Central Vertigo


Article Author:
Forshing Lui
Lisa Foris
Keith Willner


Article Editor:
Prasanna Tadi


Editors In Chief:
Rhonda Coffman
Lindsay Iverson
Heather Templin


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
7/4/2019 10:53:15 AM

Introduction

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 or 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 (vestibulo-cochlear 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: 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 refelx) 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 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.

Etiology

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] 

Epidemiology

In the United States, there are approximately 800,000 individuals per year; that experience a stroke. Of these, about 85% are ischemic strokes. Among all ischemic infarctions, 20% affected the posterior circulation. The commonest 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 than in 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 common among 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.

Pathophysiology

Any lesion affecting the central vestibular apparatus will present with vertigo as the main presenting symptom. Very often, the central occulomotor neuro-inegrators (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 vestibulococchlear 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 clinically is one a patient presented to the emergency department or urgent care with acute vertigo. Despite the fact that most patients suffer from peripheral vertigo including benign paroxysmal positional vertigo, acute vestibula neuritis(or labyrinthitis), Meniere's disease or even perilymphatic fistula or superior semicircular canal dehiscence, identification of central vertigo clinically is of utmost importance due to the serious underlying cause of a 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 exams will 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. Dix-Hallpike maneuver is indicated to rule our benign positional vertigo. A focused and expedited neurological exam especially to look for a Hoenr's 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 th patient is still suffering from ongoing vertigo especially in the setting of the emergency department. 

Before I describe the HINTS test/exam, I need to explain the vestibulo-ocular reflex (VOR).[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 had 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 case 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 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. 

Evaluation

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 focused neurological exam and a 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.

Treatment / Management

The initial step in approaching a patient complaining of vertigo is to determine whether they are in fact experiencing vertigo and not another form of dizziness from 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, th 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 IV steroid(such as IV methylprednisolone 1 gram a day for 3 o 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 vestibula neuritis. 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. Menier's 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.

Prognosis

The prognosis of central vertigo depends on the underlying cause. The commonest one is acute lateral medullary syndrome due to occlusion of the vertebral artery or the posterior inferior cerebellar artery. The patient improved to relatively good functional outcome with appropriate therapy. On the other hand basila 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 withour 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. The should be educated to go to the Emergency Department immediately.

Pearls and Other Issues

1. Cenral vertigo is much less common compared with peripheral vertigo yet its recogntion is extremely important to improive 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 we miss this the prognosis is poor. So 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 interdisciplinary team including the emergency medicine team, the radiologists, the stroke neurologist, and very often the interventional neuroradiologists.


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Central Vertigo - Questions

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A 60-year-old female presents with symptoms of vertigo. She has a history of hypertension, diabetes, and coronary disease. She also has diplopia, dysarthria, dysmetria, and vertical nystagmus. Symptoms were abrupt in onset occurring 2 hours ago. Which of the following is the reason for her vertigo?



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A 25-year-old male presents to the clinic complaining of vertigo and nausea for the past 4 hours, not precipitated by any event that she can recall. The patient denies any pre-syncopal faintness, disequilibrium, or lightheadedness. Which of the following signs, symptoms, or tests, are more consistent with a central, as opposed to a peripheral, cause of vertigo?



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A 40-year-old female presents to the emergency department because of acute onset vertigo that started a day prior. Her symptoms persisted despite resting in bed for the past one day. There is no tinnitus. Three years ago, she had an episode of left-sided visual loss associated with periorbital pain. She was treated with a course of IV methylprednisolone with a resolution of her symptoms. Physical examination shows normal visual acuity in both eyes. Extraocular movements are normal. There is phasic nystagmus with a fast phase beating in the direction of gaze. The rest of the neurological exam is normal, except an upgoing left plantar response. Which of the following is the next best step in the management of this patient?



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A 70-year-old female with a longstanding history of hypertension, type 2 diabetes and 30-pack year history of smoking presents to the emergency department with an acute onset of vertigo and slurring of speech 1 hour before arrival. Her blood pressure is 190/120 mmHg and pulse 78/min. Physical examination is most significant for mild dysarthria. Cranial nerve exams are otherwise normal with no nystagmus. There is impairment of pinprick sensation on the right side of her face and the left side of his body. She also has mild ataxia affecting her right side. Her head CT is normal. Urgent labs are sent for random glucose, PT/aPTT, CBC and serum electrolytes. Which of the following is the next best step in the management of this patient?



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Central Vertigo - References

References

Huon LK,Wang TC,Fang TY,Chuang LJ,Wang PC, Vertigo and stroke: a national database survey. Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. 2012 Sep     [PubMed]
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     [PubMed]
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     [PubMed]
Renga V, Clinical Evaluation of Patients with Vestibular Dysfunction. Neurology research international. 2019     [PubMed]
Cohen HS, A review on screening tests for vestibular disorders. Journal of neurophysiology. 2019 Apr 17     [PubMed]
Kattah JC, Use of HINTS in the acute vestibular syndrome. An Overview. Stroke and vascular neurology. 2018 Dec     [PubMed]
Omron R, Peripheral Vertigo. Emergency medicine clinics of North America. 2019 Feb     [PubMed]

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