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Central Vertigo

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Last Update: July 3, 2023.

Continuing Education Activity

Central vertigo is a clinical condition in which an individual experiences the sensation of motion despite remaining still. It results from a dysfunction in the central vestibular aspects of the nervous system. This activity explains when central vertigo should be considered on differential diagnosis and reviews the proper evaluation and management of this condition.


  • Review the causes of central vertigo and peripheral vertigo.
  • Summarize the clinical methods used to differentiate central and peripheral vertigo.
  • Outline the important emergency medicine approach to the treatment of central vertigo.
  • Explain the importance of enhancing care coordination amongst the interprofessional team to improve outcomes for patients with central vertigo.
Access free multiple choice questions on this topic.


Central vertigo is a clinical condition in which an individual experiences hallucinations of motion of their surroundings, or a sensation of spinning, while remaining still, as a result of dysfunction of the vestibular structures in the central nervous system (CNS).[1] The patient complains typically of dizziness with hallucination or sense of spinning. This is different from the light-headed "dizziness" which is more commonly secondary to global impairment of cerebral perfusion.

The peripheral vestibular system consists of the saccule, utricle, and semicircular canals. The neuroepithelial hair cells within the peripheral vestibular apparatus send projections to the vestibular nuclei in the caudal pons and rostral dorsolateral medulla by way of the vestibular division of the VIIIth cranial (vestibulocochlear nerve). The vestibular nucleus on each side is divided into 4 sub-nuclei with three lateral nuclei and one medial nuclear column, they are labeled as the superior vestibular nucleus, lateral vestibular nucleus, medial vestibular nucleus, and descending vestibular nucleus. Some nuclei receive only primary vestibular afferents, but most receive afferents from the cerebellum, reticular formation, spinal cord, and contralateral vestibular nuclei. The projections from the vestibular nuclei extend to the cerebellum, extraocular nuclei, and spinal cord. With these neuroanatomic arrangements, it will be easy to understand the functions of the vestibular system i.e. maintaining visual fixation through the vestibulo-ocular reflex with changing head and body positions in space and extended or erect body posture. The maintenance of visual fixation also requires the normal function of the oculomotor central neural integrator which consists mainly of the medial vestibular nucleus and the nucleus prepositus hypoglossi.

Any lesion affecting the vestibular nuclei or their projections especially those to and from the cerebellum will result in symptoms of vertigo and associated signs of nystagmus.


Central vertigo occurs when there is any lesion or dysfunction of the brainstem vestibular apparatus as described above. Peripheral vertigo may occur as a result of problems in the peripheral vestibular system from the inner ear to the vestibular division of the VIIIth cranial nerve. Peripheral vertigo accounts for over 90% of all causes of vertigo. Central vertigo most commonly occurs as a result of ischemia of the central vestibular structures in the cerebellum, brainstem, or vestibular nuclei especially in the elderly with vascular risk factors. Acute demyelination such as multiple sclerosis is another relatively common cause of central vertigo in younger patients. The other not so uncommon cause is medication-induced, especially toxicity due to common anticonvulsants such as phenytoin, phenobarbital, and carbamazepine. Other less common causes include infection, trauma, posterior fossa brain tumors, and migraine.[2] 


In the United States, approximately 800,000 individuals per year experience a stroke. Of these, about 85% are ischemic. Among all ischemic infarctions, 20% affected the posterior circulation. The most common posterior circulation stroke is lateral medullary syndrome (Wallenberg), which arises as a result of occlusion of the posterior inferior cerebellar artery or more commonly the vertebral artery. Central vertigo is the most predominant symptom. Men tend to experience cerebrovascular disease more frequently than women, at a rate of about 2:1. Multiple sclerosis, on the other hand, affects three times as many women as men.

Additional causes of vertigo include multiple sclerosis, which has an incidence of approximately 10 to 80 cases per 100,000 individuals in the United States per year.

Migraine occurs in 12% of the adult population (6% men and 18% women). Vertigo as a presentation of migraine is not uncommon, yet the actual incidence is unknown due to differences among physicians in their diagnosis. It is probably more commonly diagnosed in ENT practice versus internal medicine practice. These patients usually present with recurrent vertigo lasting for a few hours without any other ENT symptoms nor focal neurological signs or symptoms. Neuroimaging studies are generally normal. The diagnosis is often made when other causes of vertigo were ruled out.


Any lesion affecting the central vestibular apparatus will present with vertigo as the main presenting symptom. Very often, the central oculomotor neuro-integrators (medial vestibular nucleus and the nucleus prepositus hypoglossi) are involved resulting in impairment of visual fixation and the clinical sign of nystagmus.

The vertebrobasilar arterial (VBA) system supplies blood to the brainstem, cerebellum, and peripheral labyrinths. Occlusion of the system, therefore, can result in either central or peripheral vertigo, depending on the specific artery affected. Occlusion can occur as a result of atherothrombosis or an embolism (e.g., cardioembolism or plaque from the vertebral arteries).[3] The most important differentiating facts are peripheral vertigo presents with predominant vestibulocochlear signs and symptoms of vertigo, tinnitus and/or hearing impairment whereas central vertigo is often associated with other brainstem signs and symptoms.

Vertigo may occur in the setting of multiple sclerosis, generally with a waxing and waning course as a result of demyelination in the brainstem.

Central vertigo is also commonly seen in the setting of trauma, particularly as a result of shearing forces in the brain stem and resultant petechial hemorrhages in the vestibular nuclei. 

History and Physical

The most important clinical scenario is one a patient presented to the emergency department or urgent care with acute vertigo. Most patients suffering from vertigo have a peripheral cause including benign paroxysmal positional vertigo, acute vestibular neuritis (or labyrinthitis), Meniere disease or even perilymphatic fistula or superior semicircular canal dehiscence. However, identification of central vertigo clinically is of utmost importance due to the serious underlying cause of brainstem ischemia or infarction.

The important history will include: mode of onset, duration of the vertigo, any relationship to posture, any tinnitus or hearing impairment, any previous episodes, any sick contact, any fever, any skin rash, vascular risk factors, medications and dosage, any headache, and lastly any brainstem symptoms including weakness, numbness, diplopia or dysarthria. 

Important physical exam elements include the vitals and skin rash to suggest herpes zoster of the external ear. Presence of a neck bruit may indicate underlying carotid or vertebral stenosis. Cardiac exams are always important to rule out an arrhythmia especially atrial fibrillation or valvular heart disease which may cause an embolic event. The Dix-Hallpike maneuver is indicated to rule our benign positional vertigo. A focused and expedited neurological exam especially to look for a Horner syndrome and other brainstem signs are extremely important. Finally, the "HINTS" test needs to be performed on every patient suspected to be suffering from central vertigo. The test is valid only when the patient is still suffering from ongoing, continuous vertigo at the time the exam is performed.

Before describing the HINTS test/exam, the vestibulo-ocular reflex (VOR) must be reviewed.[4][5]  The afferent pathways of the VOR started with the semicircular canals which provide a head velocity signal.  The signal is transmitted through the vestibular division of the VIIIth cranial nerve to the vestibular nuclei. The vestibular nuclei on BOTH sides with the oculomotor neural integrator provides an equal and opposite eye velocity signal to keep the eyes still in space when the head moves. This is important when we walk or drive, we are still able to keep our objects of interest such as road signs in visual focus. Stimulation of the right peripheral vestibular apparatus such as turning the head to the right will result in equal and opposite movement of the eyes to the left (normal VOR gain). The VOR gain will be decreased in the presence of any peripheral vestibular dysfunction resulting in a corrective eye movement (saccade) visible in the bedside exam. VOR gain is normal in central vestibular lesions. The VOR test or head thrust (also called head-impulse) forms the basis of a clinical exam to differentiate central versus peripheral vertigo in the HINTS test.

HINTS stands for head impulse test, nystagmus and skew deviation. This is the best bedside test to differentiate peripheral versus central vertigo. The head impulse (head thrust) test is performed by asking the patient to look at the examiner's nose. The examiner gently and quickly thrust the patient's head about 30 degrees to one side and try to look for any catch-up saccade. The test is positive when there is a catch-up saccade to one side. The side with a positive test is the side with peripheral vestibular dysfunction. It is important to note that positive head impulse test indicates a peripheral cause for vertigo and is generally not as serious prognostically. The nystagmus in peripheral vertigo is always unidirectional often with a rotary element regardless of which direction of the gaze the patient has.

On the other hand, the nystagmus in central vertigo will more commonly present with direction changing nystagmus. The nystagmus will be right beating when the patient looks to the right and change to left beating when the patient looks to the left. Any vertical nystagmus indicates a central cause for vertigo. The last part of the HINTS test is a skew deviation. Presence of a skew deviation (one eye higher than another eye) indicates a central cause for vertigo. This skew deviation can be assessed by alternately covering the patient's eyes and assessing for a vertical corrective saccade on the affected side.


As described above in the history and physical, tests for causes of peripheral vertigo such as Dix-Hallpike test and simple screening test for hearing are important. A detailed neurological exam including assessment of extremity and truncal ataxia, gait, and HINTS test should all be performed. 

When the examination findings suggest central vertigo, most of the time the patient will need to be further evaluated and very often requires hospitalization. Magnetic resonance imaging (MRI) is the imaging modality of choice for visualization of a potential infarction, tumor, hemorrhage, or evidence of demyelination that would reveal the cause of central vertigo. Computed tomography (CT) may be employed if MRI is unavailable. CT angiogram and MR angiogram may be performed at the same time or sequentially to look for any occlusion of the vertebrobasilar arterial system which may be the cause of vertigo. Rapid evaluation, especially in preparation for thrombolytic therapy in the emergency department or interventional therapy, is extremely important to improve the outcome. MRI has reduced sensitivity in the first 48 hours following posterior circulation stroke and a positive HINTS result, regardless of imaging findings, is worrisome.

Treatment / Management

The initial step in approaching a patient complaining of vertigo is to determine whether they are in fact experiencing primary vertigo and not another form of dizziness caused by a migraine, medication, or alcohol. Once a diagnosis of central vertigo has been established, treatment is aimed at the underlying cause. Imaging studies should be done as soon as possible with a patient complaining of vertigo, and the patient should not be left unattended until a thorough examination is complete and a diagnosis is made. Most of the time, the patient will need to be admitted to the hospital for the treatment of the underlying cause of vertigo.

Thrombolytic therapy should be considered if the patient is suffering from an acute posterior circulation ischemic stroke within 3 to 4.5 hours of onset, although it is critical to be aware of any contraindications (e.g., recent surgery, severe hypertension, evidence of acute hemorrhage or edema, or rapidly improving symptoms).[6] The patient may be a candidate for mechanical thrombectomy beyond the 4.5-hour thrombolytic window if there is evidence of large vessel occlusion by neuroimaging within the 12 hour time window.

Patients with an altered level of consciousness warrant an ECG, pulse oximetry, and extremely close supervision. If a patient continues to deteriorate, emergent interventions may be required to decreased intracranial pressure (ICP) and minimize compression of the brainstem These interventions may include endotracheal intubation with or without hyperventilation, aggressive diuresis, and corticosteroids.

Finally, a neurologic consultation is warranted for a patient complaining of vertigo, and a neurosurgical consultation is necessary if an underlying hemorrhage, edema, or brainstem compression is discovered, as surgical decompression (e.g., ventriculostomy or craniectomy) may be required.

A course of an intravenous corticosteroid (such as IV methylprednisolone 1 gram a day for 3-5 days) is indicated if the cause is an acute demyelinating event of multiple sclerosis.

Differential Diagnosis

The most important differential diagnoses are causes of peripheral vertigo.[7] The most important ones in the emergency setting are acute labyrinthitis or vestibular neuritis, which are both causes of an acute vestibular syndrome like that seen in central vertigo. These patients present with acute onset of extremely severe vertigo with nausea and vomiting. They have prominent peripheral unidirectional nystagmus. Benign paroxysmal positional vertigo is a common cause of peripheral vertigo. The diagnosis can easily be made by Dix-Hallpike maneuver and treated with repositioning maneuver. Meniere disease classically presents with recurrent vertigo with tinnitus and low-frequency hearing impairment easily documented with audiometry. A slowly progressive hearing loss with infrequent vertigo and later facial paresis and ataxia will suggest a slowly enlarging tumor in the cerebellopontine angle such as a vestibular schwannoma or meningioma. Migraine as a cause of recurrent vertigo is more a diagnosis of exclusion when other causes are excluded with a thorough history, physical exam and normal imaging studies.


The prognosis of central vertigo depends on the underlying cause. The most common is acute lateral medullary syndrome due to occlusion of the vertebral artery or the posterior inferior cerebellar artery. Patients often recover relatively good functional outcome with appropriate therapy. On the other hand, basilar thrombosis will carry a much worse prognosis with much higher mortality. Brainstem involvement as a presentation of acute demyelination as in multiple sclerosis does make the prognosis worse compared with other patients without brainstem relapse. The acute relapse does tend to remit commonly after a course of IV steroid, yet the long term prognosis will depend on other factors including the age, gender, frequency, and severity of relapses.

Deterrence and Patient Education

Vertigo is a very unpleasant symptom. Patients most commonly will seek medical attention. However, it is utmost important in educating the patients about the symptoms of acute stroke as an essential cause of vertigo. These will include acute onset of impairment in speech, weakness or numbness, gait disturbance and vision. The patients need to be educated about the "FAST" test. These consist of looking for Facial asymmetry, Arm drift, Speech disturbance and Time by calling 911 and note the time of onset. They should be educated to go to the emergency department immediately.

Pearls and Other Issues

1. Central vertigo is much less common compared with peripheral vertigo yet its recognition is extremely important to improve the outcome of the patient.

2. HINTS test is the important bedside clinical test to differentiate central versus peripheral vertigo.

3. MRI brain is the best imaging test for central vertigo.

Enhancing Healthcare Team Outcomes

It is extremely important to identify central vertigo in a timely manner. Basilar occlusion presents with central vertigo as the presenting symptom. If missed, the prognosis is poor. It is very important to distinguish central vertigo from peripheral vertigo. It is extremely beneficial to approach vertigo in a systematic way. The management of underlying condition causing central vertigo requires expedited approach by an interprofessional team including the emergency medicine team, the radiologists, the stroke neurologist, and very often the interventional neuroradiologists. Emergency and neuroscience specialty care nurses monitor patients and provide feedback to the team, thus improving communication and improving patient outcomes. [Level 5]

Review Questions


Renga V. Clinical Evaluation of Patients with Vestibular Dysfunction. Neurol Res Int. 2019;2019:3931548. [PMC free article: PMC6377969] [PubMed: 30863640]
Huon LK, Wang TC, Fang TY, Chuang LJ, Wang PC. Vertigo and stroke: a national database survey. Otol Neurotol. 2012 Sep;33(7):1131-5. [PubMed: 22858717]
Lee H, Sohn SI, Cho YW, Lee SR, Ahn BH, Park BR, Baloh RW. Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology. 2006 Oct 10;67(7):1178-83. [PubMed: 17030749]
Cohen HS. A review on screening tests for vestibular disorders. J Neurophysiol. 2019 Jul 01;122(1):81-92. [PMC free article: PMC6689777] [PubMed: 30995137]
Kattah JC. Use of HINTS in the acute vestibular syndrome. An Overview. Stroke Vasc Neurol. 2018 Dec;3(4):190-196. [PMC free article: PMC6312070] [PubMed: 30637123]
Hacke W, Zeumer H, Ferbert A, Brückmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke. 1988 Oct;19(10):1216-22. [PubMed: 3176080]
Omron R. Peripheral Vertigo. Emerg Med Clin North Am. 2019 Feb;37(1):11-28. [PubMed: 30454774]

Disclosure: Forshing Lui declares no relevant financial relationships with ineligible companies.

Disclosure: Lisa Foris declares no relevant financial relationships with ineligible companies.

Disclosure: Keith Willner declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK441861PMID: 28722891


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