Central Vertigo

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Background

Central vertigo is vertigo due to a disease originating from the central nervous system (CNS). In clinical practice, it often includes lesions of cranial nerve VIII as well. Individuals with vertigo experience hallucinations of motion of their surroundings.

Central vertigo may be caused by hemorrhagic or ischemic insults to the cerebellum (see the image below), the vestibular nuclei, and their connections within the brain stem. Other causes include CNS tumors, infection, trauma, and multiple sclerosis.[1, 2]



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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 ar....

Vertigo due to acoustic neuroma is also included in the broader category of central vertigo. An acoustic neuroma develops within the eighth cranial nerve, usually within the course of the internal auditory canal, yet it often expands into the posterior fossa with secondary effects on other cranial nerves and the brain stem.

See Vertigo: 5 Case-Based Diagnostic Puzzles, a Critical Images slideshow, to help recognize diagnostic clues in vertigo cases.

Pathophysiology

The brainstem, cerebellum, and peripheral labyrinths are all supplied by the vertebrobasilar arterial system. Thus, the central and peripheral ischemic vertigo syndromes overlap.

Vertebrobasilar arterial system

The basilar artery is formed from the 2 vertebral arteries within the cranium at the level of the medulla. The artery has 3 branches on each side that supply the cerebellum. The posterior inferior cerebellar artery branches from the vertebral artery, while the anterior inferior cerebellar artery and the superior cerebellar artery branch from the basilar artery.

All 3 of the cerebellar arteries may have branches that supply brainstem tissue. A labyrinthine artery on each side branches from the basilar artery and supplies the labyrinth and associated structures via the internal auditory canal. In approximately two thirds of people, the basilar artery ends by bifurcating into the posterior cerebral arteries, with small posterior communicating arteries connecting to the internal carotid system in the circle of Willis.

Arterial occlusion and ischemic infarction

Arterial occlusion and ischemic infarction can result from cardioembolism, embolism of plaque from a vertebral artery, or local arterial thrombosis. One or both vertebral arteries, the basilar artery, or any of the smaller branches may be occluded. Even complete occlusion of a large artery may not result in death because of anastomotic retrograde flow via the circle of Willis and posterior communicating arteries.

Temporary vertebrobasilar ischemia may present as migraine syndrome or transient ischemic attacks (TIAs). While less common than cerebellar infarction, spontaneous cerebellar hemorrhage is an important life-threatening cause of vertigo associated with hypertensive vascular disease and anticoagulation.[3]

Multiple sclerosis

Multiple sclerosis is a demyelinating disease of the CNS. The course generally waxes and wanes, with varying neurologic symptoms and signs. Isolated vertigo may be the initial symptom in approximately 5% of cases. This disease is discussed in detail in the relevant article (see Multiple Sclerosis).

Acoustic neuromas

Acoustic neuromas are Schwann cell tumors that usually originate on the vestibular division of the eighth cranial nerve in the proximal internal auditory canal.[4] Usually unilateral in development, bilateral acoustic neuromas do occur in young adults, although rarely, in association with neurofibromatosis type 2. If untreated, an acoustic neuroma may expand into the cerebellopontine angle and compress facial and other cranial nerves.[5] If it compresses the brainstem, ataxia, gait disturbances, spasticity, and weakness from long-tract effects may result. See the image below.



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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,....

Other causes

Isolated vertigo due to CNS infection, such as a microabscess, or temporal lobe seizures is rare and is not discussed in this article. Vertigo and dizziness are common complications of head and neck trauma. Traumatic central vertigo may be caused by petechial hemorrhages in the vestibular nuclei of the brainstem. These may result from shearing forces on the brainstem.[6]

Epidemiology

Frequency

United States

Approximately 500,000 people have strokes each year. About 85% of these strokes are ischemic, and 1.5% of ischemic strokes affect primarily the cerebellum. Ratio of ischemic to hemorrhagic cerebellar strokes is 3-5:1.[7] Up to 10% of patients with an isolated cerebellar infarction present with only isolated vertigo and imbalance.[8] Incidence of multiple sclerosis ranges from 10-80/100,000 per year, depending on the latitude. About 3000 cases of acoustic neuroma are diagnosed each year in the United States.

Mortality/Morbidity

Vascular injuries and infarcts in the posterior circulation can cause severe permanent debilitating disease. The excellent recovery typical of acute vertigo caused by peripheral disease should not necessarily be expected in central vertigo.

Sex

Incidence of cerebrovascular disease is slightly higher in men than in women. In one series of patients with cerebellar infarction, the ratio of men to women was about 2:1. Multiple sclerosis is about twice as common in women as in men.

Age

Incidence of stroke increases with age. The mean age of patients with cerebellar infarction in one series was 65 years, with half of the cases occurring in those aged 60-80 years.[7] In one series, the mean age of patients with cerebellar hematoma was 70 years.[3]

History

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:

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

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):

Physical

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

Causes

See the list below:

Laboratory Studies

See the list below:

Imaging Studies

See the list below:

Other Tests

See the list below:

Emergency Department Care

First, distinguish true vertigo from disequilibrium and other forms of dizziness. Ascertaining this history from patients sometimes requires patience and persistence. Once the presence of vertigo or disequilibrium has been confirmed, consider a central cause. Evaluate on the basis of a careful history and physical examination and liberal use of imaging studies of the posterior fossa.

Consultations

Obtain neurologic consultation for patients with central vertigo, and consider neurosurgical consultation for all patients with space-occupying lesions or hydrocephalus.

The emergency physician should seek immediate neurosurgical consultation for patients with hemorrhage, brainstem compression, or edema, as surgical decompression via suboccipital craniectomy or ventriculostomy may be lifesaving.

Medication Summary

Patients with depressed mental status may have documented or suspected increased intracranial pressure (ICP). Administer diuretics or corticosteroids to decrease pressure while planning more definitive actions. Administer this therapy preferably in consultation with a neurosurgeon.

Dimenhydrinate (Dramamine, Dimetabs, Dymenate, Triptone)

Clinical Context:  A 1:1 salt of 8-chlorotheophylline and diphenhydramine, thought to be particularly useful in treatment of peripheral vertigo. Diminishes vestibular stimulation and depresses labyrinthine function through central anticholinergic activity.

Diphenhydramine (Benadryl, Bydramine, Hyrexin)

Clinical Context:  Used for treatment and prophylaxis of vestibular disorders.

Promethazine hydrochloride (Phenergan)

Clinical Context:  Used for symptomatic treatment of nausea in vestibular dysfunction.

An antidopaminergic agent effective in treatment of vertigo, blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Class Summary

These agents may suppress vestibular responses through an effect in the CNS; however, the mechanism remains unknown. Some investigators believe this action is mediated primarily by central anticholinergic activity.

Diazepam (Valium, Diastat, Diazemuls)

Clinical Context:  Probably most commonly used benzodiazepine to treat vertigo. Highly lipophilic and undergoes rapid redistribution after administration. Duration of effects in CNS relatively short, which may make it relatively less desirable.

Lorazepam (Ativan)

Clinical Context:  Sedative hypnotic in benzodiazepine class that has short time to onset and relatively long half-life.

Depresses all levels of CNS, including limbic and reticular formation, probably through increased action of GABA, a major inhibitory neurotransmitter.

Class Summary

Centrally, these agents inhibit vestibular responses, presumably by potentiating inhibitory GABA receptors.

Mannitol (Osmitrol)

Clinical Context:  Nonreabsorbable solute, decreases water reabsorption in water-soluble portions of nephron. Reduces reabsorption of sodium chloride as well. Perhaps more importantly, does not cross blood-brain barrier. Creates osmotic gradient, drawing water from brain into intravascular compartment. Used to lower ICP in variety of conditions.

Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h over 2-3 h.

In children, assess by administering same test dose and rate. Should produce a urine flow of at least 1 mL/kg/h over 1-3 h.

Furosemide (Lasix)

Clinical Context:  Loop diuretic that blocks transport of sodium, potassium, and chloride in thick ascending limb of loop of Henle in kidney. May enhance effect of mannitol and produce greater and more sustained decrease in ICP.

Class Summary

Diuretic agents are used as a temporary measure to lower ICP until definitive intervention is performed.

Dexamethasone (Decadron)

Clinical Context:  Preferred corticosteroid for this purpose because it demonstrates high glucocorticoid potency and minimal mineralocorticoid activity.

Class Summary

These agents are used to decrease brain edema associated with intracranial tumors.

Further Inpatient Care

See the list below:

Transfer

See the list below:

Deterrence/Prevention

See the list below:

Prognosis

See the list below:

Patient Education

See the list below:

What is central vertigo?What is the role of multiple sclerosis in the pathophysiology of central vertigo?What is the role of acoustic neuromas in the pathophysiology of central vertigo?What is the pathophysiology of central vertigo?What is the role of the vertebrobasilar arterial system in the pathophysiology of central vertigo?What is the role of arterial occlusion and ischemic infarction in the pathophysiology of central vertigo?What is the role of trauma in the etiology of central vertigo?What is the prevalence of central vertigo in the US?What is the mortality and morbidity in central vertigo?How does the incidence of central vertigo vary by sex?Which age groups has the highest incidence of central vertigo?Which clinical history findings are characteristic of central vertigo?How is peripheral vertigo distinguished from central vertigo?Which factors increase the risk for central vertigo associated with a cerebrovascular accident (CVA)?What causes depressed consciousness in patients with central vertigo?How is nystagmus characterized in patients with central vertigo?What is the role of the Hallpike (Nylen-Bárány) maneuver in the diagnosis of central vertigo?What is included in the Drachman dizziness battery for evaluation of central vertigo?What is the role of the head impulse test in the evaluation of central vertigo?What does a finding of internuclear ophthalmoplegia suggest in patients with central vertigo?What does the presence of cranial nerve deficits suggest in patients with central vertigo?Which neurologic findings are characteristic of central vertigo?Which cardiac findings are characteristic of with central vertigo?What are the symptoms of central vertigo due to Ménière disease and acoustic neuroma?What is the role of positional vertigo in the etiology of central vertigo?What is the role of cranial nerve deficits in the etiology of central vertigo?Which symptoms suggest a transient ischemic attack (TIA) etiology of central vertigo?Which symptoms suggest an acute cerebellar disease etiology of central vertigo?What is the role of caudal cerebellar infarction to the etiology of central vertigo?What is the role of cerebrovascular disease in the etiology of central vertigo?What are risk factors for central vertigo?Which symptoms suggest a multiple sclerosis etiology of central vertigo?What are the differential diagnoses for Central Vertigo?What is the role of lab studies in the workup of central vertigo?What is the role of imaging studies in the workup of central vertigo?Which cardiac tests are performed in the workup of central vertigo?Which neurologic tests are performed in the workup of central vertigo?What is the initial emergency department care of central vertigo?What is the role of thrombolytic therapy in patients with central vertigo?What is the emergency department care for central vertigo in lethargic patients with altered consciousness?What is the role of recombinant activated factor VII for the treatment of central vertigo?Which specialists should be consulted in the treatment of central vertigo?How is increased intracranial pressure (ICP) treated in patients with central vertigo?Which medications in the drug class Corticosteroids are used in the treatment of Central Vertigo?Which medications in the drug class Diuretics are used in the treatment of Central Vertigo?Which medications in the drug class Benzodiazepines are used in the treatment of Central Vertigo?Which medications in the drug class H1- receptor antagonists are used in the treatment of Central Vertigo?When is inpatient care indicted for central vertigo?When is transfer indicated in the treatment of central vertigo?How is central vertigo prevented in patients with transient ischemic attacks (TIAs)?What is the prognosis of central vertigo?What is included in patient education about central vertigo?

Author

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

Disclosure: Received research grant from: Zoll Foundation; Laerdal Foundation<br/>Received ownership interest from General Electric and Medtronic for none. for: GE; Medtronic.

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.

J Stephen Huff, MD, FACEP, Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of 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, Sanz Laniado Medical Center, Netanya, Israel

Disclosure: Nothing to disclose.

Additional Contributors

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

Disclosure: Nothing to disclose.

References

  1. Smouha E. Inner ear disorders. NeuroRehabilitation. 2013. 32(3):455-62. [View Abstract]
  2. Schneider JI, Olshaker JS. Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke. Emerg Med Clin North Am. 2012 Aug. 30(3):681-93. [View Abstract]
  3. St. Louis EK, Wijdicks EF, Li H. Predicting neurologic deterioration in patients with cerebellar hematomas. Neurology. 1998 Nov. 51(5):1364-9. [View Abstract]
  4. Chen CC, Cheng PW, Tseng HM, Young YH. Posterior cranial fossa tumors in young adults. Laryngoscope. 2006 Sep. 116(9):1678-81. [View Abstract]
  5. Selesnick SH, Jackler RK, Pitts LW. The changing clinical presentation of acoustic tumors in the MRI era. Laryngoscope. 1993 Apr. 103(4 Pt 1):431-6. [View Abstract]
  6. Fitzgerald DC. Head trauma: hearing loss and dizziness. J Trauma. 1996 Mar. 40(3):488-96. [View Abstract]
  7. Amarenco P. The spectrum of cerebellar infarctions. Neurology. 1991 Jul. 41(7):973-9. [View Abstract]
  8. Lee H, Sohn SI, Cho YW, Lee SR, Ahn BH, Park BR. Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology. 2006 Oct 10. 67(7):1178-83. [View Abstract]
  9. 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. [View Abstract]
  10. Kase CS, Norrving B, Levine SR. Cerebellar infarction - clinical and anatomic observations in 66 cases. Stroke. 1993. 24 (1):76-83. [View Abstract]
  11. Hornig CR, Rust DS, Busse O, Jauss M, Laun A. Space-occupying cerebellar infarction. Clinical course and prognosis. Stroke. 1994 Feb. 25(2):372-4. [View Abstract]
  12. Halker RB, Barrs DM, Wellik KE, Wingerchuk DM, Demaerschalk BM. Establishing a diagnosis of benign paroxysmal positional vertigo through the dix-hallpike and side-lying maneuvers: a critically appraised topic. Neurologist. 2008 May. 14(3):201-4. [View Abstract]
  13. Drachman DA. A 69-year-old man with chronic dizziness. JAMA. 1998 Dec 23-30. 280(24):2111-8. [View Abstract]
  14. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008 Jun 10. 70(24 Pt 2):2378-85. [View Abstract]
  15. Norrving B, Magnusson M, Holtas S. Isolated acute vertigo in the elderly; vestibular or vascular disease?. Acta Neurol Scand. 1995 Jan. 91(1):43-8. [View Abstract]
  16. Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke. 1990 Aug. 21(8):1135-42. [View Abstract]
  17. Lee SH, Choi SK, Lim YJ, Chung HY, Yeo JH, Na SY, et al. Otologic manifestations of acoustic neuroma. Acta Otolaryngol. 2015 Feb. 135 (2):140-6. [View Abstract]
  18. Simmons Z, Biller J, Adams HP Jr, Dunn V, Jacoby CG. Cerebellar infarction: comparison of computed tomography and magnetic resonance imaging. Ann Neurol. 1986 Mar. 19(3):291-3. [View Abstract]
  19. Hacke W, Zeumer H, Ferbert A. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke. 1988. 19 (10):1216-22. [View Abstract]
  20. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14. 333(24):1581-7. [View Abstract]
  21. Mayer SA, Brun NC, Begtrup K, Broderick J, Davis S, Diringer MN, et al. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. Feb 2005. 352:777-85. [View Abstract]
  22. Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. Jan 2007. 369:283-92. [View Abstract]
  23. Giles MF, Rothwell PM. Systematic review and pooled analysis of published and unpublished validations of the ABCD and ABCD2 transient ischemic attack risk scores. Stroke. 2010 Apr. 41 (4):667-73. [View Abstract]
  24. Kim AS, Fullerton HJ, Johnston SC. Risk of vascular events in emergency department patients discharged home with diagnosis of dizziness or vertigo. Ann Emerg Med. 2011 Jan. 57(1):34-41. [View Abstract]
  25. Anagnostou E, Varaki K, Anastasopoulos D. A minute demyelinating lesion causing acute positional vertigo. J Neurol Sci. 2008 Mar 15. 266(1-2):187-9. [View Abstract]
  26. Bradley WG. MR of the brain stem: a practical approach. Radiology. 1991 May. 179(2):319-32. [View Abstract]
  27. Bruzzone MG, Grisoli M, De Simone T, Regna-Gladin C. Neuroradiological features of vertigo. Neurol Sci. 2004 Mar. 25 Suppl 1:S20-3. [View Abstract]
  28. Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med. 2003 Dec. 10(12):1388-95. [View Abstract]
  29. Froehling DA, Silverstein MD, Mohr DN. Does this dizzy patient have a serious form of vertigo?. JAMA. 1994 Feb 2. 271(5):385-8. [View Abstract]
  30. Gacek RR. A Perspective on Recurrent Vertigo. ORL J Otorhinolaryngol Relat Spec. 2013 Jun 21. 75(2):91-107. [View Abstract]
  31. Gizzi M, Riley E, Molinari S. The diagnostic value of imaging the patient with dizziness. A Bayesian approach. Arch Neurol. 1996 Dec. 53(12):1299-304. [View Abstract]
  32. Herr RD, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Emerg Med. 1989 Jun. 18(6):664-72. [View Abstract]
  33. Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998 Sep 3. 339(10):680-5. [View Abstract]
  34. Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 1987. 18 (5):849-55. [View Abstract]
  35. Mayer SA, Brun NC, Begtrup K. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. 2005 Feb. 352(8):777-85. [View Abstract]
  36. Rother J, Wentz KU, Rautenberg W. Magnetic resonance angiography in vertebrobasilar ischemia. Stroke. 1993. 24 (9):1310-15. [View Abstract]
  37. 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]
  38. Solomon D. Distinguishing and treating causes of central vertigo. Otolaryngol Clin North Am. 2000 Jun. 33(3):579-601. [View Abstract]

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.

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.

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 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.