Published: August 2010
Last Reviewed: May 2017
Dizziness can be described as a sensation or illusion of movement (such as spinning, rotating, tilting, or rocking), unsteadiness, or dysequilibrium. It is commonly accompanied by gait imbalance.
Dizziness is a symptom and not a diagnosis; it can be compared with pain in that respect. It is difficult to quantify because of its subjective nature. Dizziness is not exclusive to the vestibular system. Furthermore, it may be a component of a larger or more diffuse problem.
The nomenclature of dizziness can be divided according to the following list. This breakdown is arbitrary. These descriptions are not quantifiable, are not mutually exclusive, and can lead to further diagnostic dilemmas, yet this approach has persisted probably because of the complex nature of the symptom.
Symptoms may be episodic or constant. If they are episodic, they can last anywhere from seconds to minutes or hours to months at a time.
Dizziness is a common complaint in the medical environment. It is the third most common symptom presentation (combined with imbalance and falls) for outpatient medical consultation, behind chest pain and fatigue. In the adult population, 42% report dizziness at some time.1 Dizziness is common in all age groups; however, its frequency does increase with age. Dizziness and related vestibular symptoms are the main reasons for visiting a doctor after 75 years of age. Prevalence rates vary depending on the patient’s age and the cause of the dizziness.
Essentially any and every part of the vestibular system can malfunction, potentially providing symptoms of dizziness. Typically, when discussing vestibular symptomatology, the dichotomy of peripheral vestibular dysfunction versus central vestibular dysfunction is discussed. This method is used here for discussion purposes, although it can be misleading in practice because there is often an overlap between the two. Systemic etiologies, which might or might not act via central vestibular pathways, can also be a helpful way to discuss these issues.
Peripheral vestibular dysfunction refers to dysfunction of the vestibular end-organ (utricle, saccule, semicircular canals) and vestibular nerve.
Vestibular neuronitis (neuritis) can affect one or both vestibular end-organs and can involve them simultaneously or sequentially. The actual portion involved is believed to be the cell bodies of the hair cells that transduce movement within the end-organ and/or the vestibular nerve itself. The neuronitis can occur as a single attack or as multiple attacks. A quantifiable peripheral vestibular loss may be appreciated with caloric testing. The term neurolabyrinthitis may be used if there is an associated hearing loss.
Bilateral vestibular hypofunction (partial or complete loss) may be related to bilateral vestibular neuronitis or to toxic or immune mechanisms. Gentamicin and streptomycin are notorious for causing vestibular dysfunction (ototoxicity). In fact, this is exactly why they are used intratympanically to induce vestibular loss, particularly in the treatment of Menière’s disease.
Autoimmune ear disease is another cause of peripheral vestibular dysfunction. It is characterized by rapidly progressive, bilateral, sensorineural hearing loss within 3 months.2 In contrast, ototoxicity can manifest with sudden bilateral loss, whereas age-related and noise-induced hearing loss can develop over many months to years. The most common age at onset of symptoms is 20 to 50 years. Many older patients present with new symptoms when autoimmune ear disease might, in retrospect, have been present for many years. The disease can affect both sexes, but a female preponderance is noted when systemic immune diseases (e.g., rheumatoid arthritis, systemic lupus erythematosus) are present.
Central or systemic vestibular dysfunction includes the vestibular nuclei (superior, inferior, lateral, and medial) where they synapse with numerous pathways including the cerebellar, oculomotor, posterior column, proprioceptive, and vestibulospinal.
Menière’s disease is a disorder that is often incorrectly diagnosed. It includes the tetrad of vertigo (lasting at least 20 minutes), unilateral tinnitus, low-frequency hearing loss (initial stages with progression to all frequencies), and aural fullness. The symptoms are believed to be associated with a change in fluid pressure within the endolymphatic space. Menière’s disease usually starts between the ages of 20 and 60 years (average, 40 years), and women outnumber men by 1.3 to 1. In most patients, only one ear is involved; it is bilateral in about 15% to 20%.
The cause of this disease is not known, although viral injuries of the inner ear and other factors affecting the homeostasis of the inner ear have been proposed. Sodium management is believed to be at the core of the disorder. The vertigo is treatable through either medical or surgical management, although the tinnitus is often difficult to control. Various case series have reported spontaneous resolution rates of up to 30%.
The term endolymphatic hydrops is often used to describe Menière’s disease. This is actually a misnomer. This term is the pathologic description of the inner ear, which can be seen in Menière’s disease. It discusses the physical appearance of the endolymphatic space and the way it is dilated. Other disorders can also lead to endolymphatic hydrops.
Benign paroxysmal positional vertigo (BPPV) is a common cause of dizziness, particularly in people older than 65 years. Its incidence is estimated at 6000 per million population in those whose illness persists longer than 30 days, although this is probably a gross underestimate. It is easily identifiable with bedside evaluation (Dix-Hallpike testing). All three canals (anterior [superior], posterior, and lateral [horizontal]) may be the source of BPPV, although the posterior semicircular canal is by far the most common source.
Various theories exist regarding the pathogenesis and localization of BPPV. Calcium carbonate is embedded in a proteinaceous matrix on the surface of the utricle, with otoconia as the building block. Through head trauma, infectious or inflammatory processes, or idiopathic mechanisms, the otoconia can dislodge and move to various areas within the endolymphatic space. This pathologic movement of otoconia within the endolymphatic space induces the sensation of movement out of proportion to actual head movement.
Variants of BPPV have been described in the literature, although their existence is controversial. These include cupulolithiasis, in which otoconia are believed to be attached to the cupula; ampullolithiasis, or short-arm BPPV, in which otoconia are within the ampulla of the semicircular canal on the other side of the cupula; and utriculolithiasis, in which otoconia are freely moving within the utricle outside of any of the semicircular canals.
Perilymphatic fistulas represent a defect of the oval or round window that produces abnormal communication between the fluid surrounding the membranous labyrinth and middle ear space. Fistulas can be spontaneous (implosive or explosive) or acquired.
Implosive fistulas arise from increased pressure in the middle ear resulting from barotrauma; they include rapid airplane descent, external ear trauma, and scuba diving. In these cases, the membranes of the oval or round windows are driven inward to permit escape of perilymph into the middle ear space.
Explosive fistulas arise from increased intracranial pressure such as weight lifting, vigorous coughing, or straining, and it is believed that there is communication with the perilymphatic space by the internal auditory canal. In these cases, the membranes of the oval and round windows are driven outward. Treatment is similar for implosive and explosive fistulas. Acquired fistulas can result from stapes or chronic ear surgery.3
Drug-induced dizziness is common. Given that medication use is ubiquitous and the mechanisms are complex, it is no wonder that so many drugs are implicated in causing dizziness. Certain antiseizure medications (carbamazepine, phenytoin, primidone) and alcohol can cause acute reversible dysequilibrium and chronic irreversible dysequilibrium as a result of cerebellar dysfunction. Sedating drugs (barbiturates, benzodiazepines, and tricyclic antidepressants) can cause a nonspecific dizziness that is believed to be related to diffuse depression of the central nervous system. Antihypertensive medications and diuretics can induce lightheadedness and presyncope by induction of postural hypotension and reduced cerebral blood flow.
A number of drugs can produce a characteristic drug-intoxication syndrome with disorientation, memory and cognitive deficits, gaze-evoked nystagmus, and gait and extremity ataxia. This can be confused with more serious disorders. Alcohol is one example of these drugs; it can cause central nervous system depression and cerebellar toxicity, and it can change the specific gravity of the cupula (motion sensor within the ampulla of the semicircular canal). This change in the cupula explains the positional vertigo and positional nystagmus that are noted with alcohol ingestion.
Drug-induced dizziness or imbalance can be caused by ototoxic drugs such as aminoglycosides (gentamicin, streptomycin) and cisplatin. Vertigo can ensue if hair-cell loss is asymmetrical. If injury is bilateral and symmetrical, oscillopia (the optical illusion that stationary objects are moving back and forth or up and down) and dysequilibrium may be experienced.
Mal de debarquement (MDD) syndrome is a disorder characterized by a persistent sensation of motion after a prolonged period of passive movement.5 It is commonly experienced after water travel, air travel, or prolonged train rides, although other modes of travel can induce this syndrome, including space flight. The sensation of motion persistence after prolonged travel is physiologic and often short-lived; it is arbitrarily considered pathologic when it remains for at least 1 month. MDD is often incorrectly described as motion sickness; instead, motion, by self-motion or driving, actually often reduces symptoms in MDD. Diagnosis of MDD is essentially made by history: a preceding period of prolonged travel with onset of a similar sensation of motion afterward. Patients often indicate improvement with self-motion (rocking) or while driving. Treatment of MDD is predominantly medical. Vestibular suppressants with diazepam or clonazepam may be helpful in some patients. Spontaneous recovery can occur.
Motion sickness begins with epigastric discomfort and may be accompanied by increased salivation and a feeling of bodily warmth. As discomfort progresses, gastric emptying is inhibited. Symptoms progress to nausea, pallor, sweating, and eventually to vomiting. Some researchers have suggested that there is an additional syndrome of motion sickness that lacks the gastrointestinal complaints and is characterized by drowsiness, headache, apathy, depression, and generalized discomfort. Motion sickness is exacerbated by further activity and movement.
Cardiogenic dizziness results from ineffective cerebral or brainstem perfusion. Low cardiac output states include cardiac failure, cardiac tamponade, arrhythmia, and aortic stenosis.
Carotid occlusion rarely causes vertigo because the posterior circulation supplies the brainstem. Only when the posterior and anterior circulations are both severely compromised can carotid disease cause vertigo.
Cerebrovascular conditions such as posterior-circulation ischemia or stroke can cause dizziness because vestibular structures are involved. A number of small- and large-vessel syndromes can include dizziness. Small-vessel syndromes include the following:
Large-vessel syndromes include the following:
Neurocardiogenic dizziness can result from a relative change in the tone of the peripheral vasculature and the heart as the system responds to feedback from the brainstem. Disorders of reduced orthostatic tolerance include neurally mediated syncope, postural tachycardia syndrome,4 postexercise syndrome, and so on.
Acoustic neuroma (vestibular schwannoma) is a nonmalignant tumor of the eighth cranial nerve and is commonly from the inferior vestibular nerve. Hearing loss is the most common symptom and is often high-frequency and sensorineural in nature. Tinnitus is also very common and tends to be unilateral and on the same side as the tumor. Despite the name vestibular schwannoma, dizziness is not common and occurs in less than 20% of patients with this diagnosis. However, unsteadiness may be present in as many as 70% of these patients.
Cervicogenic dizziness is difficult to classify (see discussion later).
Metabolic dizziness can be caused by hypoglycemia and can lead to a spectrum of symptoms that include mild fatigue, tremulousness, diaphoresis, confusion, or lightheadedness, to more-extreme symptoms of lethargy, amnesia, and seizures. It is usually a complication of diabetes mellitus or its treatment, although it can also occur with fasting or after meals. Hypomagnesemia and thyroid dysfunction (hyperthyroid and hypothyroid) can also be culprits of dizziness. Numerous other metabolic conditions can cause similar symptoms.
Migraine-associated dizziness is discussed later.
Psychophysiologic dizziness is the consequence of the integration of various subsystems that pertain to the sense of balance (visual, vestibular, proprioceptive, autonomic), and is not always pathologic. One robust example of this is the sensation of movement that a person might experience when standing at the ledge of a tall building versus just standing on the ground. It is the visual input that fools the brain into thinking that it is moving (visual-vestibular conflict), and the brain must then rely more on ankle proprioception (joint position sense).
Anxiety disorders, panic disorders, and phobias can also interact with disorders of balance and dizziness. Dizziness with anxiety and panic disorders are not related exclusively to hyperventilation. These symptoms may be primary to a psychological or psychiatric disorder or may be exacerbated by a vestibular syndrome. Phobic postural vertigo or phobic dizziness is a morbid fear of falling unassociated with postural or gait instability. It is often associated with panic disorder and agoraphobia, although the patient might focus on the physical symptoms. Patients have a fear of falling while sitting or standing, and this can provoke unpleasant sensations of body acceleration and acceleration of the environment. Neurocardiac disorders, particularly orthostatic intolerance, can mimic or contribute to these disorders. Tachycardia, palpitations, shortness of breath, and presyncope are not limited to disorders of the cardiovascular system.
Vestibular epilepsy may be vague dizziness or true vertigo that may precede the seizure (aura) or actually be or accompany the seizure event.
On evaluation of the dizzy patient, the following issues should be considered:
On evaluation of the dizzy patient, the presence or absence of the following should be assessed:
The diagnosis of BPPV is made on clinical grounds in a patient with complaints of episodic positional vertigo. It can be confirmed by Dix-Hallpike position testing of the involved ear. This test can be performed at the bedside, by trained physical therapists, or in the vestibular laboratory. Diagnosis is aided by visualization of the eyes, with either Frenzel or infrared video goggles. Both allow diminished visual fixation, although the infrared video goggles allow observation of the eye without light stimulation and allow review of the eye movements at a later time.
The provocation of paroxysmal nystagmus, after a brief delay, in the head-hanging position helps to identify the posterior semicircular canal that is involved. From the patient’s frame of reference, stimulation of the right posterior semicircular canal produces a clockwise torsional and upbeat nystagmus, and the left posterior semicircular canal produces a counterclockwise torsional and upbeat nystagmus. On return to a sitting position, the initial nystagmus often reverses. If both responses are seen, the specificity for BPPV is quite high. Dizziness that is out of proportion to the observed nystagmus may also be observed. Caution is advised if the dizziness is reproduced with no observed nystagmus; a diagnosis other than active BPPV should then be considered.6
Lateral (horizontal) canal BPPV can also be diagnosed. Symptoms of positional vertigo tend to come with rolling over in bed and are often more intense and more nauseating than posterior-canal BPPV. For diagnosis, the patient can be placed in the supine position with the head up 30 degrees to allow the lateral canal to be placed in the vertical plane. The Lempert, or barbecue roll, procedure may be used to treat this, with the direction of the roll away from the ear that exacerbates symptoms. In other words, if symptoms are produced when the patient rolls to the side that is involved, rolling 360 degrees in the opposite direction might help to reposition the stray otoconiae.
The following criteria may be used in the diagnosis of Menière’s disease.7
*Criteria for diagnosing Menière’s disease from American Academy of Otolaryngology-Head and Neck Surgery.
Superior canal dehiscence was first described by Lloyd Minor in 1998.8 Dehiscence of the bone overlying the superior semicircular canal can result in a syndrome of vertigo and be induced by loud noises (Tullio’s phenomenon) or by maneuvers that change middle-ear or intracranial pressure. The symptoms are believed to occur because the dehiscence acts as a third mobile window into the inner ear. Diagnosis is made by high-resolution computed tomography (CT) of the temporal bone demonstrating the dehiscence or thinning of the bone overlying the superior semicircular canal. A low-frequency air-bone gap (at 500 Hz and 1 kHz) with or without a conductive hearing loss may be noted, despite normal middle-ear function. Vestibular-evoked myogenic potential testing may reveal abnormally reduced thresholds. Although both sides are not necessarily symptomatic at the same time, bilateral involvement is common.
The term migraine is synonymous with headache for many people. Its manifestation is not limited to headache, however, and it often occurs without it.
The criteria of Neuhauser and colleagues9 for migrainous vertigo are:
These criteria should be considered a starting point. Controversy surrounds the issues of migrainous vertigo. Simply the coexistence of dizziness and migraine symptoms does not guarantee that the two are fully related. In many instances, a peripheral vestibular syndrome may actually be exacerbating an underlying migraine disorder.
Cervicogenic dizziness is a disorder that the literature has alluded to for decades. Basic scientists have suggested for years that stimulation of afferents in the neck chemically, with electrical stimulation, or by ablation can induce a sensation of dizziness, although often not vertigo. The mechanics of the upper cervical spine (particularly C1-C2) and associated distortions of proprioception and kinesthetic function (sensation of relative movement as it pertains to joint function) are believed to be dysfunctional.11 This can occur with or without neck pain.
Symptoms tend to be vague and are often described as head fullness or heaviness or as lightheadedness. Symptoms may be worsened with computer use, reading, or sustained neck positions, and they are often worse with increased activity and later in the day. Cervicogenic dizziness can manifest in isolation or associated with headache (possibly cervicogenic headache), or it may actually be a factor in precipitating increased migraine activity or orthostatic intolerance. Undiagnosed cervicogenic dizziness can complicate vestibular rehabilitation, and an increase in dizziness with increased head movements is required for vestibular habituation.
Cervicogenic dizziness remains controversial because neck pain, bulging cervical disks, and whiplash remain ubiquitous. The lack of consensus on objective diagnostic criteria and the lack of a sensitive and specific test have only added to the controversy. Neck-vibration testing and vibration-induced nystagmus (nystagmus elicited from neck-vibration testing, which does not always parallel the presence or absence of symptoms) may be beneficial in identifying patients with cervicogenic dizziness.12 Neck-vibration testing is vibration of various head and neck muscle groups such as the suboccipital, masseter, and sternocleidomastoid, which might reproduce the dizziness; vibration-induced nystagmus is nystagmus elicited from neck-vibration testing, which does not always parallel the presence or absence of symptoms. Apparent risk factors for cervicogenic dizziness include head trauma, neck trauma (commonly whiplash), peripheral vestibular dysfunction, and focal paraspinal muscle weakness. Imaging of the cervical spine with plain films, CT, or magnetic resonance imaging [MRI]) is uninformative. The lack of neck pain does not rule out the possibility of cervicogenic dizziness.
No significant double-blinded studies have been undertaken regarding cervicogenic dizziness. Experience at the Cleveland Clinic Foundation (CCF) and case series in the literature13 suggest that advanced-level physiotherapy directed toward the upper cervical spine may be beneficial. Therapy modalities should target normalization of biomechanics, range of movement, tone, mitigation of pain or tenderness, strengthening, and resetting of proprioception. Clinical trials at CCF are under way to assess the potential benefit of botulinum toxin combined with neck physiotherapy in the treatment of cervicogenic dizziness. The hypothesis is that botulinum toxin may be beneficial in relieving spasmodic torticollis (neurally sustained spasm), allowing the physiotherapy to progress.
Rotational chair testing, video nystagmography (infrared video recording of eye movements) to analyze eye movement responses to various maneuvers including Dix-Hallpike test, and supine positional testing with the body supine and head up 30 degrees is helpful in identifying vestibular loss (unilateral and bilateral), active BPPV, otolith dysfunction, and central vestibular disorders (global and focal).
Comprehensive audiometry (behavioral thresholds, pure tone audiometry, acoustic reflexes, tympanometry) and additional testing include auditory brainstem responses, otoacoustic emissions, and electrocochleography. Audiologic testing is helpful in quantifying associated or known audiologic deficits or for surveying for possible auditory pathway involvement.
Recommended imaging includes head MRI (internal auditory canal protocol), cervical spine MRI, and temporal bone CT (high-resolution). Temporal bone CT is particularly important for superior canal dehiscence.
Tilt-table testing is used to assess blood pressure and heart rate function in response to change in position. Head-up tilt (70 degrees) for 10 to 45 minutes can diagnose forms of orthostatic intolerance, vasovagal responses, and postural tachycardia syndrome. Additional testing can assess intravascular volume, autonomic responses, and pulmonary circuit times.
Vestibular-evoked myogenic potentials test vestibular hypersensitivity, and possibly saccular function, by activating sternocleidomastoid muscle contraction. It is helpful in diagnosing Menière’s disease and superior canal dehiscence. This test is complementary to conventional vestibular testing.
Fistula testing consists of application of pressure waveforms (positive and negative constant pressure and sinusoidal pressure) to the external auditory canal to elicit nystagmus and vertigo in the absence of middle ear or mastoid disease (Hennebert’s sign).
Dynamic platform posturography assesses balance function under conditions in which sensory cues are modified. Conditions include eyes open or closed, visual surround stable or moving, and support surface stable or moving.
Specific therapies and associated outcomes depend on the diagnosis. A number of modalities are beneficial even when the specific diagnosis is not clear.
Vestibular suppressants are commonly used. These include antihistamines (e.g., meclizine), anticholinergics (e.g., scopolamine), and benzodiazepines (e.g., lorazepam, diazepam). These medications may be used on a short-term basis or as needed. When used chronically, their benefits can wane, however, and they are commonly used incorrectly. Furthermore, chronic use of these drugs can hamper vestibular adaptation. The side effects may also be deleterious, and they include fatigue, lethargy, and dry mouth.
Antinausea medications (e.g., prochlorperazine, promethazine) may also be prescribed.
Antianxiety medications (benzodiazepines such as alprazolam, diazepam, selective-serotonin reuptake inhibitors) may be provided to patients with associated anxiety.
Assistive devices such as canes and walkers can provide stability to those with balance or orthopedic issues. Canes seem to be carried at certain times, perhaps to provide a sense of security or proprioception (position cues). The use of these devices may be optimized in the hands of an experienced vestibular therapist.
Vestibular rehabilitation (balance therapy) is a discipline within physical therapy that evaluates sensory input (proprioceptive, vestibular, and visual) and how it is used to control static and dynamic balance. Goals are to decrease the risk of falls and increase activities of daily living and functioning at home, as well as managing symptoms, educating patients, and recommending and monitoring the use of assistive devices. In uncontrolled trials of vestibular rehabilitation, improvement in more than 80% of patients has been reported.
Neck physiotherapy is shown to be beneficial managing the vestibular patient (unpublished local experience). A common reason for failure of vestibular rehabilitation is previously unidentified derangements of upper cervical mechanics. Similarly, previously undiagnosed or undertreated migraine disorders have been noted to affect rehabilitation. Active trials of the use of botulinum toxin to manage cervical dysfunction are under way here at the CCF (off-label use).
When the involved canal and side have been identified by the Dix-Hallpike maneuver, particle repositioning maneuvers may be performed. Numerous treatments exist, the more common being the Epley canalith repositioning procedure, the Semont liberatory maneuver, and the Brandt-Daroff habituation exercises. The Epley maneuvers were developed by John Epley in the 1970s.15 Repositioning therapies should be directed to the semicircular canal involved. The goal of the repositioning maneuver is to return the stray otoconia to the utricular macula. The maneuvers may be performed repetitively. Canalith repositioning is more effective than observation alone, despite spontaneous resolution rates of one in three cases after 3 weeks of treatment.16 This is further supported by current AAN guidelines, which recommend canalith repositioning and the Semont maneuver in the treatment of BPPV; as both have been found to be safe and effective (or possibly effective in the case of the Semont maneuver).17
In Menière’s disease, medical management is targeted at sodium management. A combination of diuretic therapy and sodium restriction are the mainstays of management. Diuretics such as triamterene and hydrochlorothiazide are commonly used. Sodium restriction may be as simple as not salting foods, counting actual sodium, and adhering to a target sodium amount. Commonly, 1500 to 2000 mg of sodium per day may be recommended.
Symptomatic treatment with sublingual lorazepam (brand preparation only, because the carrier agent is different in the generic preparation and affects absorption) or diazepam may be used as needed to lessen the intensity and sometimes the duration of symptoms.
Numerous surgical approaches exist. The spectrum is wide, ranging from minimally invasive procedures such as endolymphatic sac decompression to vestibular nerve section to cochleosacculotomy to labyrinthectomy. The latter involves the complete removal of the vestibular and auditory apparatus, leaving the patient with deafness and without peripheral vestibular function.
Surgical treatment is often beneficial. It involves capping the superior aspect of the superior semicircular canal with a foreign material; bone fragments alone may be ineffective because of the constant movement and pressure changes transmitted from the middle ear and the middle cranial fossa. Surgery is performed via a middle fossa approach.
Once this diagnosis has been established, treatment is similar to that for migraine headache. Avoidance practices, reduction of systemic medical issues, and abortive and preventive strategies should be used. Certain foods and additives (e.g., aged cheese and meats, red wine, caffeine) as well as hunger, dehydration, and sleep deprivation should be avoided. Reduction of systemic medical issues includes identifying certain disorders such as obstructive sleep apnea, overuse of analgesics (because of increased risk of rebound headaches), and generalized and regional pain syndromes and spine disorders (cervical, thoracic, and lumbar dysfunction). Intravenous infusion treatments with various medications, including metoclopramide, magnesium sulfate, and valproic acid, may be beneficial in managing chronic pain cycles, status migrainosus, and overuse of analgesics.
Dizziness is a complex and often multicomponent symptom. Vestibular and nonvestibular etiologies should be considered, and often the two coexist.