Vertigo (Differential diagnosis) introduction



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Vertigo (Differential diagnosis)

INTRODUCTION

  1. Vertigo is symptom of illusory movement. Almost everyone has experienced vertigo as transient spinning dizziness immediately after turning around rapidly several times. Vertigo can also be sense of swaying or tilting. Some perceive self-motion whereas others perceive motion of environment. Vertigo is symptom, not diagnosis. It arises because of asymmetry in vestibular system due to damage to or dysfunction of labyrinth, vestibular nerve, or central vestibular structures in brainstem.

  2. Vertigo is only one type of dizziness. Other disorders that present with dizziness include presyncopal faintness, disequilibrium, and non-specific or ill-defined light-headedness. The initial approach to patient who complains of dizziness is to localize cause of symptom into one of these broad categories.

  3. The pathophysiology, etiology, and differential diagnosis of vertigo will be reviewed here. The clinical approach, diagnosis, and treatment of vertigo are discussed separately.

PATHOPHYSIOLOGY

  1. The end organs of vestibular system, semicircular canals and otolith organ, sense angular and linear motion respectively. As result, patient's description of spinning sensation is likely to indicate abnormality of semicircular canal or CNS structures that process signal from semicircular canal. Similarly, illusory sensation of floating or tilting may indicate otolith system disorder.

  2. Important to pathogenesis of vertigo is fact that there is vestibular labyrinth on each side of body. CNS receives signals from both right and left labyrinths and compares these signals with one another. When head is still, tonic discharges in both vestibular afferents are exactly balanced. During motion, right and left labyrinths are alternately excited and inhibited, leading to left-right difference in 8th nerve activity, which is recognized as motion. The spurious left-right differences that result from acute unilateral peripheral vestibular disorder are also interpreted by CNS as motion or vertigo.

  3. CNS, at brainstem level, processes visual motion in manner similar to that of self-motion. This normal, physiologic aspect of vestibular system underlies experience of self-motion when viewing large-screen movies. This ambiguity between motion of self and motion of surround relates directly to lack of uniformity in patients' complaints of vertigo as either self-motion or motion of surroundings.

  4. Information from vestibular labyrinth is relayed via vestibular portion of cranial nerve VIII to brainstem vestibular nuclei and from there to cerebellum, ocular motor nuclei, and spinal cord; there are also less well-defined cerebral projections. Vestibuloocular connections are responsible for coordinated eye movements during head motion, while vestibulospinal pathways help maintain upright posture. Cerebellar connections help modulate these activities.



CAUSES OF VERTIGO

  1. 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% of cases; of these, BPPV, vestibular neuritis, and Meniere disease are the most common.

  2. The clinical features of more common disorders are summarized in table (table 2).

PERIPHERAL CAUSE

  1. Benign paroxysmal positional vertigo (BPPV)

    1. BPPV is probably the most commonly recognized cause of vertigo. It is most commonly attributed to calcium debris within posterior semicircular canal, known as canalithiasis.

    2. Classically, patients describe brief spinning sensation brought on when turning in bed or tilting 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.

    3. The diagnosis is generally made by its historical description. Dix-Hallpike maneuver can provide further evidence of its presence, but is positive in only 50 to 80% of patients.

    4. 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 semicircular canal and can be treated by canalith repositioning maneuvers.

    5. Rarely, patients presenting with positional vertigo have CNS abnormalities with less favorable prognosis. Usually, symptoms are somewhat more prolonged. Patients with atypical positional vertigo or nystagmus who do not respond to treatment should undergo MRI of brain to rule out posterior fossa abnormality.

  2. Vestibular neuritis

    1. Vestibular neuritis, also known as vestibular neuronitis and labyrinthitis, is believed to be viral or post-viral inflammatory disorder, affecting vestibular portion of CN VIII.

    2. Vestibular neuritis is characterized by rapid onset of severe, persistent vertigo, nausea, vomiting, and gait instability. PE findings are consistent with acute peripheral vestibular imbalance: spontaneous vestibular nystagmus, positive head thrust test, and gait instability without loss of ability to ambulate. In pure vestibular neuritis, auditory function is preserved; when this syndrome is combined with unilateral hearing loss, it is called labyrinthitis.

    3. A diagnosis of vestibular neuritis is largely based on clinical information. There are no specific diagnostic tests. However, clinical features of cerebellar hemorrhage or infarction may be similar to vestibular neuritis, and brain imaging is therefore often required to rule this out.

    4. Patients with vestibular neuritis generally suffer from severe vestibular symptoms for 1 to 2 days, followed by gradual diminution of symptoms and return of equilibrium. Recovery may be hastened with corticosteroid.

  3. Herpes zoster oticus

    1. Often called Ramsay Hunt syndrome, this syndrome is believed to represent activation of latent herpes zoster infection of geniculate ganglion.

    2. In addition to acute vertigo and/or hearing loss, ipsilateral facial paralysis, ear pain, and vesicles in auditory canal and auricle are typical features.

    3. Therapy with corticosteroids or acyclovir should be considered, although these modalities are not of proven value.

  4. Meniere disease

    1. Meniere disease is 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.

    2. Affected patients present with spontaneous episodic vertigo lasting for minute to hour, 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 attack.

    3. The diagnosis of Meniere disease is suggested by history. A low frequency sensorineural hearing loss on audiometry and unilateral reduced vestibular response on ENG help confirm diagnosis.

    4. 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.

  5. Labyrinthine concussion

    1. Labyrinthine concussion refers to traumatic peripheral vestibular injury following direct concussive head trauma. 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 setting of transverse fractures of temporal bone. Hemotympanum and sensorineural hearing loss often accompany vertigo in this setting.

    2. In both of these injuries, symptoms of vertigo, nausea and vomiting, and imbalance are maximal at onset and improve over days to months, depending on severity of injury.

    3. Sequelae of labyrinthine concussion may include BPPV and, occasionally, post-traumatic endolymphatic hydrops (Meniere disease). These sequelae may be delayed for weeks to months after head injury.

  6. Perilymphatic fistula

    1. This is infrequent complication of head injury, barotrauma, or heavy lifting in which fistula develops at otic capsule, permitting transfer of pressure changes to macular and cupular receptors. This explains clinical syndrome of episodic vertigo and/or hearing loss provoked by sneezing, lifting, straining, coughing, and loud sounds. The latter, so-called Tullio phenomenon, occurs because sound-induced pressure waves are abnormally distributed through inner ear.

    2. The diagnosis is difficult as clinical tests are insensitive. CT may show fluid in region of round window recess. Treatment with bed rest, head elevation, and avoidance of straining is first step; failure to resolve after several weeks of conservative therapy is indication to consider surgical patch. Recurrences occur in 10%.

  7. Semicircular canal dehiscence syndrome

    1. In semicircular canal dehiscence syndrome, bone overlying superior aspect of superior semicircular canal becomes thin or even absent, thereby allowing pressure to be transmitted to inner ear. Vertigo is provoked by coughing, sneezing, and Valsalva maneuver. Patients may experience nausea and instability during brief episodes of vertigo.

    2. Loud sound may also induce vertigo in this condition (Tullio phenomenon), as sound-induced pressure waves are abnormally distributed through inner ear. This phenomenon can be tested through click-evoked vestibuloocular reflex, which is typically high magnitude and low threshold in patients compared with controls. Cochlear hypersensitivity is another diagnostic indicator for this condition. Some patients also have hearing loss, with air-bone gaps on audiometry. One case report noted torsional pendular nystagmus that was synchronous with the palpated pulse, and suppressed by Valsalva maneuver or lying supine.

    3. This is rare syndrome. A 2005 review revealed < 100 reported cases. However, condition may be underdiagnosed. The diagnosis can be established with MRI or high resolution CT of temporal bone. Some patients benefit by surgical repair of their anatomical deficit.

  8. Cogan's syndrome

    1. Cogan's syndrome is autoimmune condition that can cause interstitial keratitis and vestibuloauditory dysfunction.

    2. Patients have Meniere-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, which is perception of objects jiggling back and forth after abruptly turning head to one side or the other. Caloric testing often reveals absent vestibular function.

    3. Systemic steroids and other immunosuppressants may be required. This topic is discussed separately.

  9. Recurrent vestibulopathy

    1. Recurrent vestibulopathy is descriptive diagnosis used for patients who experience spontaneous episode of vertigo unassociated with otologic complaints (no hearing loss, tinnitus, or ear fullness, and unassociated with migrainous phenomenon). Symptoms often include nausea, vomiting, and disequilibrium. Vertigo may occur infrequently, for example, every 1 to 2 years. Once vertigo is resolved, patients return to normal without sequelae.

    2. The pathophysiology of recurrent vestibulopathy is uncertain. The condition is thought to represent vestibular disorder of uncertain localization. Some cases appear to cluster in families. This disorder may overlap with migrainous vertigo.

  10. Other disorders

    1. Vestibular schwannoma (acoustic neuroma)

      1. Because tumor grows slowly, subtle imbalances in vestibular input are compensated for by CNS and patients often do not experience significant vertigo. Imbalance or vague feeling of swaying or tilting may be only manifestations of vestibular injury. Unilateral hearing loss or tinnitus is more likely to bring patient to medical attention.

    2. Aminoglycoside toxicity

      1. Several aminoglycoside, notably gentamicin, are selectively vestibulotoxic, causing peripheral vestibular damage without affecting hearing, presumably by damaging hair cells of inner ear.

      2. Because both vestibular end organs are equally affected, there is no right/left imbalance of vestibular input to CNS, and, therefore, patient does not experience vertigo. Patients may experience oscillopsia (to-and-fro illusion of environmental motion) with head movement, indicating deficient VOR. Bilateral vestibular loss is associated with abnormal head thrust testing in both horizontal directions, as well as reduced visual acuity during head shaking, and can be documented with both caloric and rotational testing. Severe bilateral vestibular loss leads to chronic disequilibrium and oscillopsia.

    3. Otitis media (OM)

      1. OM may be associated with vestibular symptoms. Non-specific dizziness is more common than vertigo; however, 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 IV antibiotics are required.

      2. If tragal stimulation provokes dizziness in patient with otitis, CT of temporal bone should be done to rule out fistula of bony labyrinth.

CENTRAL CAUSE

  1. Migrainous vertigo

    1. Migraine is increasingly recognized as cause of recurrent vertigo. However, mechanism whereby migraine causes vertigo is not understood, and diagnosis remains somewhat controversial.

    2. Migrainous vertigo may have both central and peripheral vestibular manifestations. 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 BPPV. Episodes lasting for several minutes to few hours are more typical.

    3. A diagnosis of migrainous vertigo relies on Hx, in which at least some attack of vertigo is associated with migraine or other migrainous phenomenon (visual aura, photophobia, or phonophobia). Episodes of migraine-related dizziness generally occur spontaneously but, similar to migraine, can be triggered by certain foods and sensory stimuli.

    4. A condition called benign recurrent vertigo of childhood is considered childhood manifestation of migraine-related dizziness or vertigo. Many of these children go on to develop more typical migraine headache.

  2. Brainstem ischemia

    1. Embolic, atherosclerotic occlusions of the vertebrobasilar arterial system will produce brainstem ischemia. While vertigo may dominate clinical presentation, it is rarely sole manifestation of brainstem ischemia. Nonetheless, cerebrovascular origin of symptoms should be excluded in patients who present with vertigo if they have vascular risk factor, because of relatively high risk of recurrent stroke, which may be mitigated by appropriate interventions.

    2. TIA

      1. While infarction produces sustained symptoms that improve over several days and weeks, TIA involving 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 diagnosis in older patients or those with vascular risk factors. MRI with DWI may be helpful, but its sensitivity is < 50%; MRA may demonstrate arterial occlusive disease in posterior circulation.

    3. Rotational VA syndrome (RVAS)

      1. RVAS (also called rotational VBI or bow hunter syndrome) refers to rare but well documented phenomenon of symptomatic VA compression by bony elements of spine (usually at CI-C2) that occurs with physiologic head rotation. Most patients with this condition report vertigo or non-specific dizziness with head turning. The diagnosis is made by vascular imaging that includes neutral as well as symptomatic position. Degenerative bone disease as well as congenital foraminal narrowing can be causative; disease or hypoplasia of non-involved VA is usually described.

      2. Surgical decompression may be successful when conservative approaches (avoiding movements that precipitate symptoms) fail. Non-invasive interventions, such as traction and enhanced external counterpulsation (EECP) are under investigation.

    4. Wallenberg's syndrome

      1. Wallenberg's syndrome, or lateral medullary infarction, is associated with acute onset of vertigo and disequilibrium. The blood supply to lateral medulla is PICA. Most patients with Wallenberg's syndrome have occlusion of ipsilateral vertebral artery that gives rise to PICA.

      2. While vertigo often dominates clinical presentation, examination usually uncovers other neurologic deficits: abnormal eye movements, ipsilateral Horner's syndrome, ipsilateral limb ataxia, and dissociated sensory loss (loss of pain and temperature sensation on ipsilateral face and contralateral trunk). Hoarseness and dysphagia are often present.




      1. Wallenberg's syndrome usually occurs as result of atherosclerotic or lipohyalinotic arterial occlusion, but it is also common presentation for traumatic VA dissection. A history of neck injury or neck pain suggests the latter. The diagnosis of medullary infarction is established definitively with MRI. MRA of head and neck should be performed as well to rule out arterial dissection. Patients usually recover their equilibrium after several months.

    1. Other stroke syndrome

      1. Labyrinthine infarction may occur with occlusion of internal auditory artery, branch of AICA. This is really peripheral lesion of vestibular system and is characterized by abrupt vertigo, hearing loss, and sometimes tinnitus.

      2. A more proximal occlusion of AICA will also involve lateral pons and cerebellar peduncle, causing gait and limb ataxia and facial paralysis in addition to vertigo and hearing loss.

      3. More restrictive brainstem infarctions have been described that affect isolated vestibular structures. Thus, their clinical manifestations are very similar to neuritis.

  1. Cerebellar infarction and hemorrhage

    1. 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. Limb ataxia is helpful in suggesting cerebellar involvement but is often absent if the lesion is more medially or inferiorly placed.

    2. 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.

    3. Cerebellar infarction and hemorrhage typically occur in older patients (> 60 years) and in those who have risk factors, particularly hypertension and diabetes.

    4. 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. CT 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.

  2. Chiari malformation

    1. Chiari I malformation is congenital anomaly in which cerebellar tonsils extend below foramen magnum. This is usually asymptomatic but may be associated with constellation of neurologic deficits (headache or neck pain, weakness with long tract sign, dysphagia, and other lower cranial nerve impairments). Vertigo and gait imbalance are common complaints in symptomatic individuals and may represent cerebellar pathology.

    2. When present, vertigo is often positionally induced, particularly by neck extension, perhaps manifesting pressure on brainstem and cerebellar structures or their blood supply. Vertiginous symptoms are generally mild and often resolve when the patient alters his or her head position. Down beating 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.

    3. Surgical decompression may be required to relieve symptoms and is usually successful.

  3. Multiple sclerosis

    1. Vertigo has been estimated to occur in 20% of MS patients, most commonly with plaques near vestibular nuclei and in root entry zone of cranial nerve VIII. 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.

    2. Vertigo can also occur with plaques within brachium conjunctivum and cerebellum. This localization is more commonly associated with acute, sustained vertigo that has more central characteristics, as in cerebellar infarction.

    3. The diagnosis is usually evident in patients with established history of MS. When vertigo is presenting symptom, the diagnosis requires a high degree of suspicion; suggestive features include history of prior neurologic symptoms and abnormal findings on NE (afferent pupillary defect, long tract sign). Demyelination should not be assumed to be cause of vertigo in patient with MS. One series noted that among 25 patients with MS complaining of vertigo, BPPV, not MS, was underlying cause in > 50% of patients.

    4. Symptoms related to MS flare last days to weeks. A short course of corticosteroids may shorten disabling attacks.

  4. Episodic ataxia type 2 (EA-2)

    1. EA-2 is AD condition caused by mutations in brain-specific P/Q type calcium channel gene on Ch 19. Attacks of severe vertigo, nausea, and vomiting, and ataxia begin in childhood or early adult life. These can last few hours or few days. Gaze-evoked, rebound, or downbeat nystagmus may be evident during or between attacks.

    2. The attacks respond to acetazolamide in a dose of 250 to 750 mg/day.

  5. Disembarkment (mal de debarquement) syndrome

    1. 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. Persons with this syndrome do not in general describe rotational vertigo but rather disequilibrium and sense of swaying or rocking, or walking on uneven ground. There is often a latency of several minutes to an hour or two between return to solid ground and symptom onset. Patients are not nauseous and physical examination is normal. 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.

    2. Uncommonly, cases of persistent and disabling symptoms lasting for weeks and years are reported in individuals’ ages 15 to 77 years and demonstrate a female preponderance. A history of motion sickness or seasickness during the initial exposure or otherwise is present in some patients, but not clearly the majority. Interestingly, re-exposure to passive motion, whether the initial trigger or an alternative (riding in a car) is typically associated with temporary mitigation of symptoms during the exposure, but exacerbation afterward. Motion sickness is described separately.

    3. In addition to imbalance and a sense of motion, patients describe difficulty tolerating complex visual stimuli (video games); they also report disabling cognitive difficulties and fatigue. 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. Treatment options are limited. The longer symptoms persist, the less likely they are to remit. 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. Higher doses are not likely to be more effective. Physical therapy and vestibular rehabilitation have not been reported to be helpful.

    4. The pathogenesis of disembarkment syndrome is not understood. Vestibular tests are normal or nonspecifically abnormal, as are structural and functional neuroimaging studies. Some patients demonstrate postural instability.

SUMMARY

  1. 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 brainstem.

  2. Vertigo is only one type of dizziness. Other disorders that present with dizziness include presyncopal faintness, disequilibrium, and nonspecific or ill-defined light-headedness.

  3. It is customary to organize causes of vertigo into peripheral and central disorders. These have distinctive clinical features, but with some overlap. Peripheral causes of vertigo generally comprise 80% of cases; of these, benign paroxysmal positional vertigo, vestibular neuritis, and Meniere disease are the most common.

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