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  • Updated 05.26.2023
  • Released 03.22.2000
  • Expires For CME 05.26.2026




The author explains the clinical presentation, pathophysiology, diagnostic work-up, and management of vertigo. Vestibular vertigo is a common problem, affecting 5% or more of adults each year. Careful history, provocative testing, and detailed examination will allow distinction of the major categories of dizziness in most cases and will often allow a specific etiologic diagnosis as well.

Key points

• Vertigo is an illusion of movement due to an imbalance of tonic vestibular activity within the central or peripheral vestibular pathways.

• Vertigo is usually rotatory, implying a disturbance of the semicircular canals or their central connections. Sensations of body tilt or impulsion indicate otolithic disturbances or dysfunction of central otolithic connections.

• Vertigo is commonly associated with nystagmus, oscillopsia, postural imbalance, and autonomic symptoms (eg, sweating, pallor, nausea, vomiting).

• Vestibular vertigo is a common problem, affecting 5% or more of adults each year.

• Careful history, provocative testing, and detailed examination will allow distinction of the major categories of dizziness in most cases and will often allow a specific etiologic diagnosis as well.

• Episodic vertigo is generally of abrupt onset, but the duration of episodes varies considerably: episodes of benign paroxysmal positioning vertigo last seconds (up to a minute), whereas seizures generally last seconds or minutes, migrainous vertigo may last minutes to days, transient ischemic attacks last minutes to hours (up to a day by definition, but generally less than 6 hours), and attacks of Ménière syndrome last hours.

• Monophasic vertigo may have an abrupt onset (eg, with trauma, stroke, or demyelinating disease), a subacute onset (eg, with vestibular neuronitis), or a subacute to chronic onset (eg, with toxic vestibulopathy or posterior fossa masses).

• Peripheral vestibular nystagmus is a mixed linear-rotatory jerk nystagmus that beats in one direction away from a hypofunctioning labyrinth.

• Drugs should be reviewed in all patients with dizziness, whether clearly vertiginous or not. Drugs associated with dizziness include alcohol and other CNS depressant medications (eg, benzodiazepines, barbiturates, phenothiazines), aminoglycoside antibiotics, anticonvulsants, antidepressant medications, antihypertensive medications, chemotherapeutic agents, loop diuretics (eg, furosemide), and salicylates.

• The elderly are particularly susceptible to drug ototoxicity.

• Occupational exposure of healthcare and research staff to static magnetic stray fields from MRI scanners is associated with transient symptoms, particularly vertigo and dysgeusia (metallic taste sensations).

• In patients with acute, persistent vertigo from peripheral vestibular lesions, recovery occurs more rapidly and more completely when vestibular exercises are begun as soon as possible after the onset of symptoms.

• Severe forms of acute, persistent vertigo are especially distressing, particularly when accompanied by nausea and vomiting; antivertiginous medications with both sedative and antiemetic effects are helpful in these situations (eg, promethazine, droperidol, dimenhydrinate).

• Vestibular paroxysmia, a neurovascular compression syndrome of the eighth cranial nerve, is often readily amenable to pharmacological treatment with carbamazepine or oxcarbazepine. It is characterized by brief attacks of vertigo lasting seconds to minutes, often occurring multiple times daily, with accompanying nystagmus and unsteadiness of stance or gait.

Historical note and terminology

English physician Erasmus Darwin (1731-1802), the grandfather of naturalist Charles Darwin (1809-1882), described physiologic vertigo, its dependence on rotation, and many of the subjective phenomena associated with it, in the late 1700s and early 1800s (35). Subsequently, other important early 19th-century contributions to vestibular physiology were made by Purkinje and Flourens (13; 148). From 1820 to 1827 Czech anatomist and physiologist Jan Evangelista Purkyně (also written Johann Evangelist Purkinje; 1787-1869) established the method of rotation to study vertigo, thoroughly described apparent movement of the visual field during and after rotation and discovered that the axis of apparent after-rotation varies with the position of the head; this, in turn, suggested that the organ for perception of rotation must lie in the head (13). From 1824 to 1830 French physiologist Jean Pierre Flourens (1794-1867) performed and reported key studies, showing the section of semicircular ducts that produces muscular incoordination that is maximal in the plane of the sectioned canals (13).

In the 1870s considerable progress was made in understanding the function of the peripheral vestibular system (13; 149). In 1870 German physiologist Friedrich Leopold Goltz (1834-1902) found that caloric irrigation of the external auditory canal produced vertigo, nausea, and nystagmus. In 1871 German neurologist and neuropsychiatrist Eduard Hitzig (1839-1907) produced similar phenomena with electric currents applied to the head (13). Goltz also argued that orientation is due to the pattern of pressures in the three semicircular ducts, an idea subsequently developed independently by Mach, Breuer, and Crum-Brown from 1873 to 1875 (13; 90; 91; 88). Austrian physicist and philosopher Ernst Mach (1838-1916) proposed in 1873 that a change in speed of rotation (ie, angular acceleration) would produce pressures within the semicircular ducts that would vary in intensity as a function of the components of rotation in the planes of the respective canals (13; 90). Mach also proposed that the maculae in the vestibular otolithic organs were responsible for sensing linear acceleration (90). Austrian physician and physiologist Josef Breuer (1842-1925) and British physician and theoretical organic chemist Alexander Crum-Brown (1838-1922) described similar results in 1874 and 1875, respectively (13; 91; 88). Though Mach had assumed that each canal sensed both clockwise and counterclockwise rotations in its own plane, Crum-Brown doubted this and noted that the symmetrical pattern of the canals on the two sides of the head made this unnecessary (13; 88). Thus, canals in the same plane on the left and right sides of the head were reversed in function, with counterclockwise rotation stimulating one, and clockwise rotation stimulating the other.

The osseous labyrinth housing the vestibular receptors lies in the petrous temporal bone, with the three semicircular canals on each side oriented roughly orthogonally to one another, and in such a fashion that (1) the superior canal on one side is in approximately the same plane as the posterior canal on the opposite side, and (2) the lateral (“horizontal” or external) canals are in approximately the same plane. The membranous labyrinth lies within the osseous labyrinth and includes the three semicircular ducts for sensing rotary motions of the head, and the utricle and saccule for sensing linear accelerations.

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