Peripheral vertigo produces an intense sensation of spinning or hurtling toward the ground or surrounding walls of abrupt onset. It is worsened by rapid movement and by changes in head position and is frequently associated with nausea, vomiting, diaphoresis, bradycardia, and hypotension.
BENIGN PAROXYSMAL POSITIONAL VERTIGO
BPPV is a mechanical disorder of the inner ear causing transient vertigo (with autonomic symptoms) and associated nystagmus that is precipitated by certain head movements. The lifetime prevalence of BPPV is 2.4% with a 1-year incidence of 0.6%, with women and patients over the age of 50 more likely to be affected. The mean duration of an episode is 2 weeks; 86% of patients affected seek medical attention.20
BPPV is believed to be caused by inappropriate activation of a semicircular canal, typically the posterior semicircular canal and typically unilateral, by the presence of free-floating particles or otoconia. The otoconia become displaced from the utricular macula by aging, head trauma, or labyrinthine disease. The particles tend to clump in the long arm of the posterior semicircular canal of the endolymph system. Once the clump reaches sufficient mass, changes in head position cause gravitation of the particles, which creates a plunger effect on the endolymph, causing the cupula to be displaced. This results in inadvertent neural firing, causing both vertigo and nystagmus.
The onset of BPPV is sudden and is precipitated by rolling over in bed, lying supine, leaning forward, looking up at the sky or ceiling, or turning the head. Because the symptoms fatigue, they tend to be worse in the morning. Patients may eliminate the offending activities. There is no associated hearing loss or tinnitus and no physical findings on examination of the external auditory canal.
Several findings support a diagnosis of BPPV (Table 170–6). There is a latency period of 1 to 5 seconds between assuming the offending head position and onset of vertigo and nystagmus. Both the vertigo and nystagmus crescendo to a peak of intensity and then subside within 5 to 40 seconds. Unlike vestibular neuronitis, the head thrust test in BPPV is normal and there is no spontaneous nystagmus. The Romberg test is negative, and the gait is normal. Posterior canal BPPV can be diagnosed using the Dix-Hallpike test (see "Physical Examination" section).15 Symptoms disappear with repeated testing. The supine roll test (Pagnini-McClure test21) for horizontal canal BPPV is done as follows: place the patient supine, turn the head to the right and observe for nystagmus, and then turn the head back to neutral position. Repeat by turning the head to the left. The side with the most prominent nystagmus is the side of the affected canal.
Supportive Findings in Benign Paroxysmal Positional Vertigo
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Supportive Findings in Benign Paroxysmal Positional Vertigo
Latency period of <30 s between the provocative head position and onset of nystagmus.
The intensity of nystagmus increases to a peak before slowly resolving.
Duration of vertigo and nystagmus ranges from 5–40 s.
If nystagmus is produced in one direction by placing the head down, then the nystagmus reverses direction when the head is returned to the sitting position.
Repeated head positioning causes both the vertigo and accompanying nystagmus to fatigue and subside.
BPPV involving the anterior semicircular canal is rare, and the Dix-Hallpike maneuver may elicit downbeating nystagmus with the affected ear up. However, any downbeating nystagmus should raise strong suspicion for a cerebellar or brainstem lesion (Table 170–7).21 Patients with isolated BPPV often undergo many tests with little or no diagnostic yield.22
Benign Paroxysmal Positional Vertigo (BPPV)
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Benign Paroxysmal Positional Vertigo (BPPV)
|Canal Affected by BPPV ||Frequency (%) ||Diagnostic Maneuver ||Nystagmus (direction named by fast component)|
|Posterior ||85 ||Dix-Hallpike, affected ear down ||Upbeat, affected ear down |
|Horizontal ||10–17 ||Supine roll test (Pagnini-McClure test) ||Horizontal, changes direction when head is turned to right or left while supine |
|Anterior ||1 ||Dix-Hallpike, affected ear up ||Downbeating, great concern for brainstem or cerebellar lesions |
Perform the particle-repositioning maneuver (or Epley maneuver) for patients with posterior canal BPPV in the ED.23 This maneuver uses gravity to induce the particles to move along the semicircular canals until they end up inside the utricle where unlikely to cause vertigo. It is indicated in patients with suspected BPPV plus a positive Dix-Hallpike test (Figure 170–3). Do not perform these maneuvers in patients with neck or cervical spine abnormalities, or if carotid or vertebral dissection is suspected.
A through C. Dix-Hallpike position test; D, E. Epley Maneuver. Turn onto unaffected side. Hold position for 60 secs.
The affected ear is determined by the side of the positive Dix-Hallpike position test. Antihistamines or antiemetics administered before the maneuver may improve patient comfort. Seat the patient in the Dix-Hallpike position test, and turn the head 45 degrees toward the affected ear. Gently bring the patient to the recumbent position with the head hanging roughly 20 degrees below the examining table. Gently rotate the head 45 degrees to the midline. Then rotate the head a further 45 degrees to the unaffected side. The patient rolls onto the shoulder of the unaffected side, at the same time rotating the head a further 45 degrees. Return the patient to the sitting position and return the head to the midline. Wait 5 minutes after each portion of the maneuver to permit the particles to traverse their intended course. Observe for nystagmus in the same direction as during Dix-Hallpike testing. Nystagmus in the opposite direction suggests the particles have moved back toward the cupula; this portends an unsuccessful maneuver. Repeat the maneuver until both the vertigo and the accompanying nystagmus have disappeared. A home treatment device has been found to enable patients with an established diagnosis of BPPV to perform the maneuver themselves safely and effectively.24
While the Epley maneuver is safe and effective for posterior canal BPPV, relapses are common. Adverse effects include light-headedness and exacerbation of vertigo.
Most episodes of BPPV resolve spontaneously after a few days. Refer patients with persistent symptoms to an otolaryngologist.
Ménière's syndrome is a disorder associated with an increased endolymph within the cochlea and labyrinth. It tends to occur in older men and women with equal prevalence. The disease is usually unilateral but may become bilateral over time. The precise pathogenesis is unknown, but evidence suggests that patients have difficulty regulating the volume, flow, and composition of endolymph. The onset is usually sudden, with associated nausea, vomiting, and diaphoresis, with attacks lasting from 20 minutes to 12 hours. The frequency of attacks varies from several times per week to several times per month. Other associated symptoms include tinnitus, diminished hearing, and fullness in one ear. Between attacks, the patient is usually well, although decreased hearing may persist.
Ménière's syndrome is managed symptomatically with antihistamines and betahistine; combination therapy with triamterene and hydrochlorothiazide is also recommended in confirmed cases. Ménière's syndrome is the only condition for which betahistine has proven efficacy. A high-dose regimen of at least 48 milligrams three times daily has been shown to provide long-term prophylaxis.25 Calcium channel blockers may also be used (Table 170–5). None of these drug treatments improves hearing. Intratympanic gentamicin administration may provide significant immediate and long-term relief.26 Refer patients for treatment to an otolaryngologist. Attacks of vertigo are generally controllable, but tinnitus and hearing loss tend to be unresponsive to therapy.27
A perilymph fistula is an opening in the round or oval window that permits pneumatic changes in the middle ear to be transmitted to the vestibular apparatus. Trauma, infection, or a sudden change in the pressure inside the ventricular system may cause the tear. The diagnosis is suggested by the sudden onset of vertigo associated with flying, scuba diving, severe straining, heavy lifting, coughing, or sneezing. Associated symptoms may include hearing loss. The diagnosis is confirmed by nystagmus elicited by pneumatic otoscopy (Hennebert sign).
Perilymph fistula is managed with symptomatic treatment and bed rest and referral to an ear, nose, and throat specialist for surgical repair (emergent referral for patients with acute associated hearing loss).
Vestibular neuronitis, a disorder of suspected viral etiology, is the second most common cause of peripheral vertigo. Unlike BPPV and Ménière's syndrome, vestibular neuronitis typically lasts several days and does not recur. The onset is sudden, often with a current or recent viral illness. Intense vertigo may require bedrest for several days. Unilateral loss of hearing and tinnitus may occur. Positive findings on physical examination include positive head thrust and horizontal or mild torsional nystagmus. The Romberg test is negative; however, the gait tends to be slow, cautious, and widely based. The condition remits spontaneously with no recurrence. Treatment is symptomatic. Both methylprednisolone and valacyclovir have been recommended, but there is insufficient evidence that these agents enhance recovery.28
Vestibular ganglionitis is believed to be caused by a neurotrophic virus such as varicella zoster reactivated years following initial infection. Herpes zoster oticus, also known as the Ramsay Hunt syndrome, is a neuropathic disorder thought to be associated with vestibular ganglionitis. It is characterized by deafness, vertigo, and facial nerve palsy. The diagnosis is confirmed by the presence of grouped vesicles on an erythematous base inside the external auditory canal. Treat this disorder with antiviral therapy started within 72 hours of the appearance of vesicles along with symptomatic treatments.
Labyrinthitis, an infection of the labyrinth, causes peripheral vertigo associated with hearing loss. Viral labyrinthitis (associated with measles and mumps) has a course that is similar to vestibular neuronitis. Serous labyrinthitis occasionally causes vertigo.
Bacterial labyrinthitis may be a sequela of otitis media, in which bacteria and toxins diffuse across the membrane of the round window. Possible antecedents for bacterial labyrinthitis include otitis media with fistula, meningitis, mastoiditis, cholesteatoma, and dermoid tumor. The hallmarks of this disease include sudden onset of vertigo with associated hearing loss and middle ear findings.
Patients with bacterial labyrinthitis are at risk for meningitis and require antibiotics and referral to an ear, nose, and throat specialist for admission and possible surgical drainage.
Various drugs have been found to be ototoxic (Table 170–8).29 Aminoglycoside antibiotics produce hearing loss and peripheral vestibular dysfunction by accumulating inside the endolymph, causing the death of cochlear and vestibular hair cells. However, because both inner ears are affected, vertigo is uncommon. Clinical manifestations include ataxia and oscillopsia (defined as the inability to maintain visual fixation while moving). The damage is usually irreversible but is dose- and duration-dependent. Loop diuretics (furosemide and ethacrynic acid) also cause irreversible vestibular toxicity and ototoxicity. N-Acetylcysteine administered orally may help prevent aminoglycoside-induced ototoxicity in hemodialysis patients.30 Cytotoxic agents such as vinblastine and cisplatin cause vestibular damage; however, newer platinums, such as carboplatin, are less likely to do so. The antiarrhythmic drug quinidine and antimalarial drugs derived from quinine, such as chloroquine and mefloquine, also can cause vestibular symptoms that may be irreversible.
Ototoxic and Vestibulotoxic Agents
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Ototoxic and Vestibulotoxic Agents
|Agent ||Dose Dependent ||Reversible |
|Aminoglycosides ||Yes ||Usually not; possible improvement with N-acetylcysteine |
|Erythromycin ||No ||Yes |
|Minocycline ||No ||Yes |
|Fluoroquinolones ||No ||Yes |
|Nonsteroidal anti-inflammatory drugs; salicylates ||Yes ||Yes |
|Loop diuretics ||No ||Can be irreversible |
|Cytostatic drugs ||Yes ||No |
|Antimalarials ||No ||Yes |
|Anticonvulsants ||Yes ||Yes |
Reversible causes of vestibular damage and ototoxicity include nonsteroidal anti-inflammatory drugs, salicylates, minocycline, erythromycin, and some fluoroquinolones. Isolated cases of unsteady gait have been observed with antiviral drugs such as abacavir as well as antiparasitic agents. Solvents and other chemicals such as propylene glycol, toluene, mercury, and hydrocarbons can cause both peripheral and central vestibular symptoms.
Drugs that sometimes induce a central vestibular syndrome include tricyclic antidepressants, neuroleptics, opiates, and alcohol. Anticonvulsants cause dizziness and ataxia, especially in older patients. Lamotrigine may cause less dizziness.31 Phenytoin, toluene, and cancer chemotherapy agents can cause irreversible cerebellar toxicity. Phencyclidine is a recreational drug that causes central vestibular symptoms, including nystagmus and ataxia.
In general, most patients adapt to chronic vertigo by relying on intact proprioception and vision. However, benzodiazepines and neuroleptics that are often used as antivertigo therapy may exacerbate symptoms by delaying or inhibiting such compensation. Thus, avoid using this therapy on a long-term basis. Refer patients with suspected ototoxicity to an otolaryngologist.
EIGHTH NERVE LESIONS AND CEREBELLOPONTINE ANGLE TUMORS
Lesions of the eighth cranial nerve such as meningiomas and acoustic schwannomas may produce mild vertigo. The onset is usually gradual and remains constant until central compensation takes place. Hearing loss usually precedes the vertigo. Tumors of the cerebellopontine angle such as acoustic neuromas, meningiomas, and dermoids may also cause vertigo. These usually present with deafness and ataxia, as well as ipsilateral facial weakness, loss of the corneal reflex, and cerebellar signs. All such patients require urgent diagnostic imaging as well as referral to a neurosurgeon.
Acute posttraumatic vertigo and unsteady gait are caused by a direct injury to the labyrinthine membranes. The onset of vertigo is immediate and is accompanied by nausea and vomiting. There may be a concomitant fracture of the temporal bone. Vertigo associated with a closed head injury warrants CT or MRI to exclude an intracranial hemorrhage. Vertigo due to direct labyrinthine trauma tends to resolve within several weeks. Closed head trauma also can displace otoconia from the utricular maculae, precipitating an attack of BPPV. Postconcussive syndrome can be associated with unsteadiness of gait and a vague sense of dizziness. These patients may be treated symptomatically, with referral to a specialist if symptoms fail to resolve.
VERTIGO AFTER COCHLEAR IMPLANTATION
Vertigo is a well-known complication of cochlear implantation. The etiology is likely multifactorial and includes the dislodging of otoconia and the introduction of bone dust into the labyrinth.32