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:
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
Physical
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.
Causes
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.
Smouha E. Inner ear disorders. NeuroRehabilitation. 2013. 32(3):455-62. [QxMD MEDLINE Link].
Schneider JI, Olshaker JS. Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke. Emerg Med Clin North Am. 2012 Aug. 30(3):681-93. [QxMD MEDLINE Link].
St. Louis EK, Wijdicks EF, Li H. Predicting neurologic deterioration in patients with cerebellar hematomas. Neurology. 1998 Nov. 51(5):1364-9. [QxMD MEDLINE Link].
Chen CC, Cheng PW, Tseng HM, Young YH. Posterior cranial fossa tumors in young adults. Laryngoscope. 2006 Sep. 116(9):1678-81. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Fitzgerald DC. Head trauma: hearing loss and dizziness. J Trauma. 1996 Mar. 40(3):488-96. [QxMD MEDLINE Link].
Amarenco P. The spectrum of cerebellar infarctions. Neurology. 1991 Jul. 41(7):973-9. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Kase CS, Norrving B, Levine SR. Cerebellar infarction - clinical and anatomic observations in 66 cases. Stroke. 1993. 24 (1):76-83. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Drachman DA. A 69-year-old man with chronic dizziness. JAMA. 1998 Dec 23-30. 280(24):2111-8. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke. 1990 Aug. 21(8):1135-42. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Bradley WG. MR of the brain stem: a practical approach. Radiology. 1991 May. 179(2):319-32. [QxMD MEDLINE Link].
Bruzzone MG, Grisoli M, De Simone T, Regna-Gladin C. Neuroradiological features of vertigo. Neurol Sci. 2004 Mar. 25 Suppl 1:S20-3. [QxMD MEDLINE Link].
Delaney KA. Bedside diagnosis of vertigo: value of the history and neurological examination. Acad Emerg Med. 2003 Dec. 10(12):1388-95. [QxMD MEDLINE Link].
Froehling DA, Silverstein MD, Mohr DN. Does this dizzy patient have a serious form of vertigo?. JAMA. 1994 Feb 2. 271(5):385-8. [QxMD MEDLINE Link].
Gacek RR. A Perspective on Recurrent Vertigo. ORL J Otorhinolaryngol Relat Spec. 2013 Jun 21. 75(2):91-107. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Herr RD, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Emerg Med. 1989 Jun. 18(6):664-72. [QxMD MEDLINE Link].
Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med. 1998 Sep 3. 339(10):680-5. [QxMD MEDLINE Link].
Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 1987. 18 (5):849-55. [QxMD MEDLINE Link].
Mayer SA, Brun NC, Begtrup K. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. 2005 Feb. 352(8):777-85. [QxMD MEDLINE Link].
Rother J, Wentz KU, Rautenberg W. Magnetic resonance angiography in vertebrobasilar ischemia. Stroke. 1993. 24 (9):1310-15. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Solomon D. Distinguishing and treating causes of central vertigo. Otolaryngol Clin North Am. 2000 Jun. 33(3):579-601. [QxMD MEDLINE Link].
Author
Keith A Marill, MD, MS Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Associate Professor, Harvard Medical School
Keith A Marill, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine
Disclosure: Received ownership interest from General Electric and Medtronic for none. for: GE; Medtronic.
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.
Chief Editor
Barry E Brenner, MD, PhD, FACEP Program Director, Emergency Medicine, Einstein Medical Center Montgomery
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine
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.