CNS Causes of Vertigo

Back

Background

Dizziness is a vague and nonspecific symptom. It refers to an abnormal sensation in relation to space and position. Vertigo is a specific type of dizziness that is defined as a spinning or rotatory sensation. Patients with vertigo report that things are rotating around them or that they are rotating around things.

Vertigo could be either from a peripheral (labyrinth and vestibular nerve) or a central disorder (central nervous system). Central vertigo is usually a result of an abnormal processing of the vestibular sensory input by the central nervous system.

See the image below.



View Image

Electrode montage for electronystagmography (ENG) testing.

Pathophysiology

The sensation of balance is the result of appropriate information detected by the vestibular, ocular, and proprioceptive sensory receptors that is then properly integrated within the cerebellum and brain stem. Proper gait, posture, and visual focus during head movement all depend on an intact sense of balance. Loss of sensory information, central integration, and output control mechanisms all result in a sense of imbalance.

Central causes of vertigo result from either a disruption of central integrators (ie, brain stem, cerebellum) or a sensory information mismatch (ie, from the cortex). Lesions that affect the vestibular nerve or root entry zone (ie, cerebellopontine angle [CPA] lesions) result in imbalance by affecting primary vestibular sensory information.

Epidemiology

Race

No racial predilection exists for CNS causes of vertigo.

Sex

Men and women are affected differently by different causes of CNS vertigo. Vestibular migraine (migraine-related vertigo, or migrainous vertigo), for example, shows a predilection for women.

Age

CNS causes of vertigo typically affect older population groups because of the associated risk factors of vascular causes of vertigo, such as hypertension, atherosclerosis, and diabetes mellitus.[1]

Younger population groups are more commonly affected by migraine headaches and multiple sclerosis (MS).[2] Cerebellar tumors affect a bimodal population of children and adults. CPA tumors typically affect people in the fifth to eighth decades of life.

A study by Teggi et al involving 252 patients with vestibular migraine found the ages of onset for migraine and vertigo to be 23 years and 38 years, respectively, in this group. Onset of migraine tended to occur at a lower age in patients with a family history of migraine, while the age of vertigo onset tended to be lower in patients with a childhood history of benign paroxysmal vertigo, benign paroxysmal torticollis, and motion sickness.[3]

History

The history is of critical importance to determine if the vertigo is from a peripheral or central origin because usually physical findings and vestibular testing can only provide supportive information. Peripheral vertigo could be positional, lasting for seconds to a few minutes (such as in benign paroxysmal positional vertigo); recurrent, lasting for hours and associated with hearing loss, aural fullness, and tinnitus (such as in Meniere syndrome),[4] or a single episode lasting days without associated auditory or neurological symptoms (such as in vestibular neuronitis).

Central vertigo should be considered when the patient’s history is not consistent with any of the well-defined peripheral syndromes. The history could be acute or chronic vertigo, usually associated with neurologic symptoms. The presence of neurologic symptoms such as headaches, aura, visual, sensory or motor symptoms is more suggestive of a central disorder.[5, 6, 7]

In the aforementioned study by Teggi et al, in which the characteristics of 252 individuals with vestibular migraine were evaluated, a family history of vertigo was reported by 167 patients (66.3%).[3]

Physical

The physical examination should also focus on findings that are consistent with either peripheral or central vestibular disorders. Findings suggestive of peripheral vestibular dysfunction include a positive head thrust test indicative of an abnormal vestibuloocular reflex (VOR), turning greater than 45° on the Fukuda stepping test, ability to perform tandem gait testing with eyes open but not closed, or a positive Dix-Halpike maneuver suggestive of benign positional vertigo (BPV).

Findings suggestive of central pathology are abnormalities on the neurologic examination such as diplopia, dysarthria, aphasia, weakness, and sensation abnormalities.

Signs of a cerebellar dysfunction such as dysmetria on finger-to-nose testing and dysdiadochokinesia are also characteristic of a central problem.[7, 8]

One of the most helpful tools during physical examination is an evaluation of any nystagmus. Nystagmus is be defined as a repetitive involuntary movement of the eyes. This is initiated by the slow phase, which is generated by the underlying disorder. The slow phase takes the eye away from the preferred position, and the fast phase (or saccade) brings the eye back to the visual target. The direction of the fast phase describes the direction of the nystagmus; the velocity of the nystagmus is determined by the slow phase.[9, 10]

Causes

Migraine-related vertigo or vestibular migraine

Migraine is a neurovascular disorder of the central nervous system that is caused by constriction and dilatation of intracranial blood vessels. The problem appears to be a dysfunction of ion channels in the aminergic nuclei of the brainstem and diencephalon. It is characterized by recurrent episodes of headaches, usually unilateral, and throbbing, with associated phonophobia, photophobia, and nausea. Headaches may occur with or without prodromal symptoms (aura). The aura consists of neurologic symptoms, mostly visual (such as scotomas-flashing or colored lights), photophobia, and/or paresthesias, likely a result of decreased local cerebral perfusion that passes across the cortex. Vestibular symptoms such as dizziness, vertigo, and tinnitus are less common but are increasingly being recognized.[11, 12, 13]

Migraine affects about 6-20% of men and 18-29% of women.[14, 15] Vertigo is 3 times more common in patients who suffer from migraine than controls. Therefore, establishing which patients have migrainous vertigo (MV) and which ones just have these conditions as separate entities is important.[16]

The relationship between vertigo and headache is variable.[17] Some patients experience the vertigo and headache as a completely separate event. In others, the headache can occur simultaneously with vertigo (25% of patients) or prior to the onset of vertigo (25% of patients). Vestibular symptoms precede headache in 50% of cases. Head motion intolerance is present in 30% of patients and typically persists after the acute attack of vertigo subsides. The duration of the vertigo can last from seconds (10%), minutes (30%), hours (30%) to days (30%).[17] Therefore, 10-30% of patients present with symptoms that are of typical duration of a migraine aura (5-60 minutes).

Most patients present with other migrainous symptoms that include photophobia, phonophobia, osmophobia, visual, or other auras. Photophobia is the most prevalent, present in 70%. These symptoms are extremely important to recognize because sometimes they are the only connection between the vertigo and migraine. Also, the patients should be asked about triggering factors such as food, hormonal changes (menstrual cycle), excessive stress, and sensory stimuli.

Hearing loss and tinnitus are not prominent symptoms. Hearing loss, when present, is usually mild and transient, without progression in the course of disease. Some patients can present with fluctuating hearing loss during the episodes, confusing the diagnosis with Meniere disease. Around 20% of patients report aural pressure for seconds to minutes at the beginning of the acute attack.[17]

Benign paroxysmal vertigo of childhood (BPVC) is considered to be an early manifestation of MV and a predictor for the development of migraine headaches. It is characterized by vertigo with nystagmus, nausea/vomit, and anxiety in an otherwise healthy child. Many of these children present with migraine later in life.[18]

A Korean study, by Lee et al, of children and adolescents who were patients in the otolaryngology departments of 11 hospitals, found that dizziness was most often caused by vestibular migraine and BPVC in children aged 7-12 years and that vestibular migraine was the most common cause in adolescents aged 13-18 years. In children aged 6 years or younger, vestibular migraine was the second most common cause of dizziness, after BPVC.[19]

Another study, a literature review by Davitt et al that encompassed 2726 children aged 2 months to 19 years, reported that vestibular migraine was the most frequent diagnosis associated with childhood vertigo (23.8%), followed by BPVC (13.7%).[20]

A consensus about the diagnosis and treatment of migrainous vertigo is evolving. Like migraine itself, MV is diagnosed based on history and physical examination. Several authors proposed different criteria in retrospective studies. One proposed criteria defines definite MV and probable MV:[21]

Notice that the response to treatment is not considered a diagnostic criteria.

Basilar migraines are relative rare causes of migraines that involve pathology within the posterior circulation of the brain. Multiple neurologic symptoms including vertigo, dysarthria, dysphagia, and paresthesias precede the onset of the headache.

Examination of patients with a history of migrainous vertigo is typically normal. Spontaneous or positional nystagmus may be visualized during an acute attack. ENG testing may be normal or reflect a peripheral vestibular loss or central pathology.[9]

Treatment of headaches includes modification of lifestyle, elimination of trigger factors, treatment of acute attacks, and prophylactic medications, when indicated. Evidence-based guidelines for the management of migraine headaches have been published and are reviewed elsewhere. Prophylactic medications aim to reduce frequency of attacks and severity and may be indicated, depending on the number and severity of attacks, degree of disability, and response to acute attack treatments. The options include propranolol, valproate, amitriptyline, fluoxetine, gabapentin, and, more recently, topiramate. About 60% of patients have a reduction in symptoms.

Similarly to headaches, the vestibular symptoms of migrainous vertigo are managed with treatment of acute attacks and prophylaxis.[22] Acute attacks are managed initially with a vestibular suppressant.[23] The use of triptans for migraine-related vestibular symptoms is not well studied and may or may not benefit vertiginous attacks. Prophylactic treatment is indicated with frequent, severe, and disabling attacks. Beta-blockers, tricyclic antidepressants, and calcium-channel blockers are useful in preventing vestibular symptoms. Antiepileptic drugs such as valproate, gabapentin, and topiramate are effective and well tolerated. Changes in lifestyle and avoidance of trigger factors are important in preventing vestibular symptoms.

Vertebrobasilar disease

The vertebrobasilar system provides blood supply to the occipital, parietal and temporal lobes, thalamus, inner ear, cerebellum, and brainstem. The most common causes of vertebrobasilar disease (VBD) are embolism, large artery atherosclerotic disease, small (penetrating) artery disease, and arterial dissection.[24] Pathology within the vertebrobasilar system results in either recurrent episodes of transient neurologic deficits lasting minutes (vertebrobasilar insufficiency), TIA, or CVA.

A study by Paşaoǧlu found that among patients suspected of having central vertigo (without stroke) who were examined with computed tomography (CT) angiography, vertebral artery hypoplasia and stenosis of 50% or greater were seen more frequently than they were in the control group, with stenosis of 50% or greater found in 78 of 129 (60.5%) vertigo patients.[25]

Up to 25% of patients with VBD present with isolated vertigo. More frequently, VBD manifests with a combination of dizziness/vertigo, hearing loss, tinnitus, headache, nausea, visual disturbances, gait disturbances, paresthesias, motor weakness, and drop attacks. VBD symptoms are summarized into the “four Ds”: dizziness, diplopia, dysphasia, and drop attacks. Neurologic examination could be normal between attacks. Usually patients have risk factors for CVA and atherosclerosis, such as diabetes, hypertension, hyperlipidemia, hypercholesterolemia, hyperviscosity, and hypercoagulability.

Several specific syndromes are associated with ischemia to the territory supplied by anterior inferior cerebellar artery (AICA) or posterior inferior cerebellar artery (PICA).[26, 27] The territories vary among individuals; therefore, the clinical findings vary depending on the areas supplied by the ischemic vessel. Ischemia to the AICA distribution causes pontine syndrome.[27] The AICA supplies the lateral pons and gives off the internal auditory artery (IAA). Occlusion of this artery produces ischemia of the entire labyrinth and a degree of pontine ischemia, producing a syndrome that manifests as vertigo, tinnitus, and hearing loss. If the occlusion is distal, only the labyrinthine blood supply is compromised, producing symptoms and ENG findings that are identical to a peripheral disorder.

Ischemia to the PICA distribution causes Wallenberg syndrome (lateral medullary syndrome).[26] It is characterized with acute vertigo, nausea, and vomiting; ipsilateral facial pain and numbness; ipsilateral ataxia and decreased contralateral pain; and temperature sensation over the rest of the body; and ipsilateral Horner syndrome. Patients can also present with laryngeal and pharyngeal paralysis, leading to hoarseness and dysphagia.

In all patients in whom vertebrobasilar disease is suspected, imaging should be obtained. Imaging should include a magnetic resonance imaging (MRI) scan of the brain, as well as imaging of the vasculature with either an MR angiogram or a CT angiogram of the head and neck. A transcranial ultrasound that reveals flow in the vertebral arteries may also be helpful.

Treatment of VBD consists of treating the underlying pathology. Treatment is focused on controlling the risk factors for CVA and antiplatelet agents such as aspirin, dipyridamole, and pentoxifylline.[28] Chronic dizziness and disequilibrium usually improves with vestibular physical therapy. Treatment of TIA and stroke are beyond the scope of this review.[29]

Prognosis of ischemia to the posterior circulation differs significantly from anterior circulation. Acute basilar artery occlusion carries a very poor prognosis with a mortality rate higher than 80%. On the other hand, unlike the cerebral cortex, the brainstem is relatively resistant to ischemia, and recanalization therapy up to a period of 24 hours can still reverse the symptoms and sequelae.

Arnold-Chiari malformation

Arnold-Chiari Malformation consists of an abnormal displacement of the cerebellum and brainstem through the foramen magnum. The degree of displacement classifies the malformation in types I through IV. The most common is the type II, in which the cerebellar vermis, lower pons, and medulla is displaced.[30]

The associated symptoms are a result of the compression of the cerebellum and brainstem structures and stretching of cranial nerves. Patients can present with vertigo, ataxia, dysequilibrium, sensorineural hearing loss, headache, cranial nerve dysfunction (such as unilateral hypoglossal palsy), cervical pain, or weakness.

The diagnosis can be made by MRI, with the sagittal view being the most helpful in determining the degree of herniation.[31] The treatment is surgical. The results in terms of alleviating the vestibular symptoms are not well established, but case reports show some improvement.

Multiple sclerosis

Multiple sclerosis is an idiopathic demyelinating disorder of the central nervous system. It is thought to be an autoimmune disease, likely due to an autoantigen to one of the myelin proteins. The demyelinization occurs in different areas of central nervous system, most commonly in the white matter, with formation of plaques that disrupt signal conduction and lead to symptoms.

Typical onset is with optic neuritis, but in 5% of the cases vertigo is the presenting symptom. Over 50% of patients present with vertigo at one point in the course of the disease. The vertigo can last from hours to days. Nystagmus, when present, can be consistent with peripheral or central lesion. MS can mimic an VIIIth nerve lesion, when a plaque develops in the entry of the nerve root in the brainstem, producing vertigo, unilateral caloric weakness, and horizontal nystagmus.[32]

The diagnosis is made with imaging and CSF exam. On MRI, plaques can be seen in the white matter. On CSF, elevated levels of IgG can be identified. The treatment options are limited. Exacerbation episodes are treated with high-dose steroids and other immunosuppressants.[7]

Laboratory Studies

Few laboratory studies facilitate the diagnosis of the CNS causes of vertigo.

If vertigo is accompanied by prolonged nausea and vomiting in elderly patients, monitoring and replacing fluids and electrolytes is prudent.

In the rare case of suspected Lyme neuroborreliosis, serology for Lyme disease with enzyme-linked immunosorbent assay (ELISA), Western blot analysis, and lymphocyte antigen stimulation assay are indicated. Obtain cerebrospinal fluid for Lyme antibody tests and polymerase chain reaction analysis to evaluate for Borrelia burgdorferi DNA.

Imaging Studies

Imaging studies are indicated when the symptoms are suspected to result from ischemia. MRI and MR angiography are the most helpful studies in assessing posterior circulation disorders and acute infarction. Diffusion-weighted MRI is sensitive and specific for early detection and differentiation between vasogenic and cytotoxic edema in patients with acute neurologic deficits.

Other Tests

Electronystagmography (ENG) is the most used vestibular test. When combined with the patient’s history and examination, the results of the ENG can be used to support a diagnosis of a peripheral or central etiology.[5, 6] Nystagmus patterns may be spontaneous or may be elicited by a change in gaze, head position, or head shake. Patterns of central and peripheral nystagmus were discussed in the Clinical section. Abnormalities in smooth pursuit or saccades are typically central in origin.

See the image below.



View Image

Electrode montage for electronystagmography (ENG) testing.

Formal evaluation with vestibular testing is indicated if the diagnosis is not apparent after obtaining a history and performing a physical examination. Vestibular testing can facilitate distinction between central, peripheral, and mixed causes of imbalance and vertigo. The test battery assesses labyrinthine function with caloric testing, rotational chair testing, and vestibular evoked myogenic potential. Oculomotor integrity is evaluated with eye tracking during smooth pursuit, saccades, and optokinetic stimulation.[33] The evaluation of spontaneous and gaze-evoked nystagmus can provide critical clues to central pathology.

Abnormalities found by oculomotor testing that suggest a central balance problem include saccade inaccuracy and smooth pursuit dysmetria. Failure to suppress nystagmus with visual fixation is often a sign of disease that affects the cerebellar flocculus or neural connections between the flocculus and the vestibular nuclei.

Positional testing with infrared oculography can be used to reveal nystagmus and to clearly define nystagmus patterns. Multidirectional nystagmus, spontaneous nystagmus, or positional nystagmus that is downbeat, torsional, or dissociated suggests a central lesion.

If symptoms suggest hypoperfusion, embolic events, or arrhythmia as the cause, perform a complete cardiac and peripheral vascular examination, including ECG, Holter monitoring, echocardiography, and carotid and vertebral Doppler ultrasonography.

Medical Care

Medical treatment includes supportive care with fluid replacement and vestibular suppressants for intractable vertigo with nausea and vomiting.

Treatment of migraine-associated vertigo includes analgesics and vestibular suppressants. Drugs useful in the treatment of migraines include sumatriptan, propranolol, imipramine, amitriptyline, and nortriptyline, and the vestibular suppressants diazepam and alprazolam. For further information on the diagnosis and treatment of migraine headaches, please refer to the Medscape Reference topic Migraine Headache.

A retrospective, open-label study by Taghdiri et al indicated that the antihistamine cinnarizine (which currently is not available in the United States) can reduce headache and vertigo in vestibular migraine and migraine with brainstem aura. The investigators found that after 3 months of cinnarizine use, patients with these types of migraine experienced a significant decrease in the mean monthly frequency of vertigo episodes and migraine headaches, as well as a significant reduction in headache duration and intensity.[34]

A retrospective study by Çelebisoy et al indicated that acetazolamide can reduce the frequency and severity of vertigo attacks and, to a lesser extent, headache episodes, in vestibular migraine. The study included 39 patients, who were prescribed 500 mg/day of the drug.[35]

Control of hypertension, diabetes mellitus, and atherosclerosis is indicated for long-term prevention of further complications. Cardiac arrhythmia should also be controlled.

Drugs useful in the treatment of vertebrobasilar insufficiency include aspirin, ticlopidine, pentoxifylline, heparin, and warfarin. Acetazolamide is indicated for the treatment of familial ataxia syndrome.

Surgical Care

Surgical treatment of central vertigo is limited to urgent posterior fossa decompression of cerebellar and brainstem edema that complicates the infarction.

Cerebellopontine angle (CPA) tumors are surgically removed on an elective basis. If a medical contraindication exists, radiotherapy for tumor control is an option.

Consultations

Otolaryngologists, neurosurgeons, neurologists, and cardiologists are consulted for further diagnosis and treatment of vertigo of CNS origin.

Diet

Address dietary management of migraine-associated vertigo with the patient. Avoidance of triggers, such as red wine, chocolate, and cheese, may reduce the frequency of attacks.

Medication Summary

The goal of pharmacotherapy is to reduce morbidity and prevent complications.

Meclizine (Antivert, Antrizine, Meni-D)

Clinical Context:  Decreases excitability of middle ear labyrinth and blocks conduction in middle ear vestibular-cerebellar pathways. This decrease is associated with therapeutic effects in the relief of nausea and vomiting.

Dimenhydrinate (Dimetabs, Dramamine)

Clinical Context:  1:1 salt of 8-chlorotheophylline and diphenhydramine thought to be useful in the treatment of vertigo.

Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic effects. However, prolonged treatment may decrease rate of recovery of vestibular injuries.

Class Summary

These agents prevent the histamine response in sensory nerve endings and blood vessels. They are also effective in treating vertigo.

Scopolamine (Isopto)

Clinical Context:  Blocks action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS. Antagonizes histamine and serotonin action.

Transdermal scopolamine may be most effective agent for motion sickness. Use in vestibular neuronitis is limited by slow onset of action.

Class Summary

These agents work centrally by suppressing conduction in the vestibular cerebellar pathways.

Diazepam (Valium)

Clinical Context:  Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Individualize dosage and increase cautiously to avoid adverse effects.

Class Summary

By binding to specific receptor sites, these agents appear to potentiate the effects of γ -aminobutyric acid (GABA) and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. These effects may prevent vertigo and emesis.

Promethazine (Phenergan)

Clinical Context:  For symptomatic treatment of nausea in vestibular dysfunction.

Antidopaminergic agent effective in treating emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Prochlorperazine (Compazine)

Clinical Context:  May relieve nausea and vomiting by depressing reticular activating system and blocking postsynaptic mesolimbic dopamine receptors through anticholinergic.

Class Summary

These agents are effective in treating emesis, possibly because of effects in dopaminergic mesolimbic system.

Ephedrine (Pretz-D)

Clinical Context:  Stimulates release of epinephrine stores, producing alpha- and beta-adrenergic effects.

Class Summary

These agents may treat vertigo, possibly through modulating the sympathetic system.

Further Outpatient Care

After the underlying cause of vertigo has been identified and treated, supportive care with vestibular suppressants and antiemetics are indicated to relieve the vertigo. Early initiation of vestibular rehabilitation is an important and effective intervention.

Patient Education

For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education articles Vertigo and Dizziness.

What is vertigo?What is the pathophysiology of vertigo?What are the racial predilections of vertigo?What are the sexual predilections of vertigo?Which age groups have the highest prevalence of vertigo?How are clinical history findings used to differentiate between peripheral and central vertigo?Which physical findings are characteristic of vertigo?What is the role of migraine in the etiology of vertigo?What are the diagnostic criteria for migrainous vertigo (MV)?How is vestibular migraine diagnosed in patients with vertigo?How is vestibular migraine treated in patients with vertigo?What is the role of vertebrobasilar disease in the etiology of vertigo?How is vertebrobasilar disease diagnosed in patients with vertigo?How is vertebrobasilar disease treated in patients with vertigo?What is the prognosis of vertebrobasilar disease-related vertigo?What is the role of Arnold-Chiari malformation in the etiology of vertigo?What is the role of multiple sclerosis in the etiology of vertigo?What is the role of lab testing in the workup of vertigo?What is the role of imaging studies in the workup of vertigo?What is the role of ENG in the workup of vertigo?What is the role of vestibular testing in the diagnosis of vertigo?What is the role of cardiac testing in the diagnosis of vertigo?How is vertigo treated?What is the role of surgery in the treatment of vertigo?Which specialist consultations are beneficial to patients with vertigo?Which dietary modifications are used in the treatment of vertigo?What is the role of drug treatment for vertigo?Which medications in the drug class Monoaminergics are used in the treatment of CNS Causes of Vertigo?Which medications in the drug class Phenothiazines are used in the treatment of CNS Causes of Vertigo?Which medications in the drug class Benzodiazepines are used in the treatment of CNS Causes of Vertigo?Which medications in the drug class Anticholinergics are used in the treatment of CNS Causes of Vertigo?Which medications in the drug class Antihistamines are used in the treatment of CNS Causes of Vertigo?What is included in the long-term management of vertigo?

Author

Marcelo B Antunes, MD, Resident Physician, Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania Health System

Disclosure: Nothing to disclose.

Coauthor(s)

Michael J Ruckenstein, MD, MSc, Professor, Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania Health System

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Peter S Roland, MD, Professor, Department of Neurological Surgery, Professor and Chairman, Department of Otolaryngology-Head and Neck Surgery, Director, Clinical Center for Auditory, Vestibular, and Facial Nerve Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Chief of Pediatric Otology, Children’s Medical Center of Dallas; President of Medical Staff, Parkland Memorial Hospital; Adjunct Professor of Communicative Disorders, School of Behavioral and Brain Sciences, Chief of Medical Service, Callier Center for Communicative Disorders, University of Texas School of Human Development

Disclosure: Received honoraria from Alcon Labs for consulting; Received honoraria from Advanced Bionics for board membership; Received honoraria from Cochlear Corp for board membership; Received travel grants from Med El Corp for consulting.

Chief Editor

Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .

Additional Contributors

B Viswanatha, DO, MBBS, PhD, MS, FACS, FRCS(Glasg), Professor of Otolaryngology (ENT), Sri Venkateshwara ENT Institute, Victoria Hospital, Bangalore Medical College and Research Institute, India

Disclosure: Nothing to disclose.

References

  1. Teggi R, Meli A, Trimarchi M, Liraluce F, Bussi M. Does Ménière's Disease in the Elderly Present Some Peculiar Features?. J Aging Res. 2012. 2012:421596. [View Abstract]
  2. Gruber M, Cohen-Kerem R, Kaminer M, Shupak A. Vertigo in children and adolescents: characteristics and outcome. ScientificWorldJournal. 2012. 2012:109624. [View Abstract]
  3. Teggi R, Colombo B, Albera R, et al. Clinical Features, Familial History, and Migraine Precursors in Patients With Definite Vestibular Migraine: The VM-Phenotypes Projects. Headache. 2018 Apr. 58 (4):534-44. [View Abstract]
  4. Gazquez I, Lopez-Escamez JA. Genetics of recurrent vertigo and vestibular disorders. Curr Genomics. 2011 Sep. 12(6):443-50. [View Abstract]
  5. Solomon D. Distinguishing and treating causes of central vertigo. Otolaryngol Clin North Am. 2000 Jun. 33(3):579-601. [View Abstract]
  6. Rubin AM, Zafar SS. The assessment and management of the dizzy patient. Otolaryngol Clin North Am. 2002 Apr. 35(2):255-73. [View Abstract]
  7. Baloh RW, Harker LA. Central vestibular system disorders. Cummings CW, ed. Otolaryngology-Head and Neck Surgery,. 2nd ed. St. Louis, MO: Mosby; 1993. 3177-3198.
  8. Chang CYJ, Gadre AK. Central Vestibulopathy. Bailey BJ, ed. Head and Neck Surgery- Otolaryngology. 4th ed. Philadelphia, PA: Lippincont; 2006. 2303-2316.
  9. Serra A, Leigh RJ. Diagnostic value of nystagmus: spontaneous and induced ocular oscillations. J Neurol Neurosurg Psychiatry. 2002 Dec. 73(6):615-8. [View Abstract]
  10. Buttner U, Helmchen C, Brandt T. Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review. Acta Otolaryngol. 1999 Jan. 119(1):1-5. [View Abstract]
  11. Espinosa-Sanchez JM, Lopez-Escamez JA. New insights into pathophysiology of vestibular migraine. Front Neurol. 2015. 6:12. [View Abstract]
  12. Sohn JH. Recent Advances in the Understanding of Vestibular Migraine. Behav Neurol. 2016. 2016:1801845. [View Abstract]
  13. Eggers SD, Neff BA, Shepard NT, Staab JP. Comorbidities in vestibular migraine. J Vestib Res. 2014. 24 (5-6):387-95. [View Abstract]
  14. Lipton RB, Stewart WF. Prevalence and impact of migraine. Neurol Clin. 1997 Feb. 15(1):1-13. [View Abstract]
  15. Waters WE, O''Connor PJ. Prevalence of migraine. J Neurol Neurosurg Psychiatry. 1975 Jun. 38(6):613-6. [View Abstract]
  16. Cha YH. Migraine-associated vertigo: diagnosis and treatment. Semin Neurol. 2010 Apr. 30(2):167-74. [View Abstract]
  17. Lempert T, Neuhauser H. Migrainous vertigo. Neurol Clin. 2005 Aug. 23(3):715-30, vi. [View Abstract]
  18. Koehler B. Benign paroxysmal vertigo of childhood: a migraine equivalent. Eur J Pediatr. 1980 Aug. 134(2):149-51. [View Abstract]
  19. Lee JD, Kim CH, Hong SM, et al. Prevalence of vestibular and balance disorders in children and adolescents according to age: A multi-center study. Int J Pediatr Otorhinolaryngol. 2017 Mar. 94:36-9. [View Abstract]
  20. Davitt M, Delvecchio MT, Aronoff SC. The Differential Diagnosis of Vertigo in Children: A Systematic Review of 2726 Cases. Pediatr Emerg Care. 2017 Oct 31. [View Abstract]
  21. Neuhauser H, Leopold M, von Brevern M, Arnold G, Lempert T. The interrelations of migraine, vertigo, and migrainous vertigo. Neurology. 2001 Feb 27. 56(4):436-41. [View Abstract]
  22. Reploeg MD, Goebel JA. Migraine-associated dizziness: patient characteristics and management options. Otol Neurotol. 2002 May. 23(3):364-71. [View Abstract]
  23. Lempert T, Neuhauser H, Daroff RB. Vertigo as a symptom of migraine. Ann N Y Acad Sci. 2009 May. 1164:242-51. [View Abstract]
  24. Savitz SI, Caplan LR. Vertebrobasilar disease. N Engl J Med. 2005 Jun 23. 352(25):2618-26. [View Abstract]
  25. Pasaoglu L. Vertebrobasilar system computed tomographic angiography in central vertigo. Medicine (Baltimore). 2017 Mar. 96 (12):e6297. [View Abstract]
  26. Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP. Wallenberg's lateral medullary syndrome. Clinical-magnetic resonance imaging correlations. Arch Neurol. 1993 Jun. 50(6):609-14. [View Abstract]
  27. Amarenco P, Rosengart A, DeWitt LD, Pessin MS, Caplan LR. Anterior inferior cerebellar artery territory infarcts. Mechanisms and clinical features. Arch Neurol. 1993 Feb. 50(2):154-61. [View Abstract]
  28. Keim RJ. William F. House Lecture. Neurotologic manifestations of microvascular hypoperfusion. Am J Otol. 1995 Jan. 16(1):34-8. [View Abstract]
  29. Chang CC, Chang WN, Huang CR, Liou CW, Lin TK, Lu CH. The relationship between isolated dizziness/vertigo and the risk factors of ischemic stroke: a case control study. Acta Neurol Taiwan. 2011 Jun. 20(2):101-6. [View Abstract]
  30. Paul KS, Lye RH, Strang FA, Dutton J. Arnold-Chiari malformation. Review of 71 cases. J Neurosurg. 1983 Feb. 58(2):183-7. [View Abstract]
  31. Longridge NS, Mallinson AI. Arnold-Chiari malformation and the otolaryngologist: place of magnetic resonance imaging and electronystagmography. Laryngoscope. 1985 Mar. 95(3):335-9. [View Abstract]
  32. Williams NP, Roland PS, Yellin W. Vestibular evaluation in patients with early multiple sclerosis. Am J Otol. 1997 Jan. 18(1):93-100. [View Abstract]
  33. Tirelli G, Rigo S, Bullo F, Meneguzzi C, Gregori D, Gatto A. Saccades and smooth pursuit eye movements in central vertigo. Acta Otorhinolaryngol Ital. 2011 Apr. 31(2):96-102. [View Abstract]
  34. Taghdiri F, Togha M, Razeghi Jahromi S, et al. Cinnarizine for the prophylaxis of migraine associated vertigo: a retrospective study. Springerplus. 2014. 3:231. [View Abstract]
  35. Celebisoy N, Gokcay F, Karahan C, et al. Acetazolamide in vestibular migraine prophylaxis: a retrospective study. Eur Arch Otorhinolaryngol. 2016 Jan 4. [View Abstract]

Electrode montage for electronystagmography (ENG) testing.

Electrode montage for electronystagmography (ENG) testing.

Electrode montage for electronystagmography (ENG) testing.