What is vertigo

Vertigo is a sensation of movement or spinning, tilting or swaying. Vertigo feels like you or everything around you is spinning – enough to affect your balance. It’s more than just feeling dizzy. While there are some serious causes of vertigo, usually it just gets better with time. Vertigo is a type of dizziness that is often described as feeling that you are spinning or that the world is spinning around you, particularly if you change position.

A vertigo attack can last from a few seconds to hours. If you have severe vertigo it can last for many days or months.

How do you get vertigo

Vertigo is the result of an inner ear problem. The most common cause is benign paroxysmal positional vertigo (BPPV). BPPV (benign paroxysmal positional vertigo) occurs when tiny calcium particles clump together in the part of the inner ear that helps control our balance, affecting the messages sent from your inner ear to your brain.

Other causes of vertigo include head injuries, stroke, circulation problems, infections, inner ear disorders, and the degeneration of inner ear structures. Inner ear problems include Meniere’s disease, vestibular neuritis and labyrinthitis. Vestibular neuritis is a swelling or infection of the nerve supplying a bone in the inner ear, and labyrinthitis is a swelling or infection of the inner ear.

Treatment for vertigo depends on the cause. In most cases vertigo goes away without treatment. Stress can increase symptoms of dizziness and nausea, and reducing stress can help reduce the symptoms.

What helps vertigo

There are things you can do to ease vertigo symptoms when they’re happening, and to reduce the number of episodes you have.

DO

• lie still in a quiet, dark room to reduce the spinning feeling
• move your head carefully and slowly during daily activities
• sit down straightaway when you feel dizzy
• turn on the lights if you get up at night
• use a walking stick if you’re at risk of falling
• sleep with your head slightly raised on 2 or more pillows
• get out of bed slowly and sit on the edge of the bed for a while before standing up
• try to relax – anxiety can make vertigo worse

DON’T

• bend over to pick things up – squat to lower yourself instead
• stretch your neck – for example, while reaching up to a high shelf

Vertigo gets better in most cases without treatment.

See a doctor if vertigo keeps coming back or is affecting your daily life. Your doctor may recommend one of the following treatments:

• Vestibular rehabilitation or balance training – this is a type of physical therapy that strengthens the vestibular system.
• Canalith repositioning measures – this is useful if the cause is benign paroxysmal positional vertigo (BPPV). The treatment moves calcium deposits out of the canal so they can be absorbed by the body.
• Medicine – motion sickness medication can be used to relieve some symptoms of vertigo such as nausea, and antibiotics can treat a bacterial infection.
• Diuretics, or water pills, may be prescribed to reduce the swelling associated with Meniere’s disease.
• Surgery – surgery is only needed in a few cases.

Inner ear anatomy

You rely on the inner ear, an intricate sensory organ, to hear and to maintain balance. The inner ear is a complex system of communicating chambers and tubes called a labyrinth. Each ear has two parts to the labyrinth—the bony (osseus) labyrinth and the membranous labyrinth (Figure 1). The bony labyrinth is a cavity within the temporal bone. The membranous labyrinth is a tube of similar shape that lies within the bony labyrinth. Between the bony and membranous labyrinths is a fluid called perilymph, which is secreted by cells in the wall of the bony labyrinth. The membranous labyrinth contains another fluid, called endolymph.

The parts of the labyrinths include three membranous semicircular ducts within three bony semicircular canals, and a cochlea. The semicircular canals and associated structures provide a sense of equilibrium (balance). The cochlea functions in hearing.

Figure 1. Inner ear anatomy

Figure 2. Parts of the inner ear

Sense of Equilibrium

The sense of equilibrium (balance) is really two senses:

1. Static equilibrium and
2. Dynamic equilibrium—that come from different sensory organs.

The organs of static equilibrium sense the position of the head, maintaining balance, stability and posture when the head and body are still. When the head and body suddenly move or rotate, the organs of dynamic equilibrium detect such motion and aid in maintaining balance.

Static Equilibrium

The organs of static equilibrium are in the vestibule, a bony chamber between the semicircular canals and the cochlea. The membranous labyrinth inside the vestibule consists of two expanded chambers—a utricle and a saccule (see Figure 2).

The saccule and utricle each have a tiny structure called a macula. Maculae have many hair cells, which serve as sensory receptors. The hairs of the hair cells project into a mass of gelatinous material, which has grains of calcium carbonate (otoliths) embedded in it. These particles add weight to the gelatinous structure.

Bending the head forward, backward, or to either side tilts the gelatinous masses of the maculae, and as they sag in response to gravity, the hairs projecting into them bend. This action causes the hair cells to signal the sensory neurons associated with them in a manner similar to that of hair cells associated with hearing. The resulting action potentials are conducted into the central nervous system on the vestibular branch of the vestibulocochlear nerve, informing the brain of the head’s new position. The brain responds by adjusting the pattern of motor impulses to skeletal muscles, which contract or relax to maintain balance.

Figure 3. Inner ear maculae respond to changes in head position

Note: (a) Macula of the utricle with the head in an upright position. (b) Macula of the utricle with the head bent forward.

Dynamic Equilibrium

The organs of dynamic equilibrium are the three semicircular canals in the labyrinth. They detect motion of the head and aid in balancing the head and body during sudden movement. These canals lie at right angles to each other (see Figure 2).

Suspended in the perilymph of the bony portion of each semicircular canal is a membranous semicircular duct that ends in a swelling called an ampulla, which
houses the sensory organs of the semicircular canals. Each of these sensory organs, called a crista ampullaris, contains a number of sensory hair cells and supporting cells. Like the hairs of the maculae, the hair cells of the crista ampullaris extend upward into a dome-shaped, gelatinous mass called the cupula (Figure 4). When the head is stationary, the cupula of the crista ampullaris remains upright. When the head is moving rapidly, the cupula bends opposite the motion of the head, stimulating sensory receptors.

Rapid movement of the head or body stimulates the hair cells of the crista ampullaris (Figure 4). At such times, the semicircular canals move with the head or body, but the fluid inside the membranous ducts remains stationary. Imagine turning rapidly while holding a full glass of water. This action bends the cupula in one or more of the canals in a direction opposite that of the head or body movement, and the hairs embedded in it also bend. The stimulated hair cells signal their associated neurons, which conduct impulses to the brain. The brain interprets these impulses as a movement in a particular direction.

Parts of the cerebellum are particularly important in interpreting impulses from the semicircular canals. Analysis of such information allows the brain to predict the consequences of rapid body movements. By modifying signals to appropriate skeletal muscles, the cerebellum can maintain balance.

Other sensory structures aid in maintaining equilibrium. For example, certain mechanoreceptors (proprioceptors), particularly those associated with the joints of the neck, inform the brain about the position of body parts. In addition, the eyes detect changes in position that result from body movements. Such visual information is so important that even if the organs of equilibrium are damaged, a person may be able to maintain normal balance by keeping the eyes open and moving slowly.

The nausea, vomiting, dizziness, and headache of motion sickness arise from sensations that don’t make sense. The eyes of a person reading in a moving car, for example, signal the brain that the person is stationary, because the print doesn’t move. However, receptors in the skin detect bouncing, swaying, starting, and stopping as the inner ear detects movement. The contradiction triggers the symptoms. Similarly, in a passenger of an airplane flying through heavy turbulence, receptors in the skin and inner ear register the chaos outside, but the eyes focus on the immobile seats and surroundings.

Figure 4. Dynamic inner ear balance organs (crista ampullaris) within the Semicricular ducts

Vertigo signs and symptoms

If you have vertigo, it may feel like you are spinning, swaying or feeling unbalanced.

The most common symptoms of vertigo include a feeling of:

• Spinning (either you or the room around you)
• Tilting or swaying
• Feeling off balance

These feelings come and go, and may last seconds, hours, or days. You may feel worse when you move your head, change positions (stand up, roll over), cough, or sneeze.

People with vertigo may also have:

• Ringing in the ears
• Vomit or feel nauseous
• Have a headache or be sensitive to light and noise
• See double, have trouble speaking or swallowing, or feel weak
• Feel short of breath or sweaty, have a racing heart beat

If you seek treatment for vertigo, you should mention how long these symptoms last, what triggers the symptoms, and any other associated problems. These clues can help point to the cause of vertigo.

Vertigo causes

Inner ear problems, which affect balance, are the most common causes of vertigo:

• Benign paroxysmal positional vertigo (BPPV) – BPPV, sometimes called benign positional vertigo, positional vertigo, postural vertigo, or simply vertigo, is a type of vertigo that develops due to collections of calcium in the inner ear. These collections are called canaliths. Moving the canaliths (called canalith repositioning) is a common treatment for BPPV. Vertigo is typically brief in people with BPPV, lasting seconds to minutes. Vertigo can be triggered by moving the head in certain ways.
• Meniere disease – Meniere disease is a rare inner ear condition that causes repeated spells of vertigo, hearing loss, and ringing in the ears (tinnitus). Spells can last several minutes or hours. It is probably caused by a buildup of fluid in the inner ear.
• Vestibular neuritis – Vestibular neuritis, also known as labyrinthitis, is probably caused by a cold or flu virus that causes swelling around the balance nerve (vestibular nerve). People with vestibular neuritis develop sudden, severe vertigo, nausea, vomiting, and difficulty walking or standing up; these problems can last several days. Some people also develop difficulty hearing in one ear.
• Head injury – Head injuries can affect the vestibular system in a variety of ways, and lead to vertigo.
• Other brain problems – Stroke or TIA (transient ischemic attack), bleeding in the brain, or multiple sclerosis can also cause vertigo. There are usually other symptoms, besides vertigo, that happen with these brain problems.

Other things that can cause vertigo:

• Migraines – In a condition called vestibular migraine or migrainous vertigo, vertigo can be caused by a migraine. This type of vertigo usually happens along with a headache, but some patients have migraines without headache.
• Some types of medicine – check the leaflet to see if it’s listed as a side effect, medications can affect the function of the inner ear or brain and lead to vertigo. Rarely, some medications can actually damage the inner ear.

Sometimes the cause is unknown.

The relative frequencies of various syndromes presenting with dizziness and vertigo are listed in table 1.

Table 1. The relative frequencies of different dizziness and vertigo syndromes

Diagnosis	Number of patients	Percent
Benign paroxysmal positioning vertigo	1336	18.6
Phobic postural vertigo	1127	15.6
Central vestibular vertigo	893	12.4
Basilar/vestibular migraine	738	10.2
Meniere’s disease	677	9.4
Vestibular neuritis	531	7.4
Bilateral vestibulopathy	367	5.1
Vestibular paroxysmia	284	3.9
Psychogenic dizziness	228	3.2
Perilymph fistula	44	0.6
Dizziness syndromes of unclear etiology	239	3.3
Other	741	10.3
Overall	7205

[Source ¹]

The important criteria for distinguishing among them are as follows ²:

• The type of dizziness/vertigo: rotatory vertigo resembles the sensation of being on a merry-go-round (in vestibular neuritis and other disorders), while postural vertigo resembles the sensation of riding in a boat (e.g., in bilateral vestibulopathy). Many patients use the term “dizziness” for lightheadedness without any sensation of movement (e.g., in drug intoxication).

• The duration of dizziness/vertigo: attacks may last for seconds or minutes (as in vestibular paroxysm) or hours (as in Menière’s disease or vestibular migraine). Persistent vertigo lasting days or weeks is seen in vestibular neuritis, among other conditions. Attacks of postural vertigo lasting minutes to hours can be produced, for example, by brainstem transient ischemic attacks.

• Precipitating and exacerbating factors of dizziness and vertigo: the symptoms arise at rest in some conditions (e.g., vestibular neuritis); they can also arise when the patient walks (as in bilateral vestibulopathy) or be induced by turning the head to the right or left (as in vestibular paroxysm). Other possible precipitating factors include turning in bed (as in benign paroxysmal positioning vertigo [BPPV]), coughing, pressing, and loud tones of a particular frequency (Tullio’s phenomenon, seen in perilymph fistula), as well as certain social or environmental conditions (e.g., phobic postural vertigo).

• The accompanying symptoms, if present, may arise from the inner ear – e.g., attacks of intense tinnitus, hearing impairment, and a pressure sensation in the ear, which are typical of Menière’s disease. Diplopia, sensory disturbances, dysphagia, dysarthria, and paralysis of arms and legs are symptoms of central origin that usually arise in the brainstem. Headache or a history of migraine may point to the diagnosis of vestibular migraine but can also be caused by brainstem ischemia or posterior fossa hemorrhage.

Table 2. The presenting manifestations and causes of peripheral vestibular types of vertigo

Type of disorder	Presenting manifestations	Examples and causes
Chronic, bilateral peripheral vestibular dysfunction	Oscillopsia on head movement (loss of the vestibulo-ocular reflex) Unsteadiness of stance and gait, worsening in darkness and on uneven ground (because of the partial or total removal of visual or somatosensory cues) Impairment of spatial memory	Bilateral vestibulopathy due to (e.g.): ototoxic substances (aminoglycosides) bilateral Menière’s disease meningitis bilateral acoustic neuromas (= neurofibromatosis type 2)
Acute/subacute unilateral vestibular dysfunction (labyrinth and/or vestibular nerve) with asymmetrical vestibular tone	Rotatory vertigo (lasting a few days to weeks), Oscillopsia due to spontaneous nystagmus, Tendency to fall to a particular side Nausea	Vestibular neuritis due to reactivation of a latent herpes simplex virus type 1 infection
Inappropriate unilateral paroxysmal excitation or loss of function of the peripheral vestibular system	Attacks of rotational or swaying vertigo that (depending on their cause) may or may not be externally precipitated, are of varying duration, and are accompanied by various other symptoms	Benign peripheral paroxysmal positioning vertigo due to canalolilthiasis; Menière’s disease due to rupture of the endolymphatic membrane; Vestibular paroxysm due to neurovascular contact

[Source ¹]

Benign paroxysmal positioning vertigo (BPPV)

This is the most common type of vertigo; it mainly affects older patients (Table 1) and has a lifetime prevalence of 2.4% ³. It is characterized by brief attacks of rotational vertigo, accompanied by vertical positioning nystagmus that rotates toward the lower of the two ears and beats toward the forehead. Nystagmus is a term used to describe alternating slow and fast movements of the eyes ⁴. These alternating movements give the appearance that the eyes are beating toward one or more directions. The attacks are precipitated by reclination of the head, or by lateral positioning of the head or body, with the affected ear downward ¹. After a change in position of one of these types, rotational vertigo and nystagmus arise after a latency of a few seconds and then take a characteristic crescendo-decrescendo course, lasting a total of 30 to 60 seconds ¹. The nystagmus corresponds to a so-called ampullofugal excitation of the affected posterior vertical semicircular canal of the affected (lower) ear.

More than 90% of cases are idiopathic ¹; the remaining, symptomatic cases are most commonly due to head trauma, vestibular neuritis, or Menière’s disease ⁵. Benign paroxysmal positioning vertigo is called “benign” because it usually resolves spontaneously within a few weeks or months; in some cases, however, it can last for years. If left untreated, it persists in about 30% of patients. Benign paroxysmal positioning vertigo also arises with greater than usual frequency after prolonged bed rest necessitated by other diseases, or after surgery. Benign paroxysmal positioning vertigo of the horizontal semicircular canal is rare and is precipitated by rotation of the head in the recumbent position.

The canalolithiasis hypothesis explains all of the manifestations of positioning vertigo and nystagmus ⁶. According to this hypothesis, the condition is due to the presence of agglomerates of many otoconia (small crystals of calcium carbonate in the saccule and utricle of the inner ear) that nearly fill the lumen of the semicircular canal and are freely mobile within it, instead of the small pieces of particulate matter that adhere firmly to the cupula (so-called cupulolithiasis).

Benign paroxysmal positioning vertigo is treated with positioning maneuvers: rapid repositioning of the head can move the otoconial agglomerate out of the semicircular canal so that it can no longer cause positioning vertigo ¹. The treatments of choice are the Semont ⁷ and Epley maneuvers. For the Semont maneuver, see Figure 5; the Epley maneuver involves rotation of the patient in the recumbent position with the head hanging down. Most patients can perform these maneuvers themselves after brief training. The two are equally effective, and the cure rate is more than 95% within a few days, as shown by multiple controlled studies and meta-analyses ⁸. The rate of recurrence of benign paroxysmal positioning vertigo is about 15% to 30% per year. The symptoms eventually recur at some time after effective treatment in about 50% of patients ⁹ but can then be treated effectively a second time in the same manner.

Vestibular neuritis

The clinical syndrome of vestibular neuritis is characterized by the following:

• Persistent rotational vertigo with a pathological inclination of the visual vertical axis toward the side of the affected labyrinth
• Spontaneous, horizontally rotating nystagmus toward the unaffected side, producing apparent movement of the environment (“oscillopsia”)
• Gait deviation and falling tendency toward the affected side
• Nausea and vomiting
• Unilateral dysfunction of the horizontal semicircular canal, as revealed by the Halmagyi-Curthoys head impulse test ¹⁰ for the function of the vestibulo-ocular reflex, as well as by caloric testing.

A viral and/or autoimmune as cause for vestibular neuritis is probable but has not yet been proven. Autopsy studies have revealed inflammatory degeneration of the vestibular nerve, the presence of viral DNA from herpes simplex virus type I, and the so-called “latency-associated transcript” (LAT) in vestibular ganglion cells ¹¹.

Menière’s disease

This condition is probably due to labyrinthine endolymphatic hydrops with periodic rupturing of the membrane that separates the endolymphatic and perilymphatic spaces. These ruptures precipitate the paroxysmal attacks that last a few minutes to hours ¹². The ultimate etiology is impaired resorption in the endolymphatic sac due to perisaccular fibrosis or to obliteration of the endolymphatic duct. Attacks are produced when rupture of the endolymphatic tube causing calcium-induced depolarization of the vestibulocochlear nerve. A classic Menière’s attack consists of rotatory vertigo, tinnitus, hearing impairment, and pressure sensation in one ear. The lifetime prevalence of this condition is approximately 0.5% ³. It usually begins on one side, and the frequency of attacks is highly variable. Menière’s disease becomes bilateral in 50% of cases ¹³ and is the second most common cause of bilateral vestibulopathy.

Vestibular Schwannoma

Vestibular schwannoma is the most common intracranial neoplasm producing vestibular symptoms, affecting one in every 100,000 people per year ¹⁴. These are usually slow-growing, benign tumors that originate from the Schwann cells lining the vestibular portion of cranial nerve VIII ¹⁵. Occasionally these tumors arise from the cochlear branch of the eighth nerve, but this is reported in less than 5% of cases ¹⁶. Patients may present with either unilateral or bilateral vestibular schwannoma. Bilateral vestibular schwannoma is associated with neurofibromatosis II, which is additionally characterized by glioma, meningioma, subcapsular ventricular opacities, and less frequently, peripheral neurofibromata and café au lait spots.

Patients may present with episodic or positional vertigo, disequilibrium, tinnitus, and usually asymmetric hearing loss. Early in the disease, when the tumor is small, patients complain of dizziness, hearing loss, and tinnitus, due to compression of the vestibulocochlear nerve. The slow growth often allows for central compensation, alleviating vertigo. With continued growth, the tumor can press against the facial or trigeminal nerve causing facial weakness and numbness, respectively. Eventually, the tumor grows to a size where it compresses the brainstem and cerebellum causing truncal ataxia, dysmetria, disequilibrium, and possibly death.

Diagnosis begins with a thorough history and physical examination. An audiogram is important in documenting hearing loss and any asymmetries which may exist. If you suspect vestibular schwannoma, then imaging is necessary. Computed tomography of the head with contrast is helpful, but magnetic resonance imaging with and without enhancement is the preferred imaging modality.

Once vestibular schwannoma is confirmed radiographically, a decision should be made on how to proceed with treatment. Treatment options include surgical excision, radiation therapy, and observation with serial magnetic resonance imaging. In making this decision, one should consider the size of the lesion, age and health of the patient, and what symptoms are present. These patients should be referred to a neuro-otologist for management of their care.

Central vestibular syndromes

Central vestibular syndromes are mainly caused by lesions of the vestibular pathways, which arise in the vestibular nuclei in the caudal portion of the brainstem and proceed to the cerebellum, thalamus, and vestibular cortex, or by damage to the vestibulocerebellum ¹. Pathological excitation is a rare cause, as occurs, for example, in the paroxysmal brainstem attacks with ataxia that can be produced by multiple sclerosis or vestibular epilepsy. The common causes of central vestibular vertigo include vestibular migraine and ischemic lesions in the brainstem ¹. Furthermore, central vestibular disturbances arise in the setting of certain ocular motor disorders such as downbeat and upbeat nystagmus, as attacks in episodic ataxia type 2, and in vestibular migraine. These individual disorders, and the treatment of each, will be discussed in the following sections.

Motion sickness

Motion sickness is attributed to an incongruence in the sensory input from the vestibular, visual, and somato-sensory systems ¹⁷. Motion sickness occurs while riding in a car, boat, or airplane if the vestibular and somato-sensory systems sense movement, but the visual system does not.

On the first sensation of motion sickness, efforts should be made to bring vestibular, visual, and somato-sensory input back in congruence. For example, a person on a boat who starts to feel seasick should immediately watch the horizon. Seasickness can be prevented by applying a scopolamine patch (Transderm-Scop) behind one ear at least four hours before boating ¹⁸.

Vertebrobasilar Ischemic Stroke

The blood supply to the brainstem, cerebellum, and inner ear is derived from the vertebrobasilar system ¹⁵. Occlusion of any of the major branches of this system may result in vertigo. Symptoms of vertebrobasilar ischemic stroke are highly variable and depend on which of the three major circumferential branches are occluded; the posterior inferior cerebellar artery, anterior inferior cerebellar artery, or superior cerebellar artery. Numerous processes may occlude the vertebrobasilar system. The most common are atherosclerosis, emboli, and vertebral artery dissection. Vertebral artery dissection can result from trauma or neck manipulation, or can occur spontaneously. Less common causes include subclavian steal syndrome, hypercoagulation disorders, and inflammatory conditions.

As mentioned earlier, the symptoms associated with ischemic stroke in this area are highly variable and greatly dependent upon which branch of the system is occluded. Occlusion of the posterior inferior cerebellar artery will cause a lateral medullary infarction and result in lateral medullary syndrome, also known as Wallenberg’s syndrome. Expected manifestations include vertigo, nystagmus, gait disturbance, ipsilateral limb ataxia and facial pain or numbness, contralateral body hemianesthesia, Horner’s syndrome, dysphagia, hoarseness, and rarely, facial nerve paralysis.

Lateral pontomedullary infarction secondary to occlusion of the anterior inferior cerebellar artery will result in lateral inferior pontine syndrome. This syndrome is characterized by symptoms similar to Wallenberg’s syndrome with notable differences. Involvement of cranial nerves VII and VIII results in ipsilateral facial paralysis and tinnitus and hearing loss, respectively. Dysphagia and hoarseness, however, are not apparent as cranial nerves IX and X nuclei are uninvolved with occlusion of the anterior inferior cerebellar artery.

Lateral superior pontine syndrome occurs when the superior cerebellar artery is occluded. With this syndrome, one can expect vertigo, nystagmus, gait disturbance, ipsilateral limb ataxia and facial pain or numbness, contralateral body hemianesthesia, and Horner’s syndrome. Distinguishing this syndrome is the finding of contralateral impairment of vibration and temperature due to medial lemniscus involvement.

A high index of suspicion must be kept with any patient presenting with spontaneous vertigo to avoid missing the diagnosis of ischemic stroke. It is essential to consider stroke in any acutely vertiginous patient with concomitant neurological signs and symptoms. Once vertebrobasilar ischemic stroke is suspected, an expeditious work-up is necessary. This should include a thorough physical examination, imaging, and neurology consultation for both evaluation and treatment.

Vertebrobasilar Insufficiency

Vertebrobasilar insufficiency is synonymous with a transient ischemic attack (TIA) of the vertebrobasilar system. By definition, patients experience symptoms similar to those detailed above, but the symptoms resolve within 24 hours. If left untreated, the disease process will eventually progress to stroke with permanent or long-lasting seqeulae. Risk factors and causes are identical to those for VIS. Forty-eight percent of patients who suffer a vertebrobasilar ischemic stroke report a transient ischemic attack in the preceding days or weeks ¹⁹. In fact, 29% of patients suffer from at least one episode of vertigo, a symptom of vertebrobasilar insufficiency, prior to their vertebrobasilar insufficiency ²⁰. Patients suffering a vertebrobasilar transient ischemic attack are likely to progress to stroke more quickly than those experiencing transient ischemic attacks in the anterior territory.

Vertebrobasilar insufficiency is a common cause of vertigo in the elderly. Symptoms may last from minutes to hours, but typically average 8 minutes in duration. In as many as one third of patients, vertigo is the only manifestation of their disease. Although this disease should always be in the differential, several months of recurrent vertigo unaccompanied by other neurological signs suggests another disorder. The likelihood of immediate stroke is less in patients presenting with only episodic vertigo. Patients who also present with paresis, blindness, or altered consciousness, however, should be evaluated urgently for fear of impending stroke. Evaluation is similar to that of an ischemic stroke. Treatment includes antiplatelets, anticoagulation, possible thrombolysis and percutaneous transluminal angioplasty, and neurological consultation.

The sudden onset of vertigo in a patient with additional neurologic symptoms (e.g., diplopia, dysarthria, dysphagia, ataxia, weakness) suggests the presence of vascular ischemia.

Treatment of transient ischemic attack and stroke includes preventing future events through blood pressure control, cholesterol-level lowering, smoking cessation, inhibition of platelet function (e.g., aspirin, clopidogrel [Plavix], aspirin-dipyridamole [Aggrenox]) and, possibly, anticoagulation (warfarin [Coumadin]).

Acute vertigo caused by a cerebellar or brainstem stroke is treated with vestibular suppressant medication and minimal head movement for the first day. As soon as tolerated, medication should be tapered, and vestibular rehabilitation exercises should be initiated ²¹, ²².

Placement of vertebrobasilar stents may be considered in a patient with symptomatic critical vertebral artery stenosis that is refractory to medical management ²³. Rarely, infarction or hemorrhage in the cerebellum or brainstem may present with acute vertigo as the only neurologic symptom ²⁴. Given the risk of brainstem compression with a large cerebellar stroke, neurosurgical decompression may be indicated.

Downbeat and upbeat nystagmus

Two types of vertically beating central nystagmus are of special importance: downbeat nystagmus and upbeat nystagmus, each named after the direction of the rapid, beating phase. Downbeat nystagmus is the most common type of acquired, persistent nystagmus ²⁵. Both types manifest themselves above all with swaying nystagmus and unsteadiness of gait and only secondarily with oscillopsia, i.e., apparent movement of the environment due to oscillation of the retinal image. In distinction to spontaneous nystagmus such as in vestibular neurits, downbeat nystagmus and upbeat nystagmus are types of fixation nystagmus, i.e., their intensity increases with visual fixation. Both downbeat nystagmus and upbeat nystagmus always indicate the presence of a central disturbance and possess special localizing significance. Downbeat nystagmus is usually due to bilateral dysfunction of the flocculus ²⁶; its three common causes are cerebellar atrophy, ischemia, and Arnold-Chiari malformation ²⁵. Upbeat nystagmus – which, unlike downbeat nystagmus, generally persists for no more than a few weeks – can be caused by paramedian medullary or pontomesenchephalic lesions, e.g., brainstem infarct or hemorrhage.

A randomized, placebo-controlled study of downbeat nystagmus has shown that the potassium-channel blockers 3,4-diaminopyridine ²⁷ and 4-aminopyridine can significantly improve this type of nystagmus ²⁸. The dosage is 5 to 10 mg tid; follow-up ECG is necessary. The effectiveness of this treatment has since been confirmed by multiple studies. 4-Aminopyridine seems to be effective against upbeat nystagmus as well, but this has been documented to date only in a single case study ²⁹.

Episodic ataxia type 2

The familial episodic ataxias are rare genetic diseases of autosomal dominant transmission. There are at least two well-defined varieties. Type 2 (EA 2) is characterized by recurrent attacks of dizziness and ataxia that are precipitated by physical activity, stress, or alcohol and usually last for hours. In between attacks, more than 90% of patients have marked central ocular motor disturbances, often downbeat nystagmus. EA 2 is caused by mutations in the CACNA1A gene (PQ calcium channel gene). Most patients can be treated successfully with acetazolamide. If this treatment is ineffective, or if adverse effects such as kidney stones develop, patients with EA 2 can also be treated with 4-aminopyridine (5 mg tid) ³⁰.

Aminopyridines are thus an effective treatment for downbeat nystagmus, upbeat nystagmus, and episodic ataxias type 2 which is well tolerated at the low dose that is generally used. These studies have also led to the development of a new principle of treatment; activation of cerebellar Purkinje cells through potassium-channel blockade enhances the cerebellar inhibitory influence on the vestibular and cerebellar nuclei.

Vestibular migraine or migraine with vestibular aura

Vestibular migraine is characterized by recurrent attacks that last minutes to hours and usually consist of rotatory vertigo ³¹, ³². It is the most common cause of spontaneously occurring attacks of vertigo (Table 1). Its lifetime prevalence is 0.98% ³. In more than 60% of patients, these attacks are associated with headache and/or photophobia or phonophobia; the remaining patients have attacks of vertigo alone. Most patients also have migraine attacks with or without an aura; this fact makes the condition easier to diagnose. In some patients, the diagnosis can be made only on the basis of a positive response to the treatment of the individual attacks with medication and to pharmacological prophylaxis. The prophylactic treatment of vestibular migraine is analogous to that of migraine with aura and consists of the administration of beta-blockers, valproic acid, and topiramate. No randomized, controlled studies on the efficacy of medications for vestibular migraine have yet been published.

Phobic postural vertigo

Phobic postural vertigo is the second most common diagnosis in a specialized neurological ambulatory clinic for dizziness and vertigo. This disorder is not found in the diagnostic repertoire of most neurologists and ENT specialists. Patients with phobic postural vertigo usually complain of swaying vertigo, lightheadedness, and gait unsteadiness that are continually present but fluctuate in severity. These symptoms are often accompanied by anxiety and are situationally dependent. The precipitating factor may be the presence of a large crowd, or waiting in the check-out line at a store; often, avoidance behavior results ². The symptoms typically improve when the patient participates in sports or has had a small amount of alcohol to drink. The affected patients often have an obsessive-compulsive personality, in the sense of “accentuated” personality traits, with a marked tendency toward introspection and a need to “have everything under control.” The central problem in phobic postural vertigo is the patient’s attempt to establish conscious control over body equilibrium, which leads to a “spiral of self-observation.” When this happens, the body’s own movements may be perceived as movements of the outside world. The main features of this disorder and its treatment are summarized in the box. The clinical neurological examination and ancillary tests reveal no relevant pathological findings.

Clinical features

• The patient has postural vertigo with unsteadiness of stance and gait; the neurological examination and ancillary tests are generally unremarkable
• Fluctuating unsteadiness of stance and gait with attacks of fear of falling, but without an actual fall
• Anxiety and autonomic disturbances sometimes occur during or just after the attacks
• The attacks are precipitated or exacerbated by typical situations, e.g., crowds, empty spaces, driving
• The symptoms often improve during sporting activity or after the consumption of a small amount of alcohol
• Increasingly severe avoidance behavior is common

The patient’s personality is usually of an obsessive-compulsive or reactive-depressive type. At the onset of the disorder, there is often a vestibular disturbance (25%) or a situation giving rise to particular stress (70%).

Treatment

• A thorough diagnostic assessment to allay the patient’s fear of having a serious organic disease
• Psycho-educative therapy to inform the patient about the pathological mechanism and the precipitating factors and situations
• Desensitization by self-exposure, i.e., the deliberate seeking out of situations that precipitate vertigo. Light sporting activities are also helpful.
• If the symptoms persist, pharmacotherapy, e.g., with selective serotonin reuptake inhibitors, and/or cognitive behavioral therapy are indicated

Treatment markedly improves symptoms in about 70% of patients ³³.

Vertigo diagnosis

If you have dizziness or vertigo that comes and goes but you do not have any of the above problems, make an appointment with your doctor. He or she will perform a physical exam and ask about your symptoms and medical history. Your doctor or nurse will probably check the following:

• Your eyes – You might be asked to follow an object with your eyes, or focus on something while moving your head from side to side.
• Your balance and gait – This involves watching you walk, to see if you lean or tilt to one side, as well as checking your balance while you stand still.
• Your hearing – Your doctor or nurse will check your hearing in both ears.

Depending on what they find during your examination, your doctor might do additional tests as well. In some cases, he or she will order an imaging test, such as an MRI, to look at what is going on in your brain.

Vertigo treatment

Most cases of vertigo get better without treatment. Treatment will depend on the cause. Your doctor might prescribe antibiotics if it’s caused by an infection.

You could also be given special exercises to do to try and correct your balance. Antihistamines can sometimes help with vertigo symptoms.

Vertigo medication

If you have spells of vertigo that are severe or last for hours or days, your doctor or nurse may recommend a medication to relieve severe vertigo symptoms, like vomiting. Treatment with medication is not usually recommended if your vertigo lasts only second or minutes.

Possible medication treatments include:

• An antihistamine, such as the prescription medicine meclizine (Antivert®), or non-prescription medicines like dimenhydrinate (Dramamine®), or diphenhydramine (Benadryl®).
• Prescription anti-nausea medicines, such as promethazine (Phenergan®), metoclopramide (Reglan®), or ondansetron (Zofran®).
• Prescription sedative medicines, such as diazepam (Valium®), lorazepam (Ativan®), or clonazepam (Klonopin®)

Most of these medicines make you sleepy, and you should not take them before you work or drive. You should only take prescription medicines to treat severe vertigo symptoms, and you should stop the medicine when your symptoms improve. Continuing to take these medications can impair long-term recovery.

Treatment for vertigo

Canalith repositioning — Canalith repositioning is a treatment that may be recommended for people with benign paroxysmal positional vertigo (BPPV). The treatment will be done by a doctor, nurse, or therapist in the office by moving your head into certain positions, sometimes called the Epley maneuver.

These movements encourage the calcium collection to move into a part of the ear where it will be reabsorbed. You may begin to feel better immediately after this treatment or within a day or two. If the treatment is successful, you may be given instructions on how to perform similar movements at home, if the symptoms return.

Balance rehabilitation — Most patients with vertigo prefer to keep their head still. However, staying still and not moving your head can make it harder to cope with vertigo and in the long-term can delay recovery. Rehabilitation can help people recover from vertigo that is caused by injury to the vestibular system.

Balance rehabilitation works by helping your brain adjust its response to changes in the vestibular system. The therapy can also help train your eyes and other senses to “learn” how to adapt. This therapy is most helpful when it is started as soon as possible after you develop vertigo.

During rehabilitation, you will work with a therapist who will teach to you perform exercises at home. For example, you might start by focusing on an object with a blank background and move your head slowly to the right and left and up and down. You would perform this exercise for several minutes two to three times per day.

If you have trouble standing or walking because of vertigo, you are at risk for falling. In older adults, falls can lead to serious complications, such as a broken hip. Talk to your doctor, nurse, or therapist about your concerns. To reduce the risk of falls, get rid of hazards in your home, such as loose electrical cords and slippery rugs, and avoid walking in unfamiliar areas that are not lighted.

Treatment for vestibular neuritis

The treatment is symptomatic, causal, and physiotherapeutic:

• Symptomatic treatment: antivertiginous medications, such as 100 to 300 mg of dimenhydrinate, should be given only in the first three days and only if necessary to treat severe nausea and vomiting, because they delay the development of central compensation mechanisms.

• “Causal” treatment: a four-armed, placebo-controlled trial was performed, based on the assumption that vestibular neuritis is caused by the reactivation of a latent herpes simplex virus type 1 infection. The trial revealed that monotherapy with a glucocorticoid-methylprednisolone at an initial dose of 100 mg daily, reduced in 20-mg steps every four days, significantly improved the recovery of peripheral vestibular function. The administration of valacyclovir alone had no effect, nor did its administration in combination with the glucocorticoid have any additional effect ³⁴.

• Physical therapy: a further principle of treatment is the promotion of central compensation by physical therapy. Equilibrium training significantly lessens the time required for vestibulospinal compensation and postural regulation to develop ³⁵. Voluntary eye movements and fixation are exercised in order to improve impaired visual fixation; furthermore, active head movements are exercised to realign the vestibular reflex, as well as balance tasks and goal-directed movements.

Treatment for Meniere’s disease

Its treatment is based on two principles:

• Treatment of individual attacks: vertigo and nausea can be improved with antivertiginous medications just as in the treatment of other types of acute labyrinthine dysfunction. For example, 100 mg dimenhydrate suppositories can be used.

• Attack prophylaxis: this type of treatment is aimed at improving the underlying endolymphatic hydrops. Despite the high prevalence of Menière’s disease and the large number of clinical studies that have been performed, there is still no treatment of this type that has been conclusively shown to be effective. The spectrum of recommendations ranges from a sodium-free diet to diuretics, transtympanic gentamicin instillation (20 to 40 mg given repeatedly, at intervals of several weeks, until symptoms improve), betahistine, and surgical procedures ¹². A beneficial effect on the frequency of attacks has been reported for transtympanic gentamicin ⁸ and for the prolonged high-dose administration of betahistine hydrochloride (48 mg tid for 12 months). The latter dose of betahistine hydrochloride is currently recommended on the basis of a recently reported observational treatment study in 112 patients who were treated for at least 12 months at doses of 16, 24, or 48 mg tid ³⁶. The highest dose led to a statistically significantly greater reduction of attack frequency and was well tolerated.

Vertigo exercises

Epley Maneuver to treat BPPV Vertigo

Deep Head Hanging Maneuver to treat BPPV Vertigo

Lempert (BBQ) Maneuver to treat BPPV Vertigo

Half Somersault Maneuver to treat BPPV Vertigo

Figure 5. The treatment of benign paroxysmal positioning vertigo with the Semont maneuver

Footnote: The illustration shows the treatment of benign paroxysmal positioning vertigo (BPPV) due to canalolithiasis of the right posterior semicircular canal.

a) In the initial, sitting position, the head is turned 45° to the side of the unaffected (“healthy”) ear.

b) The patient is laid on the right side, i.e., on the side of the affected ear, while the head is kept in 45° of rotation to the other side. This induces movement of the particulate matter in the posterior semicircular canal by gravity, leading to rotatory nystagmus toward the lower ear that extinguishes after a brief interval. The patient should maintain this position for about one minute.

c) While the head is still kept in 45° of rotation toward the side of the healthy ear, the patient is rapidly swung over to the side of the unaffected ear, so that the nose now points downward. The particulate matter in the semicircular canal now moves toward the exit from the canal. This position, too, should be maintained for at least one minute.

d) The patient returns slowly to the initial, sitting position. The particulate matter settles in the utricular space, where it can no longer induce rotatory vertigo. This sequence (a-d) should be performed three times in a row three times per day, in the morning, at noon, and at night. Most patients are free of symptoms after doing this for three days.

[Source ¹]

1. Strupp M, Brandt T. Diagnosis and Treatment of Vertigo and Dizziness. Deutsches Ärzteblatt International. 2008;105(10):173-180. doi:10.3238/arztebl.2008.0173. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696792/[↩][↩][↩][↩][↩][↩][↩][↩][↩]
2. Brandt T, Dieterich M, Strupp M. Vertigo – Leitsymptom Schwindel. Darmstadt: Steinkopff; 2003.[↩][↩]
3. Epidemiology of vertigo. Neuhauser HK. Curr Opin Neurol. 2007 Feb; 20(1):40-6. https://www.ncbi.nlm.nih.gov/pubmed/17215687/[↩][↩][↩]
4. Kerber KA. Vertigo and Dizziness in the Emergency Department. Emergency medicine clinics of North America. 2009;27(1):39-viii. doi:10.1016/j.emc.2008.09.002. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2676794/[↩]
5. What inner ear diseases cause benign paroxysmal positional vertigo ? Karlberg M, Hall K, Quickert N, Hinson J, Halmagyi GM. Acta Otolaryngol. 2000 Mar; 120(3):380-5. https://www.ncbi.nlm.nih.gov/pubmed/10894413/[↩]
6. Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis ? Brandt T, Steddin S. J Vestib Res. 1993 Winter; 3(4):373-82. https://www.ncbi.nlm.nih.gov/pubmed/8275271/[↩]
7. Curing the BPPV with a liberatory maneuver. Semont A, Freyss G, Vitte E. Adv Otorhinolaryngol. 1988; 42():290-3. https://www.ncbi.nlm.nih.gov/pubmed/3213745/[↩]
8. Strupp M, Cnyrim C, Brandt T. Vertigo and dizziness: Treatment of benign paroxysmal positioning vertigo, vestibular neuritis and Menère’s disease. In: Candelise L, editor. Evidence-based Neurology – management of neurological disorders. Oxford: Blackwell Publishing; 2007. pp. 59–69.[↩][↩]
9. Benign paroxysmal positioning vertigo: a long-term follow-up (6-17 years) of 125 patients. Brandt T, Huppert D, Hecht J, Karch C, Strupp M. Acta Otolaryngol. 2006 Feb; 126(2):160-3. https://www.ncbi.nlm.nih.gov/pubmed/16428193/[↩]
10. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol. 1988;45:737–739. https://www.ncbi.nlm.nih.gov/pubmed/3390028[↩]
11. Prevalence of HSV-1 LAT in human trigeminal, geniculate, and vestibular ganglia and its implication for cranial nerve syndromes. Theil D, Arbusow V, Derfuss T, Strupp M, Pfeiffer M, Mascolo A, Brandt T. Brain Pathol. 2001 Oct; 11(4):408-13. https://www.ncbi.nlm.nih.gov/pubmed/11556685/[↩]
12. Ménière’s disease. Minor LB, Schessel DA, Carey JP. Curr Opin Neurol. 2004 Feb; 17(1):9-16. https://www.ncbi.nlm.nih.gov/pubmed/15090872/[↩][↩]
13. Ménière’s disease: a long-term follow-up study of bilateral hearing levels. Takumida M, Kakigi A, Takeda T, Anniko M. Acta Otolaryngol. 2006 Sep; 126(9):921-5. https://www.ncbi.nlm.nih.gov/pubmed/16864488/[↩]
14. Epidemiology of acoustic neuromas. Tos M, Thomsen J. J Laryngol Otol. 1984 Jul; 98(7):685-92. https://www.ncbi.nlm.nih.gov/pubmed/6747450/[↩]
15. Thompson TL, Amedee R. Vertigo: A Review of Common Peripheral and Central Vestibular Disorders. The Ochsner Journal. 2009;9(1):20-26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096243/[↩][↩]
16. Khrais T., Romano G., Sanna M. Nerve origin of vestibular schwannoma: a prospective study. J Laryngol Otol. 2008;122:128–131. https://www.ncbi.nlm.nih.gov/pubmed/18039415[↩]
17. Fife TD. Episodic vertigo. In: Rakel RE, ed. Conn’s Current therapy, 1999: latest approved methods of treatment for the practicing physician. 51st ed. Philadelphia: Saunders, 1999:923–30.[↩]
18. Flake ZA, Scalley RD, Bailey AG. Practical selection of antiemetics. Am Fam Physician. 2004;69:1169–74.[↩]
19. Kim H. Y., Chung C. S., Moon S. Y., et al. Complete nonvisualization of basilar artery on MR angiography in patients with vertebrobasilar ischemic stroke: favorable outcome factors. Cerebrovasc Dis. 2004;18:269–276. https://www.ncbi.nlm.nih.gov/pubmed/15331872[↩]
20. Grad A., Baloh R. W. Vertigo of vascular origin. Clinical and electronystagmographic features in 84 cases. Arch Neurol. 1989;46:281–284. https://www.ncbi.nlm.nih.gov/pubmed/2919982[↩]
21. Quigley EM, Hasler WL, Parkman HP. AGA technical review on nausea and vomiting. Gastroenterology. 2001;120:263–86.[↩]
22. Baloh RW. Vertigo in older people. Curr Treat Options Neurol. 2000;2:81–9.[↩]
23. Levy EI, Hanel RA, Bendok BR, Boulos AS, Hartney ML, Guterman LR, et al. Staged stent-assisted angioplasty for symptomatic intracranial vertebrobasilar artery stenosis. J Neurosurg. 2002;97:1294–301.[↩]
24. Norrving B, Magnusson M, Holtas S. Isolated acute vertigo in the elderly; vestibular or vascular disease?. Acta Neurol Scand. 1995;91:43–8.[↩]
25. Downbeat nystagmus: aetiology and comorbidity in 117 patients. Wagner JN, Glaser M, Brandt T, Strupp M. J Neurol Neurosurg Psychiatry. 2008 Jun; 79(6):672-7. https://www.ncbi.nlm.nih.gov/pubmed/17872983/[↩][↩]
26. Detection of floccular hypometabolism in downbeat nystagmus by fMRI. Kalla R, Deutschlander A, Hufner K, Stephan T, Jahn K, Glasauer S, Brandt T, Strupp M. Neurology. 2006 Jan 24; 66(2):281-3. https://www.ncbi.nlm.nih.gov/pubmed/16434677/[↩]
27. Treatment of downbeat nystagmus with 3,4-diaminopyridine: a placebo-controlled study. Strupp M, Schüler O, Krafczyk S, Jahn K, Schautzer F, Büttner U, Brandt T. Neurology. 2003 Jul 22; 61(2):165-70. https://www.ncbi.nlm.nih.gov/pubmed/12874393/[↩]
28. 4-aminopyridine restores vertical and horizontal neural integrator function in downbeat nystagmus. Kalla R, Glasauer S, Büttner U, Brandt T, Strupp M. Brain. 2007 Sep; 130(Pt 9):2441-51. https://www.ncbi.nlm.nih.gov/pubmed/17664175/[↩]
29. 4-aminopyridine restores visual ocular motor function in upbeat nystagmus. Glasauer S, Kalla R, Büttner U, Strupp M, Brandt T. J Neurol Neurosurg Psychiatry. 2005 Mar; 76(3):451-3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1739571/pdf/v076p00451.pdf[↩]
30. Treatment of episodic ataxia type 2 with the potassium channel blocker 4-aminopyridine. Strupp M, Kalla R, Dichgans M, Freilinger T, Glasauer S, Brandt T. Neurology. 2004 May 11; 62(9):1623-5. https://www.ncbi.nlm.nih.gov/pubmed/15136697/[↩]
31. The interrelations of migraine, vertigo, and migrainous vertigo. Neuhauser H, Leopold M, von Brevern M, Arnold G, Lempert T. Neurology. 2001 Feb 27; 56(4):436-41. https://www.ncbi.nlm.nih.gov/pubmed/11222783/[↩]
32. Episodic vertigo related to migraine (90 cases): vestibular migraine ? Dieterich M, Brandt T. J Neurol. 1999 Oct; 246(10):883-92. https://www.ncbi.nlm.nih.gov/pubmed/10552234/[↩]
33. Phobic postural vertigo–a long-term follow-up (5 to 15 years) of 106 patients. Huppert D, Strupp M, Rettinger N, Hecht J, Brandt T. J Neurol. 2005 May; 252(5):564-9. https://www.ncbi.nlm.nih.gov/pubmed/15742115/[↩]
34. Strupp M, Zingler VC, Arbusow V, et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med. 2004;351:354–361. http://www.nejm.org/doi/full/10.1056/NEJMoa033280[↩]
35. Strupp M, Arbusow V, Maag KP, Gall C, Brandt T. Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis. Neurology. 1998;51:838–844. https://www.ncbi.nlm.nih.gov/pubmed/9748036[↩]
36. Strupp M, Huppert D, Frenzel C, Wagner J, Zingler VC, Mansmann U, Brandt T. Long-term prophylactic treatment of attacks of vertigo in Menière’s disease-comparison of a high with a low dosage of betahistine in an open trial. Acta Otolaryngol. 2008 May;128(5):520-4. doi: 10.1080/00016480701724912. https://www.ncbi.nlm.nih.gov/pubmed/18421605[↩]