple falls in a year. Thus, patients should be assessed for fall risk, functional mobility, and balance. Home safety evaluation and home supervision should be considered. BPPV often recurs, with an estimated rate of 15% per year. Counseling patients about recurrence can lead to earlier recognition, earlier treatment and avoidance of falls. Patients with vestibular neuritis are at increased risk for BPPV and Ménière’s disease.

    Vestibular neuritis rarely recurs.

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  11. 11
    References

    Baloh R.W. Vestibular neuritis. N Engl J Med. 2003;348:1027– 1032.

    Bhattacharyya N., Baugh R.F., Orvida L., et al. Clinical practice guideline: Benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 2008;139:S47–S81.

    Chan Y. Differential diagnosis of dizziness. Otolaryngol Head Neck Surg. 2009;17:200–203.

    Epley J.M. The canalith repositioning procedure: For treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 1992;107:399–404.

    Fishman J.M., Burgess C., Waddell A. Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochran Database Syst Rev. 2011;5: CD008607. Review.

    Goudakos J.K., Konstantinos D.M., Franco-Vidal V., et al. Corticosteroids in the treatment of vestibular neuritis: A systematic review and meta-analysis. Otol Neurotol.

    2010;31:183–189.

    Hamid M. Medical management of common peripheral vestibular diseases. Curr Opin Otolaryngol Head Neck Surg. 2010;18:407–412.

    Hillier S.L., Holohan V. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2007;4: CD005397.

    Hilton M., Pinder D. The Epley (canalith repositioning) manoeuvere for benign paroxysmal positional vertigo. Cochrane Database Syst Rev. 2004;2: CD003162.

    Kerber K.A. Vertigo and dizziness in the emergency department.

    Emerg Med Clin North Am. 2009;27:39–50.

    Leveque M., Labrousse M., Siedermann L., et al. Surgical therapy in intractable benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 2007;136:693–698.

    Newman-Toker D.E., Kerber K.A., Hsieh Y.H., et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20(10):986–996.

    Seemungal B.M., Bronstein A.M. A practical approach to acute vertigo. Pract Neurol. 2008;8:211–221.

    1  Not FDA approved for this  indication.

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