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Central Vertigo Clinical Presentation

  • Author: Keith A Marill, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
Updated: Apr 13, 2016


The clinician first should ascertain the nature of the patient's vertigo or dizziness. Patients who have conditions known to cause central vertigo do not always complain strictly of vertigo.

Vertigo implies an abnormal sensation of movement or rotation of the patient or his or her environment. Some patients with central disease may complain of disequilibrium, imbalance, or difficulty maintaining an upright posture. Other important historical factors include the presence of associated symptoms and their nature; the onset, duration, and positional dependence of symptoms; and medical history.

If associated symptoms are present, they may suggest the nature of the underlying disease.

The Dix-Hallpike test can help distinguish central vertigo from peripheral vertigo. During the test, the clinician rotates the patient's head 45 degrees to one side and then helps the patient to quickly lie back down. If rotational nystagmus is observed, the test is considered positive for benign positional vertigo. If the test is negative, CNS dysfunction may be indicated.[12]

Peripheral vertigo presents with the following:

  • Associated nausea
  • Vomiting
  • Auditory complaints
  • Abrupt onset

Central vertigo often produces other neurologic symptoms, although this generalization has many exceptions. The symptoms are characterized as follows:

  • Gradual onset
  • Tend to be much less intense than those associated with peripheral vertigo

In assessing the possibility of central vertigo related to cerebrovascular disease, inquire about important risk factors. The following are associated with an increased incidence of cerebrovascular accident (CVA):

  • Hypertension
  • Atrial fibrillation
  • History of prior CVA
  • Advanced age


A thorough neurologic and cardiologic examination is important to identify patients with central vertigo.

  • Depressed consciousness
    • Evidence of depressed consciousness requires immediate clinical attention.
    • Depressed consciousness may be due to disease such as infarction within the brain stem or external compression.
    • In patients with cerebellar infarction, brainstem compression is found more often in those who have involvement of the posterior inferior cerebellar artery.
    • In one series, the earliest sign of brainstem compression was lethargy, which occurred in 11% of patients a mean of 50 hours after onset of cerebellar infarct.[10] Of patients with cerebellar hemorrhage, 46% had deterioration of their mental status an average of 5.5 hours after presentation.[3]
  • Nystagmus
    • Examination of extraocular movements is critical. Nystagmus, if present, may be an important diagnostic clue.
    • Nystagmus consists of slow eye movement in one direction followed by rapid recovery movement in the opposite direction.
    • Vertigo of peripheral origin generally manifests by horizontal, rotatory, or absent nystagmus, but horizontal nystagmus is not a specific sign of peripheral vertigo. It is the most common type of nystagmus observed in patients with cerebellar infarction.[10]
    • Vertical nystagmus is considered specific for central vertigo.
    • Nystagmus of central origin characteristically is worsened by fixation of gaze, while peripheral nystagmus may be ameliorated.
    • Central nystagmus may be unidirectional or multidirectional and may change direction with an alteration in the direction of gaze (ie, gaze evoked), while peripheral nystagmus is unidirectional.
  • Eliciting nystagmus and symptoms of vertigo
    • Hallpike (Nylen-Bárány) maneuver consists of having the patient lie back in bed from a sitting position 3 times in succession.
      • First, the positional change is performed with the patient gazing straight ahead.
      • It is then repeated with the head turned 45° to the right and then 45° to the left.
      • The neck preferably is extended slightly when the patient lies back in the supine position.
      • In contrast to that due to central vertigo, nystagmus due to peripheral disease may not develop immediately after the positional change, and, once it develops, may fatigue quickly and last less than 1 minute.
    • Drachman dizziness battery[13]
      • BP supine and standing
      • Valsalva maneuver
      • Head turn standing with eyes open
      • Sudden turn when walking
      • Three-minute hyperventilation
      • Nylen-Bárány testing
    • The head impulse test is a test for normal ocular fixation in association with rapid passive head rotation. An abnormal response is indicated by an inability to maintain fixation during head rotation with a corrective gaze shift after the head stops moving. An abnormal test seems to be sensitive, but not specific, for a peripheral vestibular disorder.[14]
  • Internuclear ophthalmoplegia
    • Internuclear ophthalmoplegia manifests as partial or absent movement of the adducting eye and coarse nystagmus of the abducting eye with attempted lateral gaze.
    • It suggests derangement of the medial longitudinal fasciculus and a diagnosis of multiple sclerosis or other brainstem disease.
  • Cranial nerve deficits
    • Aside from a disturbance in hearing, other neurologic deficits would not be expected in patients with vertigo of peripheral origin.
    • Associated cranial nerve deficits, including facial weakness, absent corneal reflex, lateral gaze palsy, or dysarthria, mandate further evaluation.
  • Neurologic examination of the extremities and coordination is important.
    • Long-tract findings such as weakness, hyperesthesia, or positive Babinski sign are ominous and mandate further workup.
    • Ataxia may be the most important indicator of cerebellar disease. Ataxia of the limbs, as evidenced by the finger-to-nose and heel-shin tests, and truncal ataxia, with difficulty walking or even sitting, are salient findings.
  • Cardiac examination
    • Careful cardiac examination may reveal the likely source of an embolic stroke.
    • Check for murmur or irregularly irregular rhythm suggesting atrial fibrillation.
    • Inappropriate bradycardia may suggest an ongoing stroke.


See the list below:

  • Positional vertigo: abrupt onset of vertigo associated with a change in position suggests benign positional vertigo, a form of peripheral vertigo.
  • Cranial nerve deficits
    • Symptoms related to derangement of cranial nerves other than the eighth nerve suggest involvement of the brainstem and/or cerebellum.
    • As the cerebellar arteries supply areas of the dorsal brain stem, cerebellar infarcts also may involve the trigeminal, facial, and other cranial nerve nuclei. Mass effect due to edema, acute hemorrhage, or an acoustic neuroma also can cause cranial nerve deficits.
    • Facial nerve dysfunction, most commonly manifested as weakness or twitching in the periorbital area, is seen in 10% of patients with acoustic neuroma.[5]
    • Crossed findings (ie, when the patient has signs on one side of the face and sensory and [less commonly] motor signs on the other side of the body) clearly suggest brainstem involvement.
      • This includes the classic lateral medullary infarction (Wallenberg syndrome) consisting of ipsilateral limb ataxia, Horner syndrome, palatal weakness, facial hypesthesia to pain and temperature, and contralateral hypesthesia to pain and temperature in the limbs and trunk.
      • Crossed findings result from unilateral lesions of the brainstem involving cranial nerve nuclei and long tracts from higher brain centers that have yet to cross to the other side of the CNS.
  • TIAs: Recurrent transient symptoms lasting a few minutes suggest TIAs.
  • Acute cerebellar disease
    • Loss of balance and difficulty maintaining posture, standing, and walking suggest cerebellar disease. These symptoms occur in 50-75% of patients with cerebellar infarction or hemorrhage.[3]
    • Occipital headache and difficulty with speech are also common complaints with acute cerebellar disease.
  • Caudal cerebellar infarction: A prospective study of 24 patients aged 50-75 years with isolated vertigo lasting longer than 48 hours found that 6 (25%) of the patients had a caudal cerebellar infarction. [15] Infarcts of the medial branch of the posterior inferior cerebellar artery territory appear to be the most common cerebellar cause of isolated vertigo and imbalance.
  • Cerebrovascular disease: A recent history of drop attacks, cranial nerve deficits, or transient vertigo should raise suspicion for cerebrovascular disease of the posterior circulation.
    • Basilar artery occlusion: In one study of basilar artery occlusion, 4 of 53 (8%) patients had prodromal symptoms consisting only of vertigo and nausea.[16]
    • Vertebral artery occlusion: Thirty-seven of 85 (44%) patients who presented with either basilar or bilateral distal vertebral artery occlusion had prodromal symptoms that cleared in the 2 months prior to admission.[16]
  • Cardiovascular risk factors
    • The risk of stroke in patients with atrial fibrillation is highest in the first year after onset in patients not receiving anticoagulation.
    • Diabetes mellitus, hyperlipidemia, and cigarette smoking are also important risk factors.
  • Ménière disease and acoustic neuroma
    • Chronic high- and low-frequency hearing loss with associated tinnitus, which fluctuates over time, suggests Ménière disease.
    • Associated auditory symptoms suggest that vertigo has a peripheral origin, though exceptions exist.
    • Hearing loss, often with associated tinnitus, is the most common early symptom of acoustic neuroma.[5, 17]
  • Multiple sclerosis: In younger patients, recent history of neurologic deficits, particularly weakness and/or numbness in one or more limbs (lesions in time and space) or unilateral visual loss, should raise suspicion for multiple sclerosis.
Contributor Information and Disclosures

Keith A Marill, MD Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Received ownership interest from Medtronic for none; Received ownership interest from Cambridge Heart, Inc. for none; Received ownership interest from General Electric for none. for: GE; Medtronic; Cambridge Heart.

Specialty Editor Board

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.

J Stephen Huff, MD, FACEP Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD, FACEP is a member of the following medical societies: American Academy of Neurology, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

Francis Counselman, MD, FACEP Chair, Professor, Department of Emergency Medicine, Eastern Virginia Medical School

Francis Counselman, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Norfolk Academy of Medicine, Association of Academic Chairs of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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CT scan of a patient with an acute spontaneous cerebellar hemorrhage. The hemorrhage in the right lobe of the cerebellum is partly obscured by bony artifact.
MRI of a patient with an acute cerebellar hemorrhage less than 24 hours after presentation. MRI allows better resolution than CT scan without bony artifact. MRI is preferred over CT scan for imaging lesions in the posterior fossa.
CT scan of a patient with a large acoustic neuroma on the right side of the brainstem. The scan was performed after injection of intravenous contrast, which is critical for identifying tumors with CT imaging.
A CT slice through the brain of a patient with an acoustic neuroma. This slice reveals a level of the brain higher than the acoustic neuroma. The dilated third and lateral ventricles provide gross evidence of obstructive hydrocephalus due to pressure exerted by the tumor on the brainstem. A ventriculostomy, seen as a white circle in the right lateral ventricle, has been placed in an attempt to drain cerebrospinal fluid and relieve the excessive pressure above the brainstem.
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