EAR, NOSE, THROAT DISORDERS Vertigo and Dizziness: A Brief Review ABSTRACT

Dizziness is the third most common symptom seen in patients of all age groups who present to emergency departments, outpatient clinics and physicians offices. Assessing dizziness requires a differentiation of potential causes through a comprehensive medical history and thorough physical exam. The most common causes of dizziness are peripheral vestibular disorders, however disorders of the central nervous system must be ruled out. Understanding how to distinguish between various underlying causes of vertigo is essential for the timely diagnosis and effective management of patients with this symptom. In this review, an overview of the epidemiology, etiology, presentation, diagnosis and treatment of the most common causes of vertigo will be presented, touching on some of the more rare determinants.

KEYWORDS:

Vertigo, dizziness, BPPV, vestibular neuronitis, Meniere’s disease, vestibular migraine, vertebrobasilar insufficiency

Definition Vertigo is a false sense of motion of oneself or one’s surroundings resulting from an acute asymmetry in vestibular function. Patients often describe vertigo as a spinning sensation.Vertigo indicates pathology of one of more of the following: vestibular end organs, cranial nerve VIII, visual system, proprioception pathways, motor nerves, or central vestibular pathways of the brainstem and cerebellum (Figure 1).

ABOUT THE AUTHORS Curtis M. Marcoux, Memorial University of Newfoundland, St. John’s, Newfoundland and Labrador, Canada. Dr. Pradeep Shenoy, MD, DLO, FRCS, FACS, is the ENT service chief, Campbellton Regional Hospital, Campbellton, New Brunswick, Canada.

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Figure 1: Block Diagram Illustrating the Organization of the Vestibular System Sensory Input

Central Processing

Motor Ouput

Visual Vestibular Proprioceptive

Primary Processor (Vestibular Nuclear Complex)

Motor Neurons

Eye Movements Positional Movements

Adaptive Processor (Cerebellum)

Figure 1.1 Block diagram illustrating the organization of the vestibular system.

Vertigo-like Symptoms

Vertigo is the dominant type of dizziness with which patients present to their family physician1or emergency room.2 Dizziness is an imprecise and subjective complaint that can be classified more precisely as belonging to one of four types, each having distinct etiologies. Since various pathological processes may result in dizziness, it is important that vertigo be differentiated from other types of dizziness, namely lightheadedness, pre-syncope, and disequilibrium. Briefly, pre-syncope, or faintness, is a sudden weakness of quick onset and short duration representing cerebral hypoperfusion typically arising from vascular, autonomic or cardiac causes. Disequilibrium refers to unsteadiness or loss of balance while standing 41  Journal of Current Clinical Care Volume 4, Issue 6, 2014

or walking and is usually aggravated by motion. It is frequently seen in elderly patients and typically points towards neuromuscular pathology. Finally, patients with light-headedness often report prolonged dizziness, often in association with other non-specific symptoms. Light-headedness may point towards anxiety and hyperventilation, and it is usually a diagnosis of exclusion.

Differentiating Between Central and Peripheral Causes of Vertigo Once vertigo has been distinguished from other forms of dizziness, physicians should establish whether symptoms originate from a central or peripheral pathology. Central and peripheral vertigo represent two broad categories by which physicians can form a dif-

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ferential diagnosis. While not as common as peripheral vestibulopathies, the presence of central disorders such as posterior fossa tumours, cerebellar infarction and hemorrhage, or vertebrobasilar artery occlusion may require emergency management and should not be overlooked. Peripheral vertigo is caused by damage to or dysfunction of the inner ear, including the vestibular apparatus or vestibular nerve. Central vertigo arises from injury to the central nervous system, namely the brainstem or cerebellum. Peripheral causes of vertigo comprise approximately 80% of all cases, of which benign paroxysmal positional vertigo, vestibular neuronitis and Meniere’s disease are the most common.3 Although central and peripheral vertigo share many clinical features, they can often be discerned based on several distinguishing factors: direction and type of nystagmus, presence of auditory symptoms, degree of imbalance, and findings of additional neurological symptoms.4 Peripheral vertigo presents with combined unidirectional horizontal and torsional nystagmus that can be suppressed by visual fixation and is often triggered by a provoking event. Conversely, central vertigo is associated with purely horizontal, vertical or torsional nystagmus that may change direction with gaze and is not suppressed by visual fixation. Audi42  Journal of Current Clinical Care Volume 4, Issue 6, 2014

tory symptoms such as hearing loss and tinnitus are rarely seen with central vertigo but more often accompany several forms of peripheral vertigo. Typically, vertigo and nausea is more severe in patients with peripheral vertigo, while patients with vertigo of a central origin often experience a greater degree of postural instability. Additionally, central vertigo is frequently associated with non-auditory focal neurological symptoms. Although these clinical features can help physicians differentiate between central and peripheral pathology, a more detailed history and physical exam should be performed to further isolate the origin. Cerebral imaging (CT scan or MRI) can confirm the diagnosis of a central cause of vertigo.

Peripheral Causes Benign Paroxysmal Positional Vertigo Benign paroxysmal positional vertigo (BPPV) is the predominate cause of dizziness and vertigo in adults (Figure 2).3,5 Population based epidemiological data estimates the lifetime prevalence of BPPV to be 2.4%.6 The one-year prevalence of BPPV increases considerably with age, from 0.5% in those aged 18 to 39 years to 3.4% in those 60 years or older.6 It is thought the true prevalence of BPPV is underestimated as a result of poor recognition rates in primary care;7 indeed, a study of

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Vertigo and Dizziness Paroxysmal Positional Vertigo (BPPV) Figure 2: Benign

Semicircular canal function in vestibular sensation

Head rotation

Location of Semicircular Canals Endolymph flow

Superior canal

Displacement of cupula

Ampulla

Posterior canal

CNVIII

Utricle

Horizontal canal

Cupula Hair cells Decreased neural firing

Head rotation

Saccule Cupula

Endolymph flow

Endolymphatic sac Displacement of cupula

Cupulothiasis CNVIII

Canalithiasis Otholothic debris

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Increased neural firing

Otholothic debris



Vertigo and Dizziness

Figure 3: The Dix-Hallpike Maneuver

patients presenting to a geriatric clinic for various medical conditions found that 9% had undiagnosed BPPV.8 BPPV can be classified based on semicircular canal involvement and further divided by its pathological mechanism. BPPV most commonly involves the posterior or horizontal semicircular canals, while superior semicircular canal involvement is

Figure 4: The Epileys Maneuver

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exceedingly rare. Posterior canal BPPV accounts for 60 to 95% of all cases, presumably because it is located at the most dependent position in the vestibular system in both an upright and supine position.9,10 The physiological mechanism of BPPV is thought to occur as a result of one of two proposed theories: cupulothiasis and canalithiasis. Cupulothiasis was first described by Schuknechtin 1969 who proposed that BPPV is a result of dislodged otoconia from the otolith organs adhering to the cupula of a semicircular canal.11 The specific gravity of otolithic debris is greater than that of endolymph, rendering the semicircular canal gravity sensitive and producing pathological vestibular ocular reflexes when the head is held in certain positions. The canalithiasis theory was later proposed by Hall et al., who described BPPV as being the result of dislodgment of otoconia crystals similar to cupulolithasis; however, the otoconia debris remain as free floating particles in the semicircular canals.12 Although there is increasing consensus that both mechanisms exist and account for different presentations of the disease, canalithiasis is thought to better explain the typical features of BPPV.13 The characteristic clinical presentation of BPPV is episodic vertigo lasting for less than one minute following rapid head movements, with or without nausea.

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The Dix-Hallpike test (Figure 3) can be performed in an office setting or at the bedside and is the primary way by which posterior canal BPPV is diagnosed. The character-

Migraine headache is more prevalent in several well-defined peripheral vestibular disorders, with reports indicating two to three times the prevalence of migraines in patients with idiopathic

BPPV…

istic response to the Dix-Hallpike maneuver is a short latency period followed by mixed torsional and vertical nystagmus that is fatigable with repetition of the test. Upon returning the patient to an upright position the nystagmus is reversed in direction. In the case of atypical BPPV, the horizontal canal variant is more reliably diagnosed by the supine roll test (the Pagnini-

Figure 5: Brandt Daroff Exercise for Home Remedy for Vertigo

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McClure maneuver),14 although the Dix-Hallpike maneuver may elicit the characteristic nystagmus and vertigo. For a more comprehensive assessment of vertigo and associated nystagmus, both electronystagmography and videonystagmography are effective diagnostic lab techniques.15 The current recommended therapies for posterior canal BPPV are Brandt-Daroff exercises16 (Figure 4) and Epley17 (Figure 5) and Semont18 canalith repositioning maneuvers. Brandt-Daroff exercises involve a series of physiotherapeutic vestibular habituation exercises that patients seeking an active treatment for BPPV symptoms can perform at home. The canalith repositioning maneuvers consist of a sequence of patterned head movements that ultimately relocate otolithic particles from the semicircular canals to the vestibule of the inner ear. Although the repositioning procedures have been met with success since their introduction, both the Epley and Semont maneuvers are associated with high recurrence rates. Accordingly, current evidence suggests that repositioning maneuvers in combination with vestibular rehabilitation are most effective for sustained functional recovery of BPPV.19 Epley and Semont maneuvers are usually unsuccessful at treating horizontal canal BPPV, as a result alternative therapies have been explored. Although the strength of evidence

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is insufficient to draw conclusion on the efficacy of various therapies for horizontal canal BPPV, the Lempert (barbecue) roll maneuver, or similar variants, are the most

Vertigo may appear at or following the onset of headache, with only 10% of cases preceding headache as would be typical of an aura.

widely published treatment and are thought to be effective in the majority of cases.20 Vestibular suppressants, namely anticholinergics, antihistamines, and benzodiazepines, may be used for symptom relief but do not correct the underlying pathological mechanism and therefore do not decrease the frequency of symptoms. Vestibular neurectomy or post-semicircular canal obliteration is reserved for rare cases with severe, uncompromising symptoms.

Vestibular Neuronitis Vestibular neuronitis, also known as acute unilateral peripheral vestibulopathy, accounts for 3 to 10% of visits to specialty vertigo clinics.5 Although data is scarce, the peak age distribution of vestibular neuronitis is between 30 and 50.21 The only published estimate of the incidence of vestibular neuronitis is 3.5 46  Journal of Current Clinical Care Volume 4, Issue 6, 2014

per 100,000 population;21 however, this is likely an underestimate of the true frequency in the population.5 The etiology of vestibular neuronitis is often unclear. It is thought to result from viral or postviral inflammation; however, fewer than 50% of patients report or show signs of a preceding or associated infection.22 Other possible causes include bacterial infections or acute localized ischemia of the vestibular nerve. Vestibular neuronitis is characterized by an acute onset of severe rotatory vertigo, imbalance, and nausea and vomiting with spontaneous horizontal nystagmus.23 Symptoms develop rapidly over several hours then gradually subside over the course of days to several weeks. Auditory function is preserved in vestibular neuronitis. Patients that present with unilateral hearing loss or tinnitus in addition to this syndrome are believed to have involvement of the entire labyrinth, in which case the term labyrinthitis is used. As the etiology of vestibular neuronitisis unknown, diagnosis is made largely based on history and presentation. With all cases of acute prolonged vertigo, it is important to differentiate peripheral from central causes in order to rule out serious or life-threatening disorders that may require immediate intervention. Stroke in the posterior fossa can closely mimic

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vestibular neuronitis, often without focal neurological symptoms, and should therefore be ruled out when patients present with peripheral vestibular symptoms lasting more than 24 hours. A simple bedside oculomotor examination including the results of a head-impulse test, pattern of nystagmus and presence of skew deviation (vertical strabismus) is highly sensitive and specific in differentiating stroke from more benign conditions.24 There is no agreed upon standard treatment regimen for vestibular neuronitis. Therapy usually consists of management of associated infection if present and symptomatic treatment with vestibular suppressants. Though controversial, corticosteroids may accelerate early recovery of vestibular function, although long-term prognosis remains unchanged.25 Prompt vestibular rehabilitation to reduce vestibular asymmetry through central compensation is recommended and is thought to be effective in accelerating the rate and increasing the level of recovery after the occurrence of a vestibular lesion.26 Despite an absence of specific guidelines for the treatment of vestibular neuronitis, most patients make a complete recovery.

as low as 17 cases per 100,000.27 The American Academy of Otolaryngology—Head and Neck Surgery (AAOHNS) has since established revised diagnostic criteria28 for Meniere’s disease, and a more recent study using these guidelines estimated the prevalence to be 513 per 100,000, considerably higher than previous reports.29 Although the etiology of Meniere’s disease remains obscure, it is generally believed to result from a distortion of the membranous labyrinth of the inner ear. Historically, the symptoms of Meniere’s disease were thought to be generated by endolymphatic hydrops, however studies have since shown that while patients with Meniere’s disease consistently have endolymphatic hydrops, some patients with endolymphatic hydrops do not display symptoms of Meniere’s disease.30,31 As a result, endolymphatic hydrops is considered the primary histological marker for Meniere’s disease rather than the common pathway for the production of its symptoms (Figures 6 and

Figure 6: Normal Membranous Labyrinth

Meniere’s Disease Meniere’s disease is a chronic and often debilitating peripheral vestibulopathy. Few epidemiological studies have been performed on Meniere’s disease. Early studies reported the prevalence of Meniere’s disease to be 47  Journal of Current Clinical Care Volume 4, Issue 6, 2014

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7). The exact factors that distort homeostatis in the labyrinth and ultimately cause both the symptoms of Meniere’s disease and endolymphatic hydrops have yet to be identified. Nevertheless, many causes have been proposed including obstruction of the endolymphatic duct or sac,32 hypoplasia of the vestibular aqueduct,33 genetic predisposition,34,35 viral etiology36 and autoimmune mechanism.37,38 The numerous histological findings that have been implicated in the pathogenesis of Meniere’s disease suggest a multifactorial etiology. Meniere’s disease presents with a characteristic set of symptoms including episodic vertigo, tinnitus and fluctuating sensorineural hearing loss, with nausea and aural fullness occasionally being reported. Vertigo can be severe and is typically rotatory lasting for minutes to hours. Although symptoms of Meniere’s disease often fluctuate, they usually appear together. Unilateral symptoms are typical, however bilateral symptoms often develop over time. The disease most commonly affects individuals in their thirties and forties although it can manifest at any age.39 There are no definitive objective tests specific to Meniere’s disease; as a result, it remains a clinical diagnosis. According the AAO-HNS guidelines,28 for a diagnosis of Meniere’s disease to be made patients must present with at least two spontaneous episodes 48  Journal of Current Clinical Care Volume 4, Issue 6, 2014

Figure 7: Dilated Membranous Labrynth in Endolymphatic Hydrops (Meniere’s Disease)

of vertigo lasting 20 minutes or longer, audiometrically documented hearing loss along with tinnitus or aural fullness in the affected ear. A thorough physical examination must be performed to exclude other disorders. While not conclusive, MRI may identify features of Meniere’s disease40,41 and is important in ruling out central nervous system lesions. Videonystagmography and electonystagmographic testing with bithermal caloric evaluation may be used to corroborate a diagnosis of Meniere’s disease.39 The fluctuating nature of Meniere’s disease, characterized by intermittent periods of exacerbation and remission, together with a lack of controlled trials has made it challenging to assess the effectiveness of therapeutic interventions. As a result, empirical treatment remains the most common therapy for Meniere’s disease. Currently, therapy is focused on reducing the number and severity of attacks of vertigo and tinnitus, alleviat-

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ing hearing loss, relieving chronic symptoms, and preventing progression of the disease. For acute management, vestibular suppressants and anti emetics are used to lessen

the widespread use of diuretics for Meniere’s disease, a recent systematic review assessing diuretic treatment found no high quality evidence for its effectiveness in Meniere’s disease;45 nevertheless, it remains a generally safe option and atients with chronic eniere s common treatment. The association between disease should first attempt immunological dysfunction and conservative before any pharma Meniere’s disease has led to the use of corticosteroids in the manceutical or surgical therapy is agement of symptoms. Oral corticosteroids have been shown to offered decrease both the duration and frequency of vertigo episodes.46 vertigo symptoms. Patients with For patients who do no respond chronic Meniere’s disease should to oral corticosteroid treatment or first consider conservative treatwho exhibit progressive or sudden ment before any pharmacological hearing loss, transtympanic steroid or surgical therapy is attempted. perfusion may be given. A prospecReducing emotional stress,42 salt tive, double blind, randomized conintake,43 chocolate consumption, trolled trial showed that systemic 39 intratympanic dexamethasone and avoiding tobacco and alcohol serves a crucial role in the preven- injections in patients with unilattion of attacks, although the relaeral intractable Meniere’s disease led to 82% of complete control of tionship between these triggers and Meniere’s disease remain to be vertigo compared to 57% in the placebo group, with considerably clarified. greater subjective improvement While lifestyle modifications in tinnitus, hearing loss and aural may control symptoms in some fullness in the treatment group.47 patients with Meniere’s disease, a significant proportion require Although the therapeutic efficacy pharmacological intervention. of steroids in Meniere’s disease Diuretics combined with salt remains controversial, studies that restriction have generally been have been performed show promisthe treatment of choice. By reduc- ing results. ing the volume status of a patient, Vestibular rehabilitation is diuretics are thought to decrease thought to be of value in improvendolymphatic fluid volume and ing balance in patients sufferpressure in the inner ear.44 Despite ing from disequilibrium between

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acute attacks of vertigo, or in patients with residual vertigo following medical or surgical treatment.48 Ablative therapy using aminoglycosides has been performed since the 1950’s49 for patients with intractable symptoms and continues to be used. Two recent prospective, doubleblind, randomized controlled trials found a significant reduction in vertigo with gentamycin treatment,50,51 although this type of ablation therapy presents a considerable risk of hearing loss.50 For cases in which medical treatment fails and patients continue to experience unremitting symptoms, surgical intervention may be performed. There exists various surgical procedures for the management of Meniere’s disease, and the choice of procedure is usually determined by the surgeon’s experience and preference. Surgical procedures include, but are not limited to, endolymphatic sac surgery, labyrinthectomy, vestibular nerve section, and cochlear implantation. As with the majority of treatment modalities for Meniere’s disease, a lack of definitive studies evaluating surgical therapy exist.52 Although treatment of Meniere’s disease continues to provoke debate among physicians, the majority of patients can be managed effectively with one or a combination of lifestyle, pharmacological, or surgical interventions. 50  Journal of Current Clinical Care Volume 4, Issue 6, 2014

Figure 8: Superior Semicircular Canal Dehiscence

Superior semicircular canal dehiscence Superior semicircular canal dehiscence is caused by thinning or complete absence of the bony roof of the superior semicircular canal (Figure 8). It presents with unsteadiness during motion and is relieved by rest. Other symptoms include conductive deafness with valsalvainduced dizziness, Tullio phenomenon (sound induced dizziness), and autophony. A fistula test, where pressure is applied to the tragus, and test for Hennebert sign, where pressure applied to in the external auditory, both result in vertigo or nystagmus and are therefore positive. Highresolution coronal CT scan of temporal bones with less than 0.6mm cuts can confirm dehiscence (Figure 9). Treatment includes lifestyle modification to avoid aggravating factors or surgery to plug the dehiscence of the superior canal.

Perilymph fistula Perilymph fistula is a rare cause of dizziness and consists of an abnor-

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Figure 9: Anatomy Showing Superior Petrosal Sinus Dehiscence

approach to seal the fistula with fat, fascia or muscle graft may be performed.

CENTRAL CAUSES Vestibular Migraine

mal communication between the fluid-filled perilymphatic space of the inner ear and the air-filled middle ear or mastoid process. This type of abnormal rupture commonly results from direct trauma, acoustic trauma, barotrauma, congenital causes, and pathological mechanisms (cholesteatoma), which leads to leakage of perilymph into the middle ear usually through the oval window or round window (Figure 10). Symptoms include fluctuating hearing loss with episodes of vertigo, and symptoms are typically aggravated by sneezing, coughing or straining. Patients experience the Tullio phenomenon and show a positive fistula sign. In some cases, management is conservative and includes bed rest, elevation of the head, and use of stool softeners (to prevent straining). For a more definitive treatment, surgical exploration using a transcanal 51  Journal of Current Clinical Care Volume 4, Issue 6, 2014

Although it has long been known that a relationship exists between migraine and vestibular symptoms in children53 and adults,54 only recently have clinicians and researchers begun to increasingly accept vestibular migraine as a distinct diagnostic entity. Despite gaining interest, studies of vestibular migraine were complicated by complex and inconsistent manifestation, lack of biomarkers and absence of universally recognized diagnostic criteria.55 Moreover, migraine headache is more prevalent in several well-defined peripheral vestibular disorders, with reports indicating two to three times the prevalence of migraines in patients with idiopathic BPPV56,57 and two times the prevalence with Meniere’s disease.58 The overlap in presentation between

Figure 10: Showing Fistula at Round

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The clinical presentation of vestibular migraine is episodes of spontaneous and positional vertigo, with many patients experiencing a sequence of spontaneous vertigo developing into positional vertigo over the course of the epihe temporal association sode.65 Duration of the vertigo can range from seconds to days and can between headache and vestibu recur at irregular intervals, days or lar symptoms is inconsistent and even years apart.66 The temporal association between headache and often does not occur in close vestibular symptoms is inconsistent and often does not occur in relation a factor that aids in close relation, a factor that aids in distinguishing vestibular migraine distinguishing vestibular migraine from migraines with visual aura. from migraines with visual aura Vertigo may appear at or following the onset of headache, with only 2012 that consensus diagnostic cri- 10% of cases preceding headache teria was established for vestibular as would be typical of an aura.66 Other symptoms can include head migraine.60 motion intolerance, photophobia, Prior to the development of phonophobia, and hearing loss. a universally recognized definiPhysical examination of tion for vestibular migraine, Neupatients with vestibular migraine is hauser and colleagues developed typically normal between episodes. diagnostic criteria that were used During the attacks of vestibular in a number of studies.61 A longmigraine, patients usually exhibit term follow-up study reevaluated Neuhauser and colleagues criteria nystagmus that suggests central positively.62 Using the ‘Neuhauser vestibular dysfunction.67 Since criteria’, the lifetime prevalence of test results are often inconsistent vestibular migraine is estimated to in these patients and no findings be 1%.63 Based on these measures, are pathognomonic of vestibular migraine, testing is solely pervestibular migraine is the second most common cause of vertigo and formed to rule out other causes of the most common cause of sponta- vestibulopathy. The pathophysiology of migraines in general remains neous episodic vertigo in adults.64 controversial, and there is even less Vestibular migraine can develop at any age, with a clear female pre- agreement on the pathophysiology of vestibular migraine.68 dominance.61 these disorders, together with the finding that dizziness can serve as a trigger for migraines,59 has traditionally made vestibular migraine difficult to diagnose. It was only in

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Because of a lack of conclusive randomized controlled trials for vestibular migraine treatment, choice of therapy remains controversial and usually involves prophylactic or symptomatic treatment of the underlying migraine. It is generally recommended that the first line of treatment involves dietary modification, improved sleep hygiene and avoidance of trigger factors.69 If non-pharmacological treatment is inadequate, pharmacological prophylactic treatment can include anticonvulsants, antihypertensives, and antidepressants.70,71 For patients with severe and frequent episodes, acute treatment of migraines with triptans,72,73 antihistamines and antiemetics70 have shown modest benefit in several small studies. Furthermore, a retrospective study found that vestibular rehabilitation in addition to antimigraine medication provided patients with improved functional outcomes.74

for 6% of patient visits for dizziness.3 Patients with vertebrobasilar insufficiency typically present with transient episodes of neurological symptoms that can be traced to the posterior circulation. Wallenberg’s syndrome, cerebellar infarction or hemorrhage, and brainstem ischemia resulting from transient ischemic attacks represent arterial insufficiency syndromes related to vertigo. Wallenberg’s syndrome, also known as lateral medullary syndrome, is a result of occlusion of the posterior inferior cerebellar artery with subsequent infarction of the lateral medulla oblongata. Clinical signs and symptoms depend on the affected nerve tracks, however the syndrome is typically characterized by acute vertigo with neurological deficit including ipsilateral Horner’s syndrome, ipsilateral ataxia, and loss of pain and temperature on the ipsilateral face and contralateral body. Brainstem ischemia due to transient ischemic attacks lead to episodes of vertigo lasting from minutes to hours and Cerebrovascular disorders usually present with concomitant The vertebrobasilar arterial system neurological symptoms including serves as the blood supply for the but not limited to visual disturvestibular end organs, the vestibu- bances, dysphagia and ataxia. Cerlar nuclei and the vestibulocerebel- ebellar infarction and hemorrhage lum. As a result, vertebrobasilar manifest as sudden onset of headinsufficiency can cause vestibuache, vertigo, nausea and vomitlar symptoms due to peripheral ing with unsteady gait. Associated vestibular dysfunction, central brainstem signs may be present vestibular dysfunction, or both. and depend on the vascular distriCerebrovascular disease accounts bution affected or on the presence

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of compression of the brainstem secondary to edema.

Figure 11: MRI Showing Left Acoustic Neuroma

Cerebellopontine angle tumours Acoustic neuromas (vestibular schwannomas) are benign tumours arising from myelin-forming cell sheaths lining the vestibulocochlear nerve. Acoustic neuromas account for 80% of tumours of the cerebellopontine angle and 5% to 10% of all intracranial tumors.75 Other lesions of the cerebellopontine angle include meningiomas and epidermoids and present with similar signs and symptoms as acoustic neuromas. Despite accounting for less than 1% of visits for dizziness and vertigo, brain tumours should always be considered, as a delay in diagnosis may cause significant morbidity. Patients with an acoustic neuroma present with progressive unilateral hearing loss, tinnitus, and imbalance. While not invasive, un treated tumours can expand in the internal auditory meatus and compress the facial nerve causing facial weakness or paralysis. MRI is the preferred diagnostic test for both acoustic neuromas and meningiomas of the cerebellopontine angle (Figure 11).

Multiple Sclerosis While only a small proportion of patients with multiple sclerosis (MS) present with vertigo as their first neurological symptom, most patients with MS will develop vestibular symptoms over the course of the disease. Both peripheral and 54  Journal of Current Clinical Care Volume 4, Issue 6, 2014

central vestibular symptoms may be present in patients with multiple sclerosis depending on the location of lesions. Vertiginous symptoms can last for days to weeks and may resemble vestibular neuronitis. Although associated neurological signs are dependent on the site of demyelination, commonly reported symptoms include eye-movement abnormalities, changes in balance, and sensory and motor deficits.76

Arnold Chiari Malformation Arnold Chiari Malformation is a type of congenital malformation of the brain that consists of displacement of the cerebellar tonsils below the foramen magnum (Figure 12). Symptoms often develop in middle age and include headache, dizziness, aural fullness, tinnitus and fluctuating hearing loss. Diagnosis is made by MRI and should prompt consultation with neurosurgery.

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Figure 12: Showing Downward Displacement of Cerebellum Below Foramen Magnum Causing Cerebellar Hypoplasia and Obliteration of Cisterna Magna

Vertigo in Children

Of note, benign paroxysmal positional vertigo and Meniere’s disease, The prevalence of vestibular discommon causes of vertigo in adults, account for a mere 1.8% and 1.5%, orders in the pediatric population reportedly ranges between 0.7% and respectively. 15%.77 Although few epidemiological studies have focused on children Drug-induced Vertigo with dizziness, reports that have Dizziness is an undesired effect of been published indicate that the many medications. The following primary causes of vertigo in chilrepresent medications that comdren are benign paroxysmal vertigo monly result in dizziness: aminoglyof childhood (BPVC),78,79 and vescosides, antiepileptic, tranqualizers, tibular migraine,80-85 vestibular neu- antihypertensives, anti-parkisonian ronitis,86 and trauma.87 Although drugs, skeletal muscle relaxants, excluded from most studies, otitis and urological medications (Sildemedia related dizziness is also a nafil and oxybutynin). common cause of vertigo in chilConclusion dren. While the prevalence of each of these disorders varies across liter- Patients with vertigo present a comature reports, BPVC and vestibular plex and often frustrating diagnostic migraine accounted for 18.7% and challenge to family physicians, oto17.6%, respectively, of all cases of laryngologists and neurologists alike. vertigo and dizziness in children.88 Eliciting a precise description of the 55  Journal of Current Clinical Care Volume 4, Issue 6, 2014

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SUMMARY OF KEY POINTS Dizziness is a common symptom cause of medical visits. Detailed history could differentiate vertigo from vertigo like symptoms. Proper examination and investigations could differentiate central type from peripheral type of vertigo.

After establishing a diagnosis the treatment is tailored accordingly. Most of Vertigo are benign or self limiting, rare cases of central vertigo may be life threatening require an immediate attention.

dizziness is crucial in identifying a specific diagnosis. A detailed history together with oculomotor, vestibular and neurological findings should help guide the physician in differentiating between central and peripheral causes. Although most causes of vertigo are benign, rare cases of central vertigo may be life-threatening requiring immediate medical attention.

Acknowledgement Authors want to thank Ms. France Carrier, the Librarian who has helped in the literature search. Dr. Pradeep Shenoy takes full responsibility for the integrity of the content of paper. Competing interest: none declared

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Kroenke, K. et al. Causes of persistent dizziness. A prospective study of 100 patients in ambulatory care. Annals of internal medicine117, 898-904 (1992). Newman-Toker, D. E. et al. Spectrum of dizziness visits to US emergency departments: cross-sectional analysis from a nationally representative sample. Mayo Clinic proceedings83, 765-775, doi:10.4065/83.7.765 (2008). Kroenke, K., Hoffman, R. M. & Einstadter, D. How common are various causes of dizziness? A critical review. Southern medical journal93, 160-167; quiz 168 (2000). Buttner, U., Helmchen, C. & Brandt, T. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta oto-laryngologica119, 1-5 (1999). Neuhauser, H. K. Epidemiology of vertigo. Current opinion in neurology20, 40-46, doi:10.1097/ WCO.0b013e328013f432 (2007). von Brevern, M. et al. Epidemiology of benign paroxysmal positional vertigo: a population based study. Journal of neurology, neurosurgery, and psychiatry78, 710-715, doi:10.1136/jnnp.2006.100420 (2007). von Brevern, M., Lezius, F., Tiel-Wilck, K., Radtke, A. & Lempert, T. Benign paroxysmal positional vertigo: current status of medical management. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery130, 381-382, doi:10.1016/j.otohns.2003.07.007 (2004).

CLINICAL PEARLS

Dizziness and vertigo can be differentiated by a thorough history and comprehensive physical exam. Vertigo of a central origin typically presents with relatively severe gait instability and ataxia. Peripheral vertigo has nausea and vomiting as more prominent symptoms. Pattern of nystagmus, presence of auditory symptoms and additional neurological signs can further distinguish a central or peripheral etiology. 56  Journal of Current Clinical Care Volume 4, Issue 6, 2014

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8.

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14. 15.

16. 17.

18. 19.

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