INTRODUCTION — Vertigo is a symptom of illusory movement. Almost everyone has experienced vertigo as the transient spinning dizziness immediately after turning around rapidly several times. Vertigo can also be a sense of swaying or tilting. Some perceive self-motion, whereas others perceive motion of the environment. Vertigo is a symptom, not a diagnosis. It arises because of asymmetry in the vestibular system due to damage to or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures in the brainstem or cerebellum.
Vertigo is only one type of dizziness. Other disorders that present with dizziness include presyncopal faintness, disequilibrium, and nonspecific or ill-defined lightheadedness. The initial approach to the patient who complains of dizziness is to localize the cause of the symptom into one of these broad categories. (See "Approach to the patient with dizziness".)
The pathophysiology, etiology, and differential diagnosis of vertigo will be reviewed here. The clinical approach, diagnosis, and treatment of vertigo are discussed separately. (See "Evaluation of the patient with vertigo" and "Treatment of vertigo".)
PATHOPHYSIOLOGY — The end organs of the vestibular system, the semicircular canals and the otolith organs, sense angular and linear motion, respectively. As a result, a patient's description of a spinning sensation is likely to indicate an abnormality of the semicircular canals or the central nervous system structures that process signals from the semicircular canals. Similarly, an illusory sensation of floating or tilting may indicate an otolith system disorder.
Important to the pathogenesis of vertigo is the fact that there is a vestibular labyrinth on each side of the body. The central nervous system receives signals from both the right and left labyrinths and compares these signals with one another. When the head is still, tonic discharges in both right and left vestibular afferents are exactly balanced. During motion, the right and left labyrinths are excited or inhibited, leading to a left-right difference in eighth nerve activity, which is recognized as motion. The spurious left-right differences that result from an acute unilateral peripheral vestibular disorder are also interpreted by the central nervous system as motion or vertigo.
The central nervous system, at the brainstem level, processes visual motion in a manner similar to that of self-motion. This normal, physiologic aspect of the vestibular system underlies the experience of self-motion when viewing large-screen movies. This ambiguity between motion of self and motion of surround relates directly to the lack of uniformity in patients' complaints of vertigo as either self-motion or motion of the surroundings.
Information from the vestibular labyrinth is relayed via the vestibular portion of cranial nerve VIII to the brainstem vestibular nuclei and from there to the cerebellum, ocular motor nuclei, and spinal cord; there are also less well-defined cerebral projections [1]. Vestibuloocular connections are responsible for coordinated eye movements during head motion, while vestibulospinal pathways help maintain upright posture. Cerebellar connections help modulate these activities. (See "Overview of nystagmus", section on 'Basic clinical vestibular physiology'.)
PERIPHERAL ETIOLOGIES — It is customary to organize causes of vertigo into peripheral and central disorders (table 1). These have distinctive clinical features, but with some overlap. Peripheral causes of vertigo generally comprise 80 percent of cases; of these, benign paroxysmal positional vertigo (BPPV), vestibular neuritis, and Meniere disease are the most common [2].
The clinical features of the more common disorders are summarized in the table (table 2).
Benign paroxysmal positional vertigo — BPPV is probably the most commonly recognized cause of vertigo [3,4]. It is most commonly attributed to calcium debris within the posterior semicircular canal, known as canalithiasis.
Classically, patients describe a brief spinning sensation brought on when turning in bed or tilting the head backward to look up. The dizziness is quite brief, usually seconds, rarely minutes. It may be severe enough to halt activity for this duration. Patients may experience nausea but rarely vomit. Ear pain, hearing loss, and tinnitus are absent.
The diagnosis of BPPV is suggested by its historical description and confirmed by the Dix-Hallpike maneuver [5]. (See "Evaluation of the patient with vertigo", section on 'Dix-Hallpike maneuver'.)
The natural history of BPPV is one of repeated, brief vertiginous episodes that are predictably provoked and continue for weeks or months. Episodes may recur. BPPV is generally attributed to otolithic debris within a semicircular canal and can be treated by canalith repositioning maneuvers. (See "Benign paroxysmal positional vertigo".)
Rarely, patients presenting with positional vertigo have central nervous system abnormalities with a less favorable prognosis [6,7]. Usually, the symptoms are somewhat more prolonged. Patients with atypical positional vertigo or nystagmus who do not respond to treatment should undergo magnetic resonance imaging (MRI) of the brain to rule out a posterior fossa abnormality. (See "Benign paroxysmal positional vertigo".)
Vestibular neuritis — Vestibular neuritis, also known as vestibular neuronitis and labyrinthitis, is believed to be a viral or postviral inflammatory disorder, affecting the vestibular portion of the eighth cranial nerve.
Vestibular neuritis is characterized by the rapid onset of severe, persistent vertigo, nausea, vomiting, and gait instability [8]. Physical examination findings are consistent with an acute peripheral vestibular imbalance: spontaneous vestibular nystagmus, a positive head impulse (or head thrust) test (figure 1 and figure 2), and gait instability without a loss of the ability to ambulate. In pure vestibular neuritis, auditory function is preserved; when this syndrome is combined with unilateral hearing loss, it is called labyrinthitis.
A diagnosis of vestibular neuritis is usually based on clinical information. The clinical features of cerebellar hemorrhage or infarction may be similar to vestibular neuritis, and brain imaging is therefore often required to rule this out [3,9,10]. (See "Vestibular neuritis and labyrinthitis", section on 'Cerebellar hemorrhage or infarction'.)
Patients with vestibular neuritis generally suffer from severe vestibular symptoms for a few to several days, followed by a gradual diminution of symptoms and a return of equilibrium. Recovery may be improved with corticosteroid therapy. (See "Vestibular neuritis and labyrinthitis".)
Herpes zoster oticus — Often called the Ramsay Hunt syndrome, this syndrome is believed to represent activation of latent herpes zoster infection of the geniculate ganglion.
In addition to acute vertigo and/or hearing loss, ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal and auricle are typical features. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Ramsay Hunt syndrome (herpes zoster oticus)'.)
Therapy with corticosteroids or acyclovir should be considered, although these modalities are not of proven value [11]. Treatment of herpes zoster infection is discussed separately. (See "Treatment of herpes zoster in the immunocompetent host".)
Meniere disease — Meniere disease is a peripheral vestibular disorder attributed to excess endolymphatic fluid pressure, which causes episodic inner ear dysfunction. Issues related to Meniere disease are discussed in detail separately but will be briefly reviewed here. (See "Meniere disease: Evaluation, diagnosis, and management".)
Affected patients present with spontaneous episodic vertigo lasting for minutes to hours, usually associated with unilateral tinnitus, hearing loss, and ear fullness. The vertigo associated with Meniere disease is often severe and associated with nausea and vomiting and disabling imbalance. The disequilibrium may last for several days. Horizontal-torsional nystagmus is typically seen on examination during an attack.
The diagnosis of Meniere disease is suggested by the history [12]. A low-frequency sensorineural hearing loss on audiometry and a unilateral reduced vestibular response on electronystagmography help confirm the diagnosis.
Exacerbations of Meniere disease may last for months or years, during which time episodes can occur as frequently as every few days. The condition can go into remission spontaneously or with treatment, and it can recur.
Labyrinthine concussion — Labyrinthine concussion refers to traumatic peripheral vestibular injury following direct concussive head trauma [13,14]. This may also occur with abrupt changes of head motion not necessarily associated with impact. A more severe, direct injury to cochlear and/or vestibular structures usually occurs in the setting of transverse fractures of the temporal bone. Hemotympanum and sensorineural hearing loss often accompany vertigo in this setting.
Symptoms of vertigo, nausea and vomiting, and imbalance are maximal at onset and improve over days to months, depending on the severity of the injury. (See "Sequelae of mild traumatic brain injury", section on 'Posttraumatic vertigo and dizziness'.)
Perilymphatic fistula — This is an infrequent complication of head injury, barotrauma, or heavy lifting in which a fistula develops at the otic capsule, permitting a transfer of pressure changes to the macular and cupular receptors. This explains the clinical syndrome of episodic vertigo and/or hearing loss provoked by sneezing, lifting, straining, coughing, and loud sounds. The last, so-called Tullio phenomenon, occurs because sound-induced pressure waves are abnormally distributed through the inner ear.
Establishing a diagnosis is difficult, as clinical tests are insensitive [15]. Computed tomography (CT) scanning may show fluid in the region of the round window recess [16]. Treatment with bed rest, head elevation, and avoidance of straining is the first step; failure to resolve after several weeks of conservative therapy is an indication to consider a surgical patch [17,18]. Recurrences occur in 10 percent.
Semicircular canal dehiscence syndrome — In semicircular canal dehiscence syndrome, the bone overlying the superior aspect of the superior semicircular canal becomes thin or even absent, thereby allowing pressure to be transmitted to the inner ear [19]. Vertigo is provoked by coughing, sneezing, and Valsalva maneuver [19-22]. Patients may experience nausea and instability during brief episodes of vertigo.
Loud sound may also induce vertigo in this condition (Tullio phenomenon), as sound-induced pressure waves are abnormally distributed through the inner ear [19,23,24]. This phenomenon can be tested through a click-evoked vestibulocollic reflex (cervical vestibular evoked myogenic potential [cVEMP]), which is typically high magnitude and low threshold in patients compared with controls [22,25-27]. Cochlear hypersensitivity is another diagnostic indicator for this condition [28,29]. Some patients also have hearing loss, with air-bone gaps on audiometry [30]. One case report noted torsional pendular nystagmus that was synchronous with the palpated pulse and suppressed by Valsalva maneuver or lying supine [31].
While this condition is increasingly recognized, it may still be underdiagnosed. The diagnosis can be established with high-resolution CT of the temporal bone [32,33]. Some patients benefit by surgical repair of their anatomic deficit [22,27].
Vestibular paroxysmia — Vestibular paroxysmia refers to a syndrome of brief attacks of vertigo that last one to several seconds and recur several times a day. In some patients, attacks are unprovoked; in others, they are precipitated by head turn or other action [34]. Common features on evaluation include hyperventilation-induced nystagmus and mild vestibular impairment on caloric testing, as well as evidence of neurovascular compression on MRI [34,35]. A pathogenic role for neurovascular compression is disputed, as similar imaging findings have been described in asymptomatic individuals [35,36]. Carbamazepine or oxcarbazepine reportedly reduces the severity and frequency of symptoms, at least in some patients [34,37]. Surgical decompression has reportedly been effective for patients who are refractory to or cannot tolerate medical therapy [38].
Cogan syndrome — Cogan syndrome is an autoimmune condition that can cause interstitial keratitis and vestibuloauditory dysfunction.
Patients have Meniere-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, which is the perception of objects jiggling back and forth after abruptly turning the head to one side or the other. Caloric testing often reveals absent vestibular function.
Systemic steroids and other immunosuppressants may be required. This topic is discussed separately. (See "Cogan syndrome".)
Recurrent vestibulopathy — Recurrent vestibulopathy is a descriptive diagnosis used for patients who experience spontaneous episodes of vertigo unassociated with otologic complaints (ie, no hearing loss, tinnitus, or ear fullness, and unassociated with migrainous phenomena) [39]. Symptoms often include nausea, vomiting, and disequilibrium. Vertigo may occur infrequently, for example, every one to two years. Once vertigo is resolved, patients return to normal without sequelae.
The pathophysiology of recurrent vestibulopathy is uncertain. The condition is thought to represent a vestibular disorder of uncertain localization. Some cases appear to cluster in families [40]. This disorder may overlap with vestibular migraine.
Other disorders
Vestibular schwannoma (acoustic neuroma) — Because the tumor grows slowly, the subtle imbalances in vestibular input are compensated for by the central nervous system, and patients often do not experience significant vertigo. Imbalance or a vague feeling of swaying or tilting may be the only manifestations of vestibular injury. Unilateral hearing loss or tinnitus is more likely to bring the patient to medical attention. (See "Vestibular schwannoma (acoustic neuroma)".)
Aminoglycoside toxicity — Several aminoglycoside agents, notably gentamicin, are selectively vestibulotoxic, causing peripheral vestibular damage without affecting hearing, presumably by damaging the hair cells of the inner ear [41,42].
Because both vestibular end organs are equally affected, there is no right/left imbalance of vestibular input to the central nervous system, and, therefore, the patient does not experience vertigo. Patients may experience oscillopsia (to-and-fro illusion of environmental motion) with head movement, indicating a deficient vestibuloocular reflex. Bilateral vestibular loss is associated with abnormal head impulse testing (figure 1) in both horizontal directions, as well as reduced visual acuity during head shaking, and can be documented with both caloric and rotational testing [43]. Severe bilateral vestibular loss leads to chronic disequilibrium and oscillopsia [44]. (See "Pathogenesis and prevention of aminoglycoside nephrotoxicity and ototoxicity".)
Otitis media — Otitis media may be associated with vestibular symptoms [45]. Nonspecific dizziness is more common than vertigo; however, a serous or suppurative labyrinthitis may complicate otitis media, producing frank vertigo. Patients with acute bacterial labyrinthitis are quite ill with fever, hearing loss, and nausea and vomiting in addition to vertigo. Hospitalization and intravenous antibiotics are required. (See "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Balance and motor problems'.)
If tragal stimulation provokes dizziness in a patient with otitis, a CT scan of the temporal bone should be done to rule out a fistula of the bony labyrinth [46].
CENTRAL ETIOLOGIES — It is customary to organize causes of vertigo into peripheral and central disorders (table 1). These have distinctive clinical features, but with some overlap. Central causes of vertigo generally comprise 20 percent of cases; of these, vestibular migraine and vascular etiologies are the most common. Central vertigo can result from lesions affecting the brainstem and cerebellum. It is rare for vertigo to result from lesions affecting the vestibular cortex [47].
The clinical features of the more common disorders are summarized in the table (table 2).
Vestibular migraine — Migraine is increasingly recognized as a cause of recurrent vertigo. However, the mechanism whereby migraine causes vertigo is not understood.
Vestibular migraine may have both central and peripheral vestibular manifestations [48]. The severity of vertigo is variable. Its duration is also highly variable, with some patients complaining of fleeting, seconds-long symptoms, as is characteristic of benign paroxysmal positional vertigo (BPPV). Episodes lasting for several minutes to a few hours are more typical [49].
A diagnosis of vestibular migraine relies on historical information, in which at least some attacks of vertigo are associated with migraine headache or other migrainous phenomena (visual aura, photophobia, and phonophobia) [50]. Episodes of vestibular migraine generally occur spontaneously but, similar to migraine headache, can be triggered by certain foods, certain sensory stimuli, and certain situations.
A condition called benign recurrent vertigo of childhood is considered a childhood manifestation of migraine [51]. Many of these children go on to develop more typical migraine headache. (See "Vestibular migraine".)
Brainstem ischemia — Embolic, atherosclerotic occlusions of the vertebrobasilar arterial system will produce brainstem ischemia. While vertigo may dominate the clinical presentation, it is rarely the sole manifestation of brainstem ischemia. Nonetheless, a cerebrovascular origin of symptoms should be excluded in patients who present with vertigo if they have vascular risk factors, because of the relatively high risk of recurrent stroke, which may be mitigated by appropriate interventions [52].
TIA — While infarction produces sustained symptoms that improve over several days and weeks, transient ischemic attacks (TIA) involving the brainstem more usually last several minutes, perhaps hours. It is debated whether vertigo without brainstem symptoms can occur with vertebrobasilar ischemia; however, it seems reasonable to consider the diagnosis in older patients or those with vascular risk factors [53]. Magnetic resonance imaging (MRI) with diffusion-weighted imaging may be helpful, but its sensitivity is less than 50 percent; magnetic resonance angiography (MRA) may demonstrate arterial occlusive disease in the posterior circulation.
Rotational vertebral artery syndrome — The rotational vertebral artery syndrome (also called rotational vertebrobasilar insufficiency or bow hunter syndrome) refers to a rare but well-documented phenomenon of symptomatic vertebral artery compression by bony elements of the spine (usually at CI-C2) that occurs with physiologic head rotation. Most patients with this condition report vertigo or nonspecific dizziness with head turning. The diagnosis is made by vascular imaging that includes the neutral as well as the symptomatic position [54-59]. Degenerative bone disease as well as congenital foraminal narrowing can be causative; disease or hypoplasia of the noninvolved vertebral artery is usually described.
Many patients can be managed conservatively (eg, avoiding movements that precipitate symptoms), and some will remit without intervention [60]. Surgical decompression may be successful when conservative approaches fail [57-59]. Noninvasive interventions, such as traction and enhanced external counterpulsation (EECP), are under investigation.
Wallenberg syndrome — Wallenberg syndrome, or lateral medullary infarction, is associated with the acute onset of vertigo and disequilibrium. The blood supply to the lateral medulla is the posterior inferior cerebellar artery. Most patients with Wallenberg syndrome have an occlusion of the ipsilateral vertebral artery that gives rise to the posterior inferior cerebellar artery [61]. (See "Posterior circulation cerebrovascular syndromes", section on 'Lateral medullary infarction'.)
While vertigo often dominates the clinical presentation, examination usually uncovers other neurologic deficits: abnormal eye movements, an ipsilateral Horner syndrome, ipsilateral limb ataxia, and a dissociated sensory loss (loss of pain and temperature sensation on the ipsilateral face and contralateral trunk with preserved vibration and position sense). Hoarseness and dysphagia are often present.
Wallenberg syndrome usually occurs as a result of atherosclerotic or lipohyalinotic arterial occlusion, but it is also a common presentation for traumatic vertebral artery dissection. A history of neck injury or neck pain suggests the latter. The diagnosis of medullary infarction is established definitively with MRI. MRA of the head and neck should be performed as well to rule out arterial dissection. Patients usually recover their equilibrium after several months.
Other stroke syndromes
●Labyrinthine infarction may occur with occlusion of the internal auditory artery, a branch of the anterior inferior cerebellar artery (AICA). This is really a peripheral lesion of the vestibular system and is characterized by abrupt vertigo, hearing loss, and sometimes tinnitus.
●A more proximal occlusion of the AICA will also involve the lateral pons and cerebellar peduncle, causing gait and limb ataxia and facial paralysis in addition to vertigo and hearing loss.
●More restrictive brainstem infarctions have been described that affect isolated vestibular structures. Thus, their clinical manifestations are very similar to vestibular neuritis [62,63].
Cerebellar infarction and hemorrhage — A cerebellar hemorrhage or infarction may produce sudden, intense vertigo accompanied by nausea and vomiting. This syndrome may be clinically indistinguishable from vestibular neuritis at presentation (figure 2). Limb ataxia is helpful in suggesting cerebellar involvement but is often absent if the lesion is more medially or inferiorly placed [9].
In cerebellar lesions, the patient falls toward the side of the lesion, and nystagmus is more pronounced to the side of the lesion, while in labyrinthine disease or vestibular neuritis, the direction of falls (toward the lesion) and nystagmus (away from the lesion) are opposite. In general, gait is more impaired with acute cerebellar lesions than in vestibular neuritis. However, these caveats are often of limited value in clinical assessment, because it is often difficult to persuade patients with acute, severe vertigo to attempt to walk.
Cerebellar infarction and hemorrhage typically occur in older patients (>60 years) and in those who have risk factors, particularly hypertension and diabetes.
Neuroimaging may be required to exclude these disorders in patients presenting with acute sustained vertigo, in particular if the patient is older and/or has other vascular risk factors (figure 2) [10,64]. A computed tomography (CT) scan can exclude cerebellar hemorrhage and should be done urgently if MRI is not immediately available, as patients can deteriorate abruptly. A brain MRI is more sensitive for cerebellar infarction, especially in the acute setting.
Epileptic vertigo — Vertigo can be an ictal symptom in patients with focal epilepsy, but it is uncommon for seizures to manifest as isolated vertigo. In one systematic review, accompanying disturbances of consciousness and/or motor and sensory phenomena occurred in most patients with ictal vertigo [65]. In this same review, episodes were brief (less than a few minutes), localized electroencephalography (EEG) abnormalities in the temporal lobe were common, and most patients responded to antiseizure medication therapy. (See "Focal epilepsy: Causes and clinical features".)
Chiari malformation — A Chiari I malformation is a congenital anomaly in which the cerebellar tonsils extend below the foramen magnum. This is usually asymptomatic but may be associated with a constellation of neurologic deficits (headache or neck pain, weakness with long tract signs, dysphagia, and other lower cranial nerve impairments) [66,67]. Vertigo and gait imbalance are common complaints in symptomatic individuals and may represent cerebellar or brainstem pathology.
When present, vertigo is often positionally induced, particularly by neck extension, perhaps manifesting pressure on brainstem and cerebellar structures or their blood supply [66]. Vertiginous symptoms are generally mild and often resolve when the patient alters his or her head position. Downbeating nystagmus is often associated with this syndrome, but other patterns of central nystagmus may be seen as well. The diagnosis is confirmed with sagittal MRI.
Surgical decompression may be required to relieve symptoms and is usually successful [68,69].
Multiple sclerosis — Vertigo has been estimated to occur in 20 percent of patients with multiple sclerosis (MS), most commonly with plaques near the vestibular nuclei and in the root entry zone of cranial nerve VIII [66,70]. A syndrome similar to vestibular neuritis may occur, with acute sustained vertigo with peripheral characteristics. It may be associated with symptoms reflecting dysfunction of adjacent cranial nerves such as hyper- or hypoacusis, facial numbness, and diplopia.
Vertigo can also occur with plaques within the brachium conjunctivum and cerebellum [71]. This localization is more commonly associated with acute, sustained vertigo that has more central characteristics, as in cerebellar infarction.
The diagnosis is usually evident in patients with an established history of MS. When vertigo is the presenting symptom, the diagnosis requires a high degree of suspicion; suggestive features include a history of prior neurologic symptoms and abnormal findings on neurologic examination (eg, afferent pupillary defect, long tract signs). Demyelination should not be assumed to be the cause of vertigo in a patient with MS. One series noted that among 25 patients with MS complaining of vertigo, BPPV, not MS, was the underlying cause in more than half of patients [72].
Symptoms related to an MS flare last days to weeks. A short course of corticosteroids may shorten disabling attacks. (See "Manifestations of multiple sclerosis in adults".)
Episodic ataxia type 2 — Episodic ataxia type 2 (EA2) is an autosomal dominant condition caused by mutations in a brain-specific P/Q type calcium channel gene on chromosome 19 [73]. Attacks of severe vertigo, nausea and vomiting, and ataxia begin in childhood or early adult life. These can last a few hours or a few days. Gaze-evoked, rebound, or downbeat nystagmus may be evident not only during but also between attacks [74,75].
The attacks respond to acetazolamide in a dose of 250 to 750 mg/day [75]. (See "Overview of the hereditary ataxias", section on 'Episodic ataxias'.)
Disembarkment (mal de debarquement) syndrome — A perception of self-motion and imbalance is described by some individuals following exposure to passive motion. Water travel is the most usual trigger, but others (air or land travel, flight simulators, water beds) have been described [76,77]. There is often a latency of several minutes to an hour or two between return to solid ground and symptom onset. A history of motion sickness or seasickness during the initial exposure is present in some patients, but not the majority. The pathogenesis of this syndrome is not understood [78]. Motion sickness is described separately. (See "Motion sickness".)
Persons with this syndrome typically describe disequilibrium and a sense of swaying or rocking, or walking on uneven ground, rather than rotational vertigo. Patients are not nauseous, and physical examination is normal [77]. Some patients demonstrate postural instability [79]. Short durations, usually several minutes or a few hours, of these symptoms are common in sea travelers, but even a day or two of symptoms may be considered normal [78,80].
Uncommonly, cases of persistent and disabling symptoms lasting for weeks, months, or years are reported in individuals ages 15 to 77 years and demonstrate a female preponderance [76,77,81]. Reexposure to passive motion is typically associated with temporary mitigation of symptoms, but exacerbation afterward.
In addition to imbalance and a sense of motion, patients describe difficulty tolerating complex visual stimuli (eg, video games); they also report disabling cognitive difficulties and fatigue [76,77]. Many patients develop depression and anxiety. These are believed to be a reaction to symptoms, not a cause. However, psychiatric comorbidity may contribute to symptom refractoriness if not addressed [76].
Diagnostic criteria have been published by the Bárány Society [82]:
●Non-spinning vertigo characterized by an oscillatory perception (rocking, bobbing, or swaying) present continuously or for most of the day
●Onset within 48 hours after the end of exposure to passive motion
●Symptoms temporarily reduce with exposure to passive motion (eg, driving)
●Symptoms persist for more than 48 hours
Diagnostic testing is of limited utility. Vestibular tests are normal or nonspecifically abnormal, as are structural and functional neuroimaging studies [76,77].
Treatment options are limited. The longer symptoms persist, the less likely they are to remit [77]. Patients who recover from an episode may be susceptible to recurrences of increasing duration. Benzodiazepines can provide limited symptomatic relief; clonazepam 0.25 to 0.5 mg twice daily is most often used [76,81]. Higher doses are not likely to be more effective. Vestibular rehabilitation has not been reported to be helpful.
SUMMARY — Vertigo is a symptom of illusory movement. Vertigo is a symptom, not a diagnosis.
●Vertigo arises because of asymmetry in the vestibular system due to damage to or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures in the brainstem. (See 'Pathophysiology' above.)
●Vertigo is only one type of dizziness. Other types of dizziness include presyncopal faintness, disequilibrium, and nonspecific or ill-defined lightheadedness. (See "Approach to the patient with dizziness".)
●It is customary to organize causes of vertigo into peripheral and central disorders (table 1). These have distinctive clinical features, but with some overlap. Peripheral causes of vertigo generally comprise 80 percent of cases; of these, benign paroxysmal positional vertigo (BPPV), vestibular neuritis, and Meniere disease are the most common. (See 'Peripheral etiologies' above and 'Central etiologies' above.)
●The clinical features of the more common disorders are summarized in the table (table 2). (See 'Peripheral etiologies' above and 'Central etiologies' above.)
