Associated Articles

"Vertigo—a type of dizziness"

American Family Physician, March 15, 2005
What is vertigo?

Vertigo is a type of dizziness. If you have vertigo, you may feel like you are moving or spinning. It is not the same as feeling like you are off balance or about to faint.

What causes vertigo?

Vertigo has many causes. You may have this type of dizziness because you have small calcium deposits in your inner ear. You may have vertigo because of swelling or fluid in your inner ear. Vertigo may happen if you have migraine headaches or an anxiety disorder. Rarely, vertigo is caused by poor blood flow or a tumor.

How can my doctor tell what is causing my vertigo?

Your doctor will ask how long your dizziness lasts and if you have any other symptoms.

Your doctor also may do a test. For this test, your doctor will turn your head to the right and then support your head as you lie back quickly on the exam table, ending with your head hanging off the table. The doctor will do the test again with your head turned to the left.

Patients with vertigo usually do not need to have costly tests. Some patients may need hearing tests or brain imaging.

COPYRIGHT 2005 American Academy of Family Physicians
COPYRIGHT 2005 Gale Group

"Post-Traumatic Vertigo"

Medicine and Health Rhode Island, Oct 2004 by Friedman, Jules M

The incidence of dizziness and dysequilibrium following head and/or neck injury lies between 40-60%, even following mild or moderate head injuries not requiring acute hospitalization. Accordingly, most practitioners should have a fairly extensive experience with this large outpatient group. Yet, in spite of their familiarity with this common problem, many clinicians routinely use a diagnostic approach which is not pathophysiologically based and a treatment approach which is often confined to attempts at providing symptomatic relief with vestibular suppressants. Indeed, the tendency to attribute most post-traumatic dizziness to the post-concussion syndrome without diagnostic consideration of specific vestibular pathologies has been the cause of a significant and largely unnecessary increase in morbidity in this population. What follows is a review of those specific pathologies which, taken together, cause the great proportion of post-traumatic symptoms and which should rightly form the basis for a diagnostic and management approach.


Fractures of the temporal bone occur in the more severe cases of head injury and have a number of clinical and radiological manifestations. They represent what should be an easily identifiable subgroup of head trauma patients discharged from acute hospitals in whom residual vestibular and/or auditory system symptoms can be expected to occur in high incidence (upwards of 95% in certain types of fractures). These symptoms commonly persist well beyond the period of acute hospitalization, and as such will most often require active (and possibly long-term) management by outpatient primary and specialty caregivers.1

Basal skull fractures may be of two kinds depending upon the relationship of the fracture line to the long axis of the petrous bone. These fractures can be well demonstrated on thin section temporal bone CT. Eighty percent are longitudinal and twenty percent are transverse. As longitudinal fractures run thru the axis of the middle ear, they often produce tympanic membrane tears with otorrhagia, and conductive or mixed hearing loss. They also can cause facial palsies. Given that the fracture line does not directly involve the inner ear, vestibular symptoms are somewhat less common in this type of fracture, but they can often occur due to concurrent labyrinthine concussion, perilymphatic fistula, or benign paroxysmal positional vertigo (see below). Transverse fractures extend thru the inner ear and produce damage to cochlear and/or vestibular labyrinthine neural structures directly with or without hemorrhage. They often produce hemotympanum and sensorineural hearing loss, and less commonly facial palsies. They also can be complicated by CSF leak and/or meningitis. Vestibular symptoms consist acutely of severe vertigo and ataxia (and possibly vegetative symptoms), which progressively improves due to CNS compensation, but in most cases persists to some degree well into the outpatient course. The nature of these persistent vestibular symptoms depends also upon the possible concurrent presence of a perilymphatic fistula, BPPV or the development of delayed hydrops (see below).

Successful outpatient management of the post-traumatic vertigo in this group of patients involves judicious restraint in the use of symptomatic treatment with vestibular suppressants (so as not to interfere with the development of CNS compensation), early resort to vestibular rehabilitation as the mainstay of treatment, and vigilance in detecting the concurrent existence or development of BPPV, perilymphatic fistula or delayed hydrops. Ongoing follow-up, including serial exams and timely utilization of vestibular laboratory diagnostic studies should be routine in patients not demonstrating progressive, if not rapid, recovery.

In spite of all such efforts, however, a small but significant percentage of patients with uncomplicated temporal bone fracture (estimates vary from 10-30% depending upon severity criteria) will remain with some degree of vestibular symptomatology indefinitely due to incomplete CNS compensation. This is the likely prognosis for those patients whose recovery during vestibular rehabilitation plateaus for two months in the absence of any other concurrent treatable vestibular post-traumatic pathology. In such cases, liberal use of vestibular suppressants long term remains the only option.


Blunt head injury can concuss the membranous labyrinth against the otic capsule (much as the brain is concussed against the skull in cerebral concussion). This results in acute hypofunction of some portion of the vestibular neural substrate within the affected labyrinth. As labyrinthine concussions and transverse temporal bone fractures both produce acute unilateral (or asymmetrical) vestibular hypofunction, their clinical manifestations and course are much the same. There is the acute onset of vertigo and ataxia whose severity is proportional to the degree of hypofunction and there is some variable degree of associated vegetative symptomatology. Symptoms are most severe at the time of the head injury and invariably improve but with a temporal profile which can vary from days to months, with a minority of patients having some degree of residual symptomatolgy which persists indefinitely. There are, however, some differences which can be seen between labyrinthine concussions and fractures. Concussions are somewhat more likely to produce reversible neural insults which can result in a very abbreviated course of recovery. They are less likely to produce associated perilymphatic fistulas and to lead to the development of delayed hydrops, but are more likely to be associated with coexistent BPPV (perhaps because fractures more often result in complete ablation of all vestibular function), and hearing loss is a less common accompaniment. Although radiological confirmation of involvement of vestibular structures is necessarily absent in uncomplicated concussions, several types of vestibular diagnostic studies are now available to confirm and quantify the severity of these lesions and even to measure the degree of CNS compensation. Outpatient management considerations are otherwise the same for labyrinthine concussions as described above for fractures.


Because BPPV is the most common cause of vertigo in general and of post-traumatic vertigo in particular, clinicians need to be well versed in its varied clinical presentations and their treatment options.

Canalolithiasis and Cupulolithiasis are the underlying mechanisms of BPPV In either case, otoconia are displaced from an injured uticular membrane into one of the semicircular canals. Even relatively mild blunt head trauma can provide enough shearing force to the utricular membrane to displace critical numbers of otoconia. There is also much anecdotal evidence that the acceleration-deceleration forces produced in whiplash injuries even without head injury may also suffice to produce such displacements. Because the posterior canal is situated directly inferior to the utricule when the head is upright, the otoconia settle into that canal in 90+ % of cases, but the lateral (5-8%) or the anterior canal (1-3%) can be sites of deposition as well.2

In Canalolithiasis - the most common cause of BPPV- the calcium carbonate crystals that compose the individual otoconia tend to form clumps that are free to move within the lumen of the involved canal. Changes in head position - especially in the axis of the canal - cause a displacement of the otoconial plug which in turn causes a displacement of the cupula. This produces a brief paroxysm of vertigo, nystagmus and ataxia. These paroxysms of positional vertigo continue to occur until a critical portion of the otoconial mass moves back out of the canal. This egress can eventually occur as a result of the random head movements characteristic of unrestrained daily activities or much more rapidly with more purposeful head positionings performed as part of the treatment regimen (see below). However, a damaged utricular membrane may contain numbers of less than adequately adherent otoconia which will provide a source of future displacements causing a potential for recurrences. Indeed, recurrences occur in 30% of cases of BPPV within the first year and 50% within five years.

BPPV as a cause of post-traumatic vertigo can be a straightforward diagnosis in many but not all cases. It often presents with the classical history of isolated paroxysms of positional vertigo and the equally classical paroxysmal positional nystagmus can be documented with Dix-Hallpike positional testing. However, there are many instances, in which the presentation and course can be confusing. One or more types of post-traumatic vestibular pathology can coexist. For example, if BPPV and labyrinthine concussion are both present (a fairly common event), the paroxysms of positional vertigo may be less evident in the context of the ongoing symptoms of motioninduced dizziness commonly seen as a result of the resolving effects of the concussion alone. If the BPPV is not recognized, then delayed or limited recovery will be unnecessarily attributed to a refractory case of concussion. Further complicating management, there may be a hiatus between the time of injury and the onset of BPPV. This is postulated to be due to the time required for partially displaced crystals to work loose, enter the affected canal and coalesce into a critical mass. This delay in onset of symptoms can certainly be weeks and may be months. Thus, ongoing follow-up and re-examination/retesting is especially necessary in patients who experience unexplained setbacks or refractory courses.

Recognition of BPPV as the sole or contributing cause of post-traumatic vertigo opens up the opportunity for treatment which is most often easily effected and rapidly successful. Canalith Repositioning Maneuvers (Epley/modified Epley Maneuvers) have success rates reported to be between 80-95% following one to three repetitions (with occasional cases requiring several more). Abrupt cessation of all symptoms is common, but other possible outcomes result in residual symptoms which give the appearance of failure but which can often be easily treated if recognized. In this regard, one must note that many patients will experience residual lightheadedness, motion sensitivity and dysequilibrium following an essentially successful maneuver which will clear following a short course of habituation/balance retraining exercises. These patients can be distinguished by the absence of positional nystagmus on retesting. In some cases, both ears are involved and must be treated sequentially. Additionally, care must be taken to distinguish lateral canalolithiasis or anterior canalolithiasis from the much more common posterior canal variant.3 Further, in what may be upwards of 5-10% of cases, Epley maneuvers can actually displace the otoconial plug from the posterior into the horizontal or the anterior canal/' These variants are a potential cause for confusion unless one recognizes the very different type of positional nystagmus produced by each of the three types of canalolithiasis. Because specific maneuvers are required for these respective variants, failure to determine that one is present in a given case will inevitably lead to treatment failure.

Cupulolithiasis represents a much less common mechanism for BPPV, and is another potential cause for treatment failure if not recognized. In these cases, the otoconia adhere to the gelatinous cupula rather than remaining free within the lumen of the canal. Once again, the pattern of positional nystagmus is different. As all Epleybased maneuvers are designed to roll the loose plug of otoconia out of the canal, they are unhelpful in cases of cupulolithiasis. Liberatory maneuvers-maneuvers that utilize rapid, high amplitude head accelerations-are necessary to loosen the otoconia from the cupula.

Those responsible for the outpatient management of patients with post-traumatic BPPV must keep in mind the above considerations. Epley maneuvers can easily be performed in the office setting. Success rates of 80-90% should be routinely expected. These are cases in which vestibular suppressants have a minimal role (confined to providing tolerance for maneuvers and/or exercises). Persistence of symptoms demands further exploration of pathogenesis and/or utilization of more appropriate vestibular rehabilitation techniques.

In 1% of cases or less, surgical intervention is warranted. Posterior canal plugging is a relatively effective and safe procedure which "dams off" the cupula from exposure to the otoconial plugs in the canal.5 Singulectomy is a procedure which deafferents the cupula in the posterior canal alone, and is less commonly performed.


Blunt head trauma with or without temporal bone fracture can cause rupture of the oval or round windows which separate the perilymphatic space from the middle ear. This can produce a variety of symptoms of vestibular and/or cochlear dysfunction. Unfortunately, most of these clinical presentations mimic closely those of other post-traumatic vestibular syndromes.

Patients with PLF can present with sudden unilateral sensorineural hearing loss (with or without tinnitus and aural blockage) and /or acute onset of persistent, gradually diminishing vertigo and ataxia which is indistinguishable from the clinical picture of temporal bone fracture or inner ear concussion. PLF has also been reported to produce positional vertigo which can be strikingly paroxysmal by history - although reports of positional nystagmus typical of BPPV are hard to substantiate as unrelated to coexistent canalolithiasis. PLF often produces paroxysms of spontaneous vertigo and/ or fluctuations in hearing loss, much as in endolymphatic hydrops (although the latter would more likely be of delayed onset when seen post-traumatically). PLF can produce sound-induced vestibular symptoms (Tullio phenomenon) as well as pressure-induced vestibular symptoms including vertigo, oscillopsia and ataxia. Patients often report that the latter symptoms occur during activities that effectively induce Valsalva maneuvers.

The sensitivity of labyrinthine structures to changes in pressure across the middle ear forms the basis for the one objective finding that is somewhat specific for PLF (although it, too can be seen in hydrops). This finding - the Hennebert sign - can be produced by a "pressure fistula test" in which pressure is introduced by pneumatic otoscope or tympanogram into the external auditory canal. A positive sign consists of ocular deviation or nystagmus observed directly or recorded as part of an ENG study. Subjective responses, including vertigo, oscillopsia or postural sway are considered suggestive but not definitive responses.6

More definitive diagnosis involves performing exploratory tympanotomy with direct observation for perilymph leakage thru the oval or round window. However, the inevitable presence of tissue fluid in the middle ear during the procedure makes even intraoperative confirmation of the diagnosis uncertain. As the definitive surgical treatment of placing a soft tissue graft over the fistula can easily be done once the tympanotomy has been performed, it is routinely carried out even in the absence of convincing intraoperative findings.

Most cases of suspected post-traumatic PLF are managed conservatively. Patients are put at bed rest for durations of a week or two, and instructed to avoid any activities that would produce Valsalva type maneuvers. Opinions vary as to whether, with the notable exception of unstable hearing, persistence of symptoms for further weeks or even months warrants exploration.7 In general, much controversy surrounds the subject of PLF. It is generally accepted as a viable post-traumatic entity (as opposed to occurring spontaneously), but even then there is wide disagreement in terms of diagnostic criteria and management.


A syndrome clinically indistinguishable from idiopathic Meniere's Syndrome can begin post-traumatically.8 ' There can be a hiatus of months and perhaps even years between the injury and the onset of symptoms (delayed hydrops). The clinical picture of fluctuating/progressive unilateral hearing loss, tinnitus, aural fullness and episodes of vertigo, ataxia and vegetative symptoms occurring spontaneously and lasting minutes to hours is classical. This clinical profile can often be difficult to distinguish from that of perilymphatic fistula-especially in the acute and subacute stage following the trauma when PLF is more likely. Management considerations are identical to the idiopathic form of Meniere's Syndrome.


Head trauma can produce focal lesions that involve the temporal or parietal association cortex which receives vestibular projections. These lesions can occasionally form seizure foci which can lead to simple or partial complex sensory seizures whose manifestation is episodic vertigo. The episodes usually last no more than seconds or minutes. They can be associated with mild nausea but not vomiting. Nystagmus can be an accompaniment due to stimulus of contiguous cerebral oculomotor control areas.10 Tinnitus can at times be associated. Contralateral paresthesias and/or olfactory and gustatory symptoms are occasionally reported. Unconsciousness will follow only if the seizure becomes generalized.

Epilepsy represents a relatively uncommon cause of post-traumatic vertigo. Seizure workups are not routinely fruitful except in selected cases in which other symptoms suggestive of sensory seizures are present or, certainly, in which loss of consciousness occurs-something that only rarely occurs in aural vertigo due to intense vegetative symptoms leading to vagal syncope.


Vestibular symptoms can possibly be produced from damage to either cervical vascular or cervical neural structures. Trauma to a vertebral artery can result in thrombosis or dissection with resultant brainstem/cerebellar ischemia." The case for vertigo mediated by C1-3 posterior roots following whiplash injury to deep cervical soft tissue is less clear.12 There is ample evidence that these roots mediate cervical proprioceptive inputs that actually synapse within the vestibular nuclei and which would provide an anatomical substrate capable of mediating vestibular-like symptoms. Further, there are many experimental models in lower species in which deep cervical lesions produce objective manifestations indistinguishable from primary vestibular lesions (nystagmus and ataxia). However, these objective findings are not reproducible in primates. Human experiments document subjective sensations of dizziness and perceptions of lateropulsion, but no measurable objective parameters that could form the basis for a diagnostic test for cervical vertigo have yet to be demonstrated. In many cases, there are cervical trigger points that produce subjective vertigo with deep palpation. In all cases in which the diagnosis is suspected, treatment is limited to cervical soft tissue physical therapy modalities


Headache is one of the most common post-traumatic symptoms, and upwards of 25% of cases meet the criteria for migraine. Vertigo associated with both idiopathic and post-traumatic migraine has been widely reported, but criteria have not yet been established for the diagnosis of vestibular migraine.13 Headache may not be temporally associated with the vertigo in upwards of a third of these reported cases. Episodic vertigo, positional vertigo and non-vertiginous dizziness have all been described; and some authors accept durations of chronic unremitting symptoms lasting days or weeks as consistent with the diagnosis. Many studies report convincing results of therapeutic trials of medication and/or other modalities used in the treatment of other types of migraine.14


Substantial numbers of patients who have sustained mild or moderate head injuries present with a similar cluster of symptoms. These most often include headache, visual symptoms, and cognitive changes. Dizziness, nausea and, at times, tinnitus and hyperacusis are also symptoms that are quite commonly included in this syndrome. However, a diagnosis of PCS for a patient presenting with any of the latter symptoms, presumes that the pathophysiology is confined to traumatic brain injury and not to any of the specific vestibular and/or auditory system pathologies described above. The pathology of traumatic brain injury includes focal lesions, diffuse axonal injury (DAI), and scattered petechial hemorrhages. These latter injuries, however, are rarely found in patients in which the duration of loss of consciousness is less than 30 minutes, and attributing symptoms to PCS in milder head injuries is probably inappropriate. Further, irregardless of the severity of injury, dizziness and vertigo as well as auditoty symptoms are due to other specifically identifiable pathologies in the overwhelming majority of patients. That being the case, PCS should be a diagnosis of exclusion. Once the diagnosis of PCS has been made, it still remains unclear how long symptoms can appropriately be attributed to it. Many authors suggest consideration should be given to post-traumatic stress disorder when symptoms extend beyond six months to a year.


The vestibular-like symptoms that commonly follow head injury are most often due to one of a number of specific pathologies affecting vestibular, CNS or cervical structures. These pathologies can be readily identified in the majority of cases by appropriate testing in the examining room, and in vestibular function or neurodiagnosic laboratories. Wheteas vestibular suppressants have a roll, they often delay recovery and have been supplanted as the mainstay of treatment in most cases by vestibular rehabilitation techniques. Given the large number of patients requiring outpatient management following head injury, it is appropriate that most generalists and many subspecialists should be aware of the differential diagnosis, workup and treatment options for post-traumatic vertigo.

"Establishing the Cause of Vertigo"

American Family Physician, March 1, 2000 by Anne D. Walling

(Australia--Australian Family Physician, September 1999, p. 883.) A careful history is essential to distinguish true vertigo from symptoms such as dizziness. Vertigo, described as a sensation of spinning, usually results from disturbances of the semicircular canals. When patients complain of disturbances of linear motion, such as sudden falling or tilting, the cause is likely to involve the otolith organs. The length of attacks may provide diagnostic clues. Benign positional vertigo or vestibular peripheral lesions usually cause attacks of vertigo lasting a few seconds. Migraine and vertebrobasilar ischemia may result in vertigo lasting several minutes. Attacks lasting hours occur in Meniere's disease, vestibular neuronitis and labyrinthitis. Neurologic examination of patients with vertigo should include assessment of balance, gait, eye movements and hearing. Specific provocation tests for nystagmus resulting from positional change are particularly useful to diagnose benign positional vertigo. Specialized investigations--computed tomographic brain scanning, audiometry, brain stem auditory evoked potentials and vestibular investigations--should target the most likely cause of vertigo. Potentially serious neurologic disease should be suspected in patients with focal neurologic signs, severe ataxia, nystagmus changing direction, vertical nystagmus and abnormal eye movement.

COPYRIGHT 2000 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group

"Stop the spinning: Diagnosing and managing vertigo"

Nurse Practitioner, Aug 2002 by Sandhaus, Sonia


Differentiating vertigo from other forms of dizziness presents a diagnostic challenge. Extensive investigation, however, can help reveal vertigo's true etiology: life-threatening central lesions or debilitating, but benign, peripheral causes. Here, learn to assess vertigo using physical examination, history, and diagnostic procedures. Also, manage symptoms of common vestibular disorders, such as benign paroxysmal peripheral vertigo, labyrinthitis, and Meniere's disease.

Vertigo, a common symptom, can be as disabling as paralysis or loss of limb,1,2 yet most types are self-limiting and treatable. The ninth most common symptom reported by primary care patients, vertigo affects more than 90 million Americans age 17 and older.3,4 Distinguishing vertigo from underlying causes, such as psychogenic factors or lifethreatening central nervous system disease, remains central to accurate diagnosis.5-7 Because vertigo symptoms are subjective and nonspecific, evaluating the vertiginous patient poses special challenges.8,9

* Etiology and Pathophysiology

To remain upright--a distinctly human attribute--the body must integrate input from the vestibular, visual, and proprioceptive systems. The peripheral vestibular labyrinth contains sensory receptors for balance that lie in three semicircular canals and in the inner ear's otolithic organs. These sensory receptor neurons have ciliated hair cells that respond to motion and transmit impulses to the eighth cranial nerve fibers, which course through the internal auditory canals and form a synapse in the cerebellum's vestibular nuclei.

Visual receptors in the vestibular ocular connections provide feedback for a stable retinal image during head movement. Somatosensory receptors in the peripheral and central vestibular structures provide information about gravity, position, and movement of muscles and joints.

Under normal conditions, receptors process and coordinate environmental cues. For example, while walking, proprioceptors in the feet indicate movement, so you observe surroundings move in relation to your body while the inner ear detects the motion.5 An insult that disrupts the balance between the ear receptors, or between the ears and other systems, results in vertigo.1,10 Therapeutic goals involve reestablishing balance and recalibrating vestibular systems.

Altered vestibular nerve input to the vagus nerve causes visceral manifestations of vertigo, such as nausea, vomiting, pallor, and perspiration. 10,11 Nystagmus, another sign of vertigo, occurs from altered input passing from the vestibular nuclei to the nuclei of the extraocular muscles. 11,12

* Understanding Vertigo

Dizziness, a term most patients use to describe sensations of imbalance, can be classified as presyncope, disequilibrium, lightheadedness, or vertigo.13,14 A feeling of faintness and impending loss of consciousness characterizes presyncope, a cardiovascular symptom. Disequilibrium, a locomotor problem, involves a falling feeling. The patient feels a lost sensation of balance when upright, either standing or walking. Light-headedness, a final dizziness category, is psychogenic or idiopathic and doesn't fit any of the other three classifications.

Vertigo, the cardinal symptom of vestibular dysfunction, is the illusion of movement.12-14 Typically rotational, vertigo can also be a sensation of tilting or swaying. Rotational vertigo results from disease of the semicircular canals. Tilting or swaying vertigo stems from disorders affecting the otolithic organs. Vertigo causes feelings of imbalance during standing and walking, and makes most patients want to lie still and avoid movement.12

Vertigo is either objective or subjective. Objective vertigo involves a perception that the surroundings are moving while the body remains still; subjective vertigo involves a feeling that the surroundings remain still while the body is moving. Vertigo type doesn't have diagnostic significance.5,6

Varying degrees of nausea, vomiting, pallor, and perspiration usually accompany vertigo; however, patients don't lose consciousness.14,15 Almost 85% of patients with vertigo have a peripheral vestibular disorder; the others have a central nervous system disorder (see Table 1, "Identify Vertigo's Origin").5,7 Peripheral vestibular disorders involve the semicircular canal or peripheral nerve, whereas central nervous system disorders include acoustic neuroma, brain tumors and trauma, transient ischemic attacks or strokes, and multiple sclerosis.

Most cases of peripheral vertigo are benign paroxysmal positional vertigo (BPPV), labyrinthitis, or Meniere's disease.16 Of these, BPPV accounts for more than half of all cases of peripheral vertigo and is mostly a clinical diagnosis.12,13,16,17


Conduct a thorough history to identify vestibular disorders, concentrating on symptom onset, duration, and quality (see Table 2, "Dizziness Questionnaire"). The physical examination will help differentiate the causes of vertigo.10,18,19 History and physical examination alone may provide enough information to diagnose vertigo in more than 80% of patients (see Figure 1, "A Differential Diagnosis of Dizziness").5

Taking the History

Ask patients to describe dizziness in their own words. Although many people experience dizziness, they're limited by a paucity of words to describe their sensations.15,19 They often resort to vague terminology but, in many cases, the descriptions are diagnostic.

An abnormal perception of movement distinguishes true vertigo from dizziness.5 Some 95% of patients who mention sensation of motion, without prompting, have vertigo.13,17 If the patient can't describe the sensations, ask about feelings of spinning, fainting, and falling.

Ask about positional changes because vertigo is almost always transient, occurring with changes of head position when lying or sitting.1 Patients with presyncope, which is often caused by orthostatic changes, report dizziness only when standing. Disequilibrium occurs only when the patient is walking or standing. Questions about the effects of lying down, sitting, standing, and walking can elicit valuable history. More important, questions about loss of consciousness help rule out cardiac causes.

Symptom duration is the most valuable diagnostic criterion in differentiating the three most common peripheral diseases.5 In labyrinthitis, vertigo usually is constant for a few days and resolves within 1 or 2 weeks. In BPPV, the sensation is episodic, lasting only seconds, and usually occurs when patients turn their heads or lie down. The sensation in Meniere's disease is episodic as well, but the spells last for hours and recur over a period of months to years.

Labyrinthitis generally prompts an emergency department visit. BPPV is commonly mentioned in the course of a visit for another complaint, in which the patient casually mentions feeling dizzy when lying down or turning over. Meni&re's disease may precipitate an acute attack of vertigo, but recurrence is a hallmark of this disease.

When the cause is peripheral, vertigo is usually intense. In central nervous system diseases, vertigo is mild, but nystagmus is prominent. With a central cause, vertigo's onset is immediate and the response persists; the more central the process, the longer the vertigo lasts.1,10

A history of hypertension, diabetes, heart disease, or endocrine disorders is pertinent to diagnosis. Drugs may cause dizziness but rarely cause vertigo.5 Common drugs that can cause dizziness include alcohol, aminoglycosides, anticonvulsants, antidepressants, antihypertensives, cocaine, cytotoxic agents, furosemide, nitroglycerine, nonsteroidal anti-inflammatory drugs (especially indomethacin), salicylates, and tranquilizers. Use of tobacco, caffeine, and alcohol also impacts symptoms.

Conducting the Physical Examination

During the physical examination, focus on cardiac, otologic, and comprehensive neurologic assessment and observe for nystagmus.1,18 Postural vital signs, carotid examination, and auscultation of carotid arteries will rule out cardiovascular disorders. Neurologic evaluation, particularly of the cranial nerves, detects clinical signs of brainstem or other central sources of vertigo. Refer patients who have worrisome signs and symptoms, such as severe headaches, seizures, fainting, or positive cranial nerve involvement.

Only 20% of vertiginous patients in the primary care setting require further evaluation and testing.5 Cardiac murmurs, dysrhythmias, carotid bruits, and orthostatic hypotension suggest central causes of vertigo. Vertebral-basilar ischemia is associated with brainstem symptoms such as diplopia, dysarthria, facial numbness, and focal sensory and motor deficits.8,9 Multiple sclerosis involves symptoms of focal weakness, diplopia, and bowel and bladder dysfunction. Migraine-induced vertigo is highly variable.

Patients with peripheral vestibular disorders experience imbalance but can walk, whereas those with central lesions often can't stand or take a step without falling.14 Hearing and tuning fork tests will be normal in BPPV and labyrinthitis, while asymmetric sensorineural hearing loss suggests Meniere's disease, acoustic neuroma, or syphilis.1

The Dix-Hallpike maneuver is the most useful office test for nystagmus, the only objective sign of vertigo (see Figure 2, "Using the Dix-Hallpike Maneuver").11,16 The test takes about 5 minutes: Vertigo and nystagmus are significant positive findings.11

Consider psychogenic vertigo as a diagnosis of exclusion in patients with depression and anxiety. 19 Ask patients to hyperventilate for 2 minutes; if vertigo results, it's probably psychogenic in etiology.11

Special Screening

Further evaluation depends on history. Target laboratory tests toward difficult diagnoses and suspected systemic conditions. Thyroid and liver function tests and blood chemistry and counts can rule out metabolic etiologies. Serology for neurosyphilis is indicated for sensorineural hearing loss.5 Evaluate patients with cardiovascular symptoms with electrocardiogram and Holter monitoring.

When vertigo persists, psychiatric screening and vestibular testing prove valuable.14,16 Audiometry, caloric stimulation, electronystagmography, magnetic resonance imaging, and auditory brainstem response are indicated for persistent vertigo when you suspect central nervous system disease.

Caloric stimulation quantifies degrees of vestibular dysfunction to differentiate peripheral lesions of the labyrinth from central lesions of the eighth cranial nerve.16 Electronystagmography records nystagmus induced by head and body movements. Auditory brainstem response measures the speed of auditory impulses in which acoustic neuroma may delay conduction)

* Common Vestibular Syndromes Benign Paroxysmal Positional Vertigo

In BPPV, the most common form of vertigo, changes in head position provoke brief vertiginous episodes.12,17,20 For example, vertigo occurs when the patient rolls over in bed, looks upward, places a jar on a higher shelf, or bends down to tie his or her shoes. The initial onset, associated with nausea and vomiting, frightens the patient. Most patients quickly learn to avoid provocative head movements, which prolong vertigo's course.

In BPPV patients, the neurologic examination is normal, except for nystagmus confirmed by the Dix-Hallpike maneuver. No other diagnostic procedures are necessary.8,9 BPPV, which is usually self-limiting, results in complete recovery in 3 months. Although BPPV can occur at any age, it's most common in older people, and women outnumber men by 3 to 1.16 Causes include head trauma or prior viral inner ear infection, but most cases are idiopathic with no accompanying inner ear damage. 14,16

Canalithiasis causes BPPV and occurs when free-floating canaliths (calcium carbonate crystals), which are normally attached to the utricle, inadvertently migrate to the posterior semicircular canal.16 With head motion elicited by the Dix-Hallpike maneuver, the canaliths move about and displace the cupula (the nerve sensors of the semicircular canal) to create vertigo. 3,16

Latency before nystagmus onset is from the delay in setting the canaliths in motion with positional changes. Fatigability of nystagmus with repeated positioning occurs with canalith settling. The induced vertigo and nystagmus are brief, as the canaliths quickly reposition themselves after bouncing off the cupula.


Also known as peripheral vestibulopathy or vestibular neuritis, labyrinthitis occurs at any age.5 This disease consists of acute onset of vertigo, nausea, and vomiting that lasts for several days without any auditory or neurologic symptoms. Most patients gradually improve within a few months. Recovery occurs even when unilateral loss of vestibular function is permanent because the brain compensates for the loss.14 About 50% of patients report a prior viral infection, but researchers haven't isolated a virus.16 This syndrome can occur in small outbreaks, may affect several family members, and often erupts in the spring.5

Meniere's Disease

A diagnosis of Meniere's disease is based on a triad of symptoms: vertigo, hearing loss, and tinnitus. 14 Hearing disturbances are rare in labyrinthitis and absent in BPPV. Meniere's disease accounts for 10% of patients with vertigo who present with episodic severe attacks and fluctuating hearing levels.16 Excessive accumulation of endolymph causes the membranous labyrinth to expand and rupture, resulting in hearing loss and vertigo. In most cases, patients can localize the affected ear because of the associated hearing difficulties. Although idiopathic, Meniere's disease must be differentiated from allergic, autoimmune, viral, and hormonal etiologies.

* Managing Vertigo Symptoms

To suppress vertigo and alleviate nausea and vomiting, consider symptomatic treatment with pharmacologic therapy (see Table 3, "Pharmacologic Therapy and Vertigo"). Limit medications to a 2-week duration and prescribe only as needed.8,9,20 Drugs don't reduce the frequency of vertigo attacks and can cause sleepiness, lethargy, worsening of balance, and increased falls in older adults. Furthermore, prolonged drug use may delay central compensation.8,9 Treatment for Meni&re's disease includes a low-salt diet and diuretics aimed at reducing inner ear fluid pressure.20

When nausea and vomiting resolve, encourage physical activity, which enhances the central nervous system's ability to compensate for labyrinthine dysfunction. To promote vestibular compensation, prescribe an exercise program of repeated, provocative head movements. Patients should perform the head movements at least twice daily until the vertigo abates.8,9,20 These habituation maneuvers deliberately repeat side-to-side head positions that initially elicited vertigo and promote compensation by lessening the duration and severity of vertigo associated with BPPV.21 Patients become asymptomatic and functional within a short time without medication.3

Canalith repositioning maneuvers provide another noninvasive treatment option. The purpose of these maneuvers is to move free-floating canaliths within the labyrinth to the utricle of the inner ear where they attach to the membrane and stabilize (see Figure 3, "Particle-Repositioning Maneuver for Right-Sided BPPV"). This recommended, cost-effective treatment for BPPV involves a series of specific head maneuvers that provide immediate and often long-lasting relief.5,8,9 These maneuvers have demonstrated an 85% cure or improvement in vertiginous patients and are useful adjuncts in treating labyrinthitis and Meniere's disease.3,8,9,22,23

Those with refractory vertigo may benefit from formal rehabilitation programs with a physical therapist.24 Some patients benefit from individualized habituation protocols and specialized tilt tables.24 Reserve surgery for those who remain substantially disabled despite a prolonged trial of pharmacologic and exercise therapies.

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