Neurologic Disorders


Vertigo and Vestibular Function

By Jason J. Barton, MD, PhD, FRCP(C)

Few problems are as common as dizziness, which results from vestibular problems, among other causes. Sufferers may end up in your chair, because many describe their symptoms in visual terms. In addition, the best signs of impaired vestibular function are abnormal eye movements.

Aiding dizzy patients entails an understanding of the vestibular system, which helps stabilize vision via the vestibulo-ocular reflexes. When the system fails, the patient experiences blurry vision during head movement and may have a sense of abnormal visual or self motion, such as the spinning sensation of vertigo. These symptoms are often associated with easily detectable signs of abnormal vestibulo-ocular responses.

In this article, I will review the symptoms of vestibular pathology and some of its ocular signs. The information should enable you to diagnose vestibular dysfunction and to determine which patients require further attention from a neurologist or otolaryngologist.

When to Suspect Vertigo: The History
The vertiginous patient's dizziness usually is an illusion of movement, such as spinning. More specifically, vertigo is the subjective sensation resulting from an acute asymmetry in vestibular function.

Normally, the right and left vestibular systems work together in a push-pull fashion. For example, when people turn their head to the right, the activity of the right horizontal canal increases and that of the left decreases from their resting firing rates. The right anterior and left posterior canals are paired, since they lie in the same plane, as are the left anterior and right posterior. These canals are activated most by head rotations in their plane. The net difference between each pair generates the signal that the head is moving in that plane.

With the head at rest, there is normally no difference, but a sudden loss (or gain) of function on one side will create a resting imbalance and the erroneous impression that the head is turning. This explains why people with vertigo suffer from the illusion that either they or their environment is spinning. The mismatch between what the vestibular system is signalling ("head moving") and what the eyes are signalling ("head not moving") generates the accompanying nausea and vomiting.

Because patients are not used to describing vestibular sensations, many give vague descriptions of what their vertigo feels like. Keep in mind that the odd person with presyncope (light-headedness) may complain that his body is spinning, floating or rocking. He is less likely to complain that the world is moving, however. In other words, what dizziness "feels like" is unreliable to the diagnosis.

For better clues, try the following questions.

Also, be careful in your consideration of certain symptoms. For instance, panic and fear don't automatically mean a panic attack rather than vertigo. Vertigo itself is a frightening experience. Neither does hyperventilation-induced dizziness necessarily mean presyncope, because it can actually bring out signs of vestibular dysfunction.

The modified Epley's procedure, used here for benign paroxysmal positional vertigo of the posterior semicircular canal of the right ear. The patient sits and turns his head 45 degrees to the right before lying back quickly, a pillow under his shoulders. After 30 seconds, the patient turns his head 90 degrees to the left, waits another 30 seconds, and then turns his head and body another 90 degrees to the left. After 30 seconds, the patient sits up on the left side. The maneuver should be repeated three times daily until BPPV does not occur within a 24-hour period.1,2,3

A 52-year-old man has one year of episodic dizziness, diagnosed previously as "cervical vertigo&uot; and treated with a neck collar. On further questioning, this transient dizziness occurs only when he is driving on the highway, on the approach to bridges, lasts several minutes, and is associated with tingling in the fingertips. It is not worsened by head movement. It does not occur when he is a passenger. He is taking trazodone and alprazolam. His exam shows a congenital left fourth-nerve palsy only. Hyperventilation reproduces his symptoms, without nystagmus. The diagnosis is an anxiety disorder. The key is the historical relation to a specific situation, the lack of worsening with head motion, and the reproduction of symptoms without nystagmus by rapid breathing. The tingling in the fingertips is a telltale symptom of hypocapnia from hyperventilation.

Vestibular Dysfunction's Other Symptoms
The acute vestibular asymmetry underlying vertigo can arise through either a sudden unilateral loss of function, as with a vestibular infarct, or abnormal unilateral activity (hyperfunction), as with Ménière's disease or BPPV. Recognizing the other symptoms of vestibular dysfunction can be important, though these are less well known than vertigo. The type of symptom depends upon the duration of dysfunction and whether one or both vestibular systems are involved. Here's an overview.

Chronic unilateral vestibular hypofunction. Rather than vertigo, patients suffer a transient spatial disorientation that is induced by rapid head turns toward the damaged side.

If an acute vestibular asymmetry is permanent, the resultant vertigo will disappear as the brainstem and cerebellum learn to use the signals from the remaining labyrinth more effectively. With only one working labyrinth, head movement toward the damaged side will be signaled only by a decrease in the firing rate of the intact side. This change is proportional to the rate of head movement and encodes head velocity.

Since no firing rate can be reduced below zero, there comes a point at which the speed of the head turn exceeds the firing rate change that can reliably signal head velocity. It is also too fast for the pursuit and optokinetic systems to track the shift in the visual environment. The inaccurate vestibular data causes a transient moment of spatial disorientation that lasts a second or so with the rapid head turn.

This disorientation can be the remnant of an acute but permanent lesion that once caused vertigo. If the patient has never had vertigo, however, you must consider the possibility that this symptom may be the insidious manifestation of a progressing lesion, such as a meningioma or acoustic neuroma (schwannoma) at the cerebellopontine angle. These cases require neurologic referral and MR imaging of the internal auditory canal.

A 50-year-old female golf pro had sudden vertigo, tinnitus, imbalance and vomiting one year ago. She was placed on bed rest for two weeks, and symptoms gradually improved over the next month. However, she found that, since then, activities with head motion (such as playing golf) caused dizziness, a sense of self motion. On exam, her acuity decreased from 20/15 with the head still to 20/100 while her head was shaken by the examiner. She had a positive head-thrust test with rapid right head turns and, after head shaking for one minute, there was left-beating nystagmus in the dark. Her history suggests an acute vestibular asymmetry, probably a viral labyrinthitis, possibly an infarct, with permanent right vestibular hypofunction afterwards. The prolonged period of bed rest may actually have hampered her adaptive recovery. She did well with a course of vestibular rehabilitation, resuming her work with an improved golfing handicap.

Bilateral vestibular dysfunction, acute or chronic. If a person loses both vestibular systems simultaneously, no asymmetry in function-and, therefore, no vertigo-will occur. Instead, the patient has difficulties with balance, frequently worse in the dark when vision cannot compensate for the loss. Walking to the bathroom at night, for instance, becomes a major challenge. This imbalance is not very specific, though, since patients with an abnormal position sense or cerebellar dysfunction are ataxic, too. A better indicator is that patients who have lost both vestibular systems frequently perceive the world as jiggling (oscillopsia) as soon as they start to move. Walking or driving on an uneven road, which cause high-frequency oscillations of the head, are particularly problematic. In addition to the jiggling, vision becomes blurry, and patients often have to stop walking to read signs.

Oscillopsia induced by head motion is pathognomonic for an impaired or absent vestibulo-ocular reflex. It differs from oscillopsia due to nystagmus, which is present even when the head is still, sometimes varying with gaze direction.

Acute, bilateral simultaneous loss often has a toxic or metabolic cause. The most common toxins are the aminoglycosides, loop diuretics, salicylates and cisplatin. Meningitis or head injury can also cause this, but will be evident from the history.

Causes of chronic bilateral loss include otosclerosis, radiation treatment and idiopathic degeneration. Bilateral acoustic neuromas are rare and indicate a high likelihood of neurofibromatosis type 2.

Some patients lose first one labyrinth and then the other. Sequential acute loss has a typical story. An episode of vertigo occurs and gradually resolves. It leaves only a mild, transient disorientation during rapid head motion to one side, an experience the patient may not be able to describe well. Then, a second vertiginous episode occurs, as the loss of the second side leads to a transient apparent asymmetry in the adapted network. When this resolves, the patient is left with severe oscillopsia and reduced acuity associated with head motion.

The causes of this sequential bilateral pattern include those of vertigo, notably ischemia, inflammation, Ménière's disease and Cogan's autoimmune syndrome, which is associated with interstitial keratitis.

Diagnostic Examination
Many different aspects of vestibular function can be tested. For ophthalmologists, naturally, ocular signs are the most obvious. There are two main groups of findings: nystagmus and signs of a defective vestibulo-ocular reflex.

The modified Epley's procedure, used here for benign paroxysmal positional vertigo of the posterior semicircular cananl of the right ear. The patient sits and turns his head 45 degrees to the right before lying back quickly, a pillow under his shoulders. After 30 seconds, the patient turns his head 90 degrees to the left, waits another 30 seconds, and then turns his head and body another 90 degrees to the left. After 30 seconds, the patient sits up on the left side. The maneuver should be repeated three times daily until BPPV does not occur within a 24-hour period.1,2,3

Nystagmus. If the patient is experiencing an acute attack of vertigo at the time of his visit, he may have nystagmus, a rhythmic oscillation of the eyes. Vestibular nystagmus is always jerk in form, meaning it has a slow phase in one direction and a fast phase in the other.

The push-pull asymmetry in the vestibular system generates the slow phase. The fast phase occurs when the brain realizes that the eye is getting off target and tries to correct it.

Pattern. The direction of nystagmus correlates with the planes in which vestibular asymmetry exists. For example, the healthy left horizontal canal is excited by head turns to the left, leading to compensatory slow vestibular eye movements rightward. Loss of this canal leads to the loss of the rightward drive to the eyes. This causes the eyes to drift leftward under the unopposed action of the right horizontal canal. The result is right-beating nystagmus.

By the same token, the loss of the left posterior canal leads to downward and clockwise torsional nystagmus. The loss of the left anterior canal leads to upward and clockwise nystagmus.

Peripheral damage to the vestibular system commonly affects all three canals on one side. The result from left-side damage is a right-beating, clockwise torsional nystagmus (the vertical components from the posterior and anterior canals cancel each other out, while the torsional components add up). When severe, this type of nystagmus is present in all directions of gaze, though worst to the right. With time and less severe lesions, it may be present only in right gaze.

This mixed pattern of nystagmus is most commonly seen with lesions of the labyrinth or peripheral vestibular nerve. Nevertheless, a lesion of the vestibular nuclei in the lateral medulla can cause a similar horizontal-torsional nystagmus with vertigo.

Patients with chronic unilateral vestibular hypofunction may not have nystagmus on first inspection. Nystagmus, however, may emerge during funduscopy, particularly if you block the other eye. This technique reveals that patient's brain has learned to suppress nystagmus with visual fixation.

Lesions. What type of nystagmus indicates a brain lesion? An important rule of thumb is that nystagmus in primary position, which is restricted to one direction, means a lesion of the brain, not the labyrinth. This is always true with pure upbeat, pure downbeat and pure torsional nystagmus. The rule is less reliable with pure horizontal nystagmus, which can sometimes occur with a peripheral lesion.

To understand why this rule holds, consider the case of pure upbeat nystagmus. As the name implies, the rapid phase is upward moving. A lesion of one anterior canal will cause upbeat nystagmus, but with a torsional component, too, because the plane of the anterior canal is set at 45 degrees from the sagittal plane. So, pure upbeat nystagmus can only occur if a lesion affects the data from both anterior canals, which cancels out the torsional phases of each, and if it spares the input from all the other canals. This is not likely to occur with peripheral disease.

Similarly, pure torsional nystagmus requires a peripheral lesion on one side that affects both vertical canals and spares the horizontal canal. This is not a likely scenario, considering the vascular and nerve anatomy of the labyrinth.

Gaze-evoked nystagmus also points to disease of the central nervous system (CNS). This type of nystagmus occurs only in eccentric gazes and beats in the direction of gaze. So, there is left-beating nystagmus when the patient looks left and right-beating nystagmus when he looks right. This nystagmus implies a failure of gaze-holding, which is a cerebellar and brainstem function, not a vestibular one. Drugs, especially anti-epileptic medications, are a common cause.

Patients with central lesions causing primary position nystagmus in one direction or gaze-evoked nystagmus probably will not be nauseated. In addition, they tend to complain of oscillopsia rather than vertigo. If you encounter such a patient, promptly refer him for a neurologic assessment, as there is a lengthy list of differential diagnoses.

BPPV. Be on the alert for BPPV, a special kind of nystagmus and an exceedingly common problem. BPPV is caused by canalithiasis, in which loose calcium debris gets into a semi-circular canal, usually the posterior one. When gravity causes the debris to move, it generates false signals of head turns.

Patients with BPPV complain of bouts of vertigo that last a few minutes or less. They will tell you that their vertigo is brought on by bending over, looking up, turning their head and getting out of bed. Dizziness upon standing up in the morning may mislead you to suspect postural presyncope. To differentiate between the two, keep in mind that the BPPV patient will also be dizzy when going to lie down or turning over in bed. These maneuvers never provoke presyncope.

By placing the eye clinic's chair flat and removing the head rest, you can induce an attack of BPPV in an affected person. The patient should remain seated, his head turned to one side with the neck extended. Place him flat with the head hanging down. Turning the head to the left places the left posterior canal parallel to the gravity vector, and any debris in the canal will begin to move. This will generate an abnormal excitation of the canal and, in a few seconds, result in upbeat, counterclockwise nystagmus, which will end in less than a minute. If the patient sits up and the maneuver is repeated a few times, the nystagmus should be of shorter duration each time (fatigability). If no nystagmus occurs, have the patient sit up and perform the maneuver with the extended head turned to the opposite side.

Unless you observe this pattern of nystagmus, you can only presume a diagnosis of BPPV from the history. If there is nystagmus without a lag, which persists on repeated testing, or beats in a different direction, you must suspect a CNS lesion and refer the patient for neurologic evaluation. If, however, you observed typical BPPV and can identify which direction of head turn generates it, you can actually perform a curative treatment while the patient is in the chair, or prescribe a set of effective home exercises.

A 31-year-old man was hit by a car while bicycling one year ago, suffering a concussion and basal skull fracture. When he was allowed to move in the hospital, he noted severe vertigo and vomiting, as well as deafness and tinnitus in the right ear. This abated after one week. Since then, he has had episodic vertigo, lasting a minute and provoked by lying down in bed, looking up at a basketball net, and rolling over in bed to the right. It is followed by nausea. Examination showed good visual acuity even during head shaking (20/20) and no nystagmus after head shaking. The head-thrust test was negative. Positional testing showed that, with the head hanging down to the right, there was a mixed upbeat/counterclockwise torsional nystagmus after 2 seconds, lasting 15 seconds, and not recurring on a second maneuver. He clearly has BPPV from right posterior canal debris, caused by head trauma. He also had a transient vestibular dysfunction at the time of injury, but that has left no permanent vestibular hypofunction. He was cured with a single Epley maneuver.

Signs of an abnormal VOR. In patients who are between attacks of vertigo or whom you suspect of having chronic or bilateral vestibular problems, you will need to look for signs of a defective vestibulo-ocular reflex (VOR). The following should aid you in your examination.

Visual acuity during head motion. Ask the patient to read the eye chart at a distance while you rapidly oscillate his head. Keep in mind that their VOR will be calibrated for their customary distance correction, so they must wear this during the test. The patient's visual acuity should not fall more than three to four lines from what it is with the head still. An abnormal result may occur from central or peripheral, unilateral or bilateral vestibular disease, though it is usually much worse with bilateral disease.

Head-thrust test. Ask the patient, who again wears his normal correction, to keep his gaze on a distant point while you rapidly turn his head to one side and then the other. Be sure that the patient cannot predict when and by how much you will move his head.

If the vestibular system on the side to which you turn the head is defective, then the patient's eyes will not stay on target but will move with the head. Watch for a small saccade back to the target after the head turn has stopped. Because the head-thrust test deals with each side separately, it will enable you to distinguish unilateral from bilateral disease. Abnormal head thrusts are common with peripheral lesions, but they can occur with a lesion of the vestibular nuclei, too.

Post-head-shaking nystagmus. This test works best with visual fixation suppressed. This can be done with Frenzel lenses or, barring that, in the dark with ophthalmoscopy to see the nystagmus once the head stops moving. Shake the patient's head side to side 30 times or more. When the patient's head stops, his eyes should be stable. If there is an asymmetry in the vestibular input to the cerebellum, then you will see a nystagmus beating away from the defective side. Bilateral disease will not give an abnormal result.

Course of Action
The diagnosis of dizziness and vertigo requires an expert. By the knowledgeable history-taking and examination described above, however, you can establish whether there is a vestibular problem. The next step is to determine which patients need a neurologic evaluation. The following information should help.

Tumors. For the most part, tumors are chronic, progressive problems. They seldom cause vertigo. If they affect the peripheral vestibular system, the patient is more likely to present with transient spatial disorientation after rapid head movements.

A tumor of the brainstem or cerebellum may cause other types of nystagmus and oscillopsia. The exceptions to this "no vertigo" rule are tumors with acute complications, such as bleeding and rapid swelling. When these occur, though, the resultant increase in pressure in the posterior fossa usually leads quickly to other signs of brainstem and cerebellar dysfunction, including a decrease in consciousness. These patients should be in the emergency room, not an eye clinic chair.

CNS disease. If your examination discovers signs indicating CNS disease, refer the patient to a neurologist. Sometimes the problem is benign; sometimes it is dangerous; and sometimes it can be fixed. Refrain from ordering a generic "brain MRI" before a referral, because a neurologic exam will determine the best MR sequences and focus of view.

Vestibular disease. The presence of signs indicating disease of the peripheral vestibular system does not automatically mean that the problem is benign. Certainly, the most common conditions (like vestibular neuronitis, Ménière's disease and BPPV) are not life-threatening.

Nevertheless, once in a while, vertigo with a peripheral-looking nystagmus will come from something meaner. A cerebellar hemorrhage or infarct, for example, can cause horizontal nystagmus, dizziness and vomiting. Telltale signs in this case would be bilateral sixth-nerve palsies or drowsiness, but these are not always present.

Another cause might be a lateral medullary infarction, which can cause vertigo with horizontal-torsional nystagmus. Associated clues could include Horner's syndrome, hoarseness, or the loss of pain sensation on the same side of the face or the other side of the body.

Sudden vertigo and unilateral hearing loss might indicate an infarct of the nerve or labyrinth. This is essentially a stroke in the distribution of the anterior inferior cerebellar artery, so the patient needs a stroke workup. If you suspect any of these conditions, refer the patient to a neurologist for a consultation.

Dr. Barton is an assistant professor for the departments of neurology and ophthalmology at Beth Israel Deaconess Medical Center, Harvard Medical School, and the department of bioengineering at Boston University.

Posted: Oct. 20, 2000. Originally published September 2000.


1. Epley, JM. The canalith repositioning procedure: For the treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992; 107:399.
2. Herdman, SJ, Tusa, RJ, Zee, DS, et al. Single treatment approaches to benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg 1993; 119:450.
3. Radtke A, Neuhauser H, von Brevern M, Lempert T. A modified Epley's procedure for self-treatment of benign paroxysmal positional vertigo. Neurology 1999; 53:1358.

Further Reading

1. Dix, MR, Hallpike, CS. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Ann Otol Rhinol Laryngol 1952; 61:987.
2. Gizzi, M, Riley, E, Molinari, S. The diagnostic value of imaging the patient with dizziness. A Bayesian approach. Arch Neurol 1996; 53:1299.
3. Hall, SF, Ruby, RR, McClure, JA. The mechanics of benign paroxysmal vertigo. J Otolaryngol 1979; 8:151.
4. Harner, SG, Laws, ER Jr. Clinical findings in patients with acoustic neuroma. Mayo Clin Proc 1983; 58:721.
5. Herr, RD, Zun, L, Matthews, JJ. A directed approach to the dizzy patient. Ann Emerg Med 1989; 18:664.
6. Hotson, JR, Baloh, RW. Acute vestibular syndrome. N Engl J Med 1998; 339:680.
7. Hughes, CA, Proctor, L. Benign paroxysmal positional vertigo. Laryngoscope 1997; 107:607.
8. Johnson, GD. Medical management of migraine-related dizziness and vertigo. Laryngoscope 1998; 108:1.
9. Knox, GW, McPherson, A. Ménière's disease: Differential diagnosis and treatment. Am Family Physician 1997; 55:1185.
10. Kroenke, K, Lucas, CA, Rosenberg, ML, et al. Causes of persistent dizziness: A prospective study of 100 patients in ambulatory care. Ann Intern Med 1992; 117:898.
11. Nedzelski, JM, Barber, HO, McIlmoyl, L. Diagnoses in a dizziness unit. J Otolaryngol 1986; 15:101.
12. Semont, A, Freyss, E, Vitte, P. Curing the BPPV with a liberatory maneuver. Adv Otorhinolaryngol 1988; 42:290.
13. Sloane, PD. Evaluation and management of dizziness in the older patient. Clin Geriatric Med 1996; 12:785.
14. Yardley, L, Beech, S, Zander, L, et al. A randomized controlled trial of exercise therapy for dizziness and vertigo in primary care. Brit J Gen Pract 1998; 48:1136.

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