Dizziness is an imprecise term patients often use to describe various related sensations, including
Faintness (a feeling of impending syncope)
Light-headedness
Feeling of imbalance or unsteadiness
A vague spaced-out or swimmy-headed feeling
A spinning sensation
Vertigo is a sensation of movement of the self or the environment when there is no actual movement. Usually the perceived movement is rotary—a spinning or wheeling sensation—but some patients simply feel pulled to one side. Vertigo is not a diagnosis—it is a description of a sensation.
Both sensations may be accompanied by nausea and vomiting or difficulty with balance, gait, or both.
Perhaps because these sensations are hard to describe in words, patients often use “dizziness,” “vertigo,” and other terms interchangeably and inconsistently. Different patients with the same underlying disorder may describe their symptoms very differently. A patient may even give different descriptions of the same “dizzy” event during a given visit depending on how the question is asked. Because of this discrepancy, even though vertigo seems to be a clearly delineated subset of dizziness, many clinicians prefer to consider the two symptoms together.
However they are described, dizziness and vertigo may be disturbing and even incapacitating, particularly when accompanied by nausea and vomiting. Symptoms cause particular problems for people doing an exacting or dangerous task, such as driving, flying, or operating heavy machinery.
Dizziness accounts for about 5 to 6% of physician visits. It may occur at any age but becomes more common with increasing age; it affects about 40% of people over age 40 at some time. Dizziness may be temporary or chronic. Chronic dizziness, defined as lasting > 1 month, is more common among older people.
Pathophysiology of Dizziness and Vertigo
The vestibular system is the main neurologic system involved in balance. This system includes
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The vestibular apparatus of the inner ear
The 8th (vestibulocochlear) cranial nerve, which conducts signals from the vestibular apparatus to the central components of the system
The vestibular nuclei in the brain stem and cerebellum
Disorders of the inner ear and 8th cranial nerve are considered peripheral disorders. Those of the vestibular nuclei and their pathways in the brain stem and cerebellum are considered central disorders.
The sense of balance also incorporates visual input from the eyes and proprioceptive input from the peripheral nerves (via the spinal cord). The cerebral cortex receives output from the lower centers and integrates the information to produce the perception of motion.
Vestibular apparatus
Perception of stability, motion, and orientation to gravity originates in the vestibular apparatus, which consists of
The 3 semicircular canals
The 2 otolith organs—the saccule and utricle
Rotary motion causes flow of endolymph in the semicircular canal oriented in the plane of motion. Depending on the direction of flow, endolymph movement either stimulates or inhibits neuronal output from hair cells lining the canal. Similar hair cells in the saccule and utricle are embedded in a matrix of calcium carbonate crystals (otoliths). Deflection of the otoliths by gravity stimulates or inhibits neuronal output from the attached hair cells.
Etiology of Dizziness and Vertigo
There are numerous structural (trauma, tumors, degenerative), vascular, infectious, toxic (including drug-related), and idiopathic causes (see table Some Causes of Dizziness and Vertigo), but only a small percentage of cases are caused by a serious disorder.
The most common causes of dizziness with vertigo involve some component of the peripheral vestibular system:
Other causes include a central vestibular disorder (most commonly migraine), a disorder with a more global effect on cerebral function, a psychiatric disorder, or a disorder affecting visual or proprioceptive input. Sometimes, no cause can be found.
The most common causes of dizziness without vertigo are less clear cut, but they are usually not otologic and probably are
Drug effects
Multifactorial or idiopathic
Nonneurologic disorders with a more global effect on cerebral function sometimes manifest as dizziness and rarely as vertigo. These disorders typically involve inadequate substrate (eg, oxygen, glucose) delivery caused by hypotension, hypoxemia, anemia, or hypoglycemia; when severe, some of these disorders may manifest as syncope. Additionally, certain hormonal changes (eg, as with thyroid disease, menstruation, pregnancy) can cause dizziness. Numerous central nervous system-active drugs can cause dizziness independent of any toxic effect on the vestibular system.
Occasionally, dizziness and vertigo may be psychogenic. Patients with panic disorder, hyperventilation syndrome, anxiety, or depression may present with complaints of dizziness.
Persistent perceptual postural dizziness (PPPD), sometimes described as chronic internal swaying that goes away when lying flat and lasting for over 3 months with no clinical explanation for its persistence, is classified as a chronic functional disorder. It can be precipitated by other acute conditions, such as benign paroxysmal positional vertigo (BPPV) or vestibular migraine, or can be a manifestation of an anxiety disorder.
Uncompensated peripheral vestibular weakness causes dysequilibrium rather than vertigo and often visual blurring with head turning. It can be the result of vestibular neuronitis, migraine with vertigo, Meniere disease, head trauma or inner ear surgery.
In older patients, dizziness is often multifactorial secondary to drug adverse effects and age-diminished visual, vestibular, and proprioceptive abilities. Two of the most common specific causes are disorders of the inner ear: benign paroxysmal positional vertigo and Meniere disease.
Some Causes of Dizziness and Vertigo
Cause | Suggestive Findings | Diagnostic Approach |
|---|---|---|
Peripheral vestibular system disordersa,b | ||
Severe, brief (< 1 minute) spinning triggered by moving head in a specific direction Nystagmus that has a latency of 0 to 30 seconds, is fatigable, and is torsional, beating toward the undermost ear Frenzel lenses needed to prevent visual fixation Hearing and neurologic examination intact | Dix-Hallpike maneuver to assess characteristic positional nystagmus | |
Recurrent episodes of unilateral tinnitus, hearing loss, ear fullness | Audiometry Gadolinium-enhanced MRI to rule out other causes | |
Vestibular neuronitis (viral cause suspected) | Sudden, incapacitating, severe vertigo with no hearing loss or other findings Lasts up to 1 week, with gradual lessening of symptoms Positional vertigo may result | Sometimes clinical examination alone Sometimes gadolinium-enhanced MRI Positional vertigo in neuronitis can be differentiated from BPPV by a Dix-Hallpike maneuver |
Labyrinthitis (viral or bacterial) | Hearing loss, tinnitus | Audiometry Temporal bone CT if purulent infection suspected Gadolinium-enhanced MRI if unilateral hearing loss and tinnitus |
Otitis media (acute or chronic, sometimes with cholesteatoma) | Ear pain, abnormal ear examination, including discharge if chronic otitis History of infection | Audiometry With cholesteatoma, CT optional to rule out semicircular canal fistula formation |
Trauma (eg, tympanic membrane rupture, labyrinthine contusion, perilymphatic fistula, temporal bone fracture, postconcussion) | Trauma obvious on history Other findings depending on location and extent of damage | Sometimes clinical examination alone Sometimes CT |
Vestibular schwannoma (acoustic neuroma) | Slowly progressive unilateral hearing loss, tinnitus, dizziness, dysequilibrium Rarely, facial numbness, weakness, or both | Audiometry Gadolinium-enhanced MRI if significant hearing asymmetry or unilateral tinnitus |
Treatment with aminoglycoside drugs recently instituted, usually with bilateral hearing loss and vestibular loss | Audiometry Sometimes vestibular evaluation with electronystagmography and rotary chair tests | |
Herpes zoster oticus (Ramsay Hunt syndrome) | Also affects geniculate ganglion, so facial weakness and taste loss often manifest along with hearing loss Vertigo possible but not typical Vesicles present on pinna and in ear canal | Clinical examination alone |
Chronic motion sickness (mal de debarquement) | Persistent symptoms after acute motion sickness | Clinical examination alone |
Central vestibular system disordersd | ||
Brain stem hemorrhage or infarction | Sudden onset Involvement of cochlear artery possibly causing ear symptoms | Immediate imaging (Gadolinium-enhanced MRI if available, otherwise CT) |
Cerebellar hemorrhage or infarction | Sudden onset, with ataxia and other cerebellar findings, often headache Deteriorates rapidly | Immediate imaging (Gadolinium-enhanced MRI if available, otherwise CT) |
Episodic, recurrent vertigo, usually without unilateral auditory symptoms (may have tinnitus that is usually bilateral) Possibly headache, but often personal or family history of migraine Photophobia, phonophobia, visual or other auras possible, helping make diagnosis | Usually clinical examination but with brain imaging as needed to rule out other causes Sometimes trial of migraine prophylaxis | |
Varied CNS motor and sensory deficits, with remissions and recurring exacerbations | Gadolinium-enhanced MRI of brain and spine | |
Vertebral artery dissection | Often head and neck pain | Magnetic resonance angiography |
Vertebrobasilar insufficiency | Intermittent brief episodes, sometimes with drop attacks, visual disturbance, confusion | Magnetic resonance angiography |
Global disturbance of CNS functione | ||
Pallor, weakness, sometimes heme-positive stool | Complete blood count | |
CNS-active drugsf (not ototoxic) | Drug recently instituted or dose increased; multiple drugs, particularly in an older patient Symptoms unrelated to movement or position | Sometimes clinical examination alone Sometimes drug levels (certain anticonvulsants) Sometimes trial of withdrawal |
Hypoglycemia (usually caused by drugs for diabetes) | Recent dose increase Sometimes sweating | Fingerstick glucose test (during symptoms if possible) |
Hypotension (caused by cardiac disorders, antihypertensives, blood loss, dehydration, or orthostatic hypotension syndromes including postural orthostatic tachycardia syndrome and other dysautonomias) | Symptoms on arising, sometimes with vagal stimulation (eg, urination) but not with head motion or while recumbent Manifestation possibly dominated by cause (eg, blood loss, diarrhea) | Orthostatic vital signs, sometimes with tilt table test, ECG |
Tachypnea Often history of lung disease | Pulse oximetry | |
Other causese | ||
Persistent perceptual postural dizziness (PPPD) | Chronic non-spinning dizziness (an internal sensation of swaying) persisting for > 3 months Can be precipitated by other acute conditions such as BPPV or vestibular migraine Can be a manifestation of anxiety disorder | Clinical examination alone |
Pregnancy | May be unrecognized | Pregnancy test |
Psychiatric (eg, panic attack, hyperventilation syndrome, anxiety, depression) | Symptoms chronic, brief, recurrent Unrelated to movement or position but may occur with stress or upset Neurologic and otologic examinations normal Initially, patient may be diagnosed with peripheral vestibular dysfunction and fail to respond to appropriate management | Clinical examination alone |
Chronic symptoms with bilateral hearing loss, fluctuating, with episodic vertigo | Audiometry Syphilis serology | |
Weight change Heat or cold intolerance | Thyroid function testing | |
Uncompensated peripheral vestibular weakness | Dysequilibrium Visual blurring (an internal sensation of swaying) with head turning Can follow episodes of vestibular neuronitis, migraine with vertigo, Meniere disease or after head trauma or inner ear surgery | Vestibular testing |
a Symptoms are typically paroxysmal, severe, and episodic rather than continuous. Ear symptoms (eg, tinnitus, fullness, hearing loss) usually indicate a peripheral disorder. Loss of consciousness is not associated with dizziness due to peripheral vestibular pathology. b Peripheral vestibular system disorders are listed in rough order of frequency of occurrence. cNumerous drugs, including aminoglycosides, chloroquine, furosemide, and quinine. Many other drugs are ototoxic but have more effect on the cochlea than the vestibular apparatus. d Ear symptoms are rarely present, but gait/balance disturbance is common. Nystagmus is not inhibited by visual fixation. e These causes should not cause otic symptoms (eg, hearing loss, tinnitus) or focal neurologic deficits (sometimes occurs with hypoglycemia). Vertiginous symptoms are rare but have been reported. f There are numerous drugs, including most antianxiety, anticonvulsant, antidepressant, antipsychotic, and sedative drugs. Drugs used to treat vertigo are also included. BPPV = benign paroxysmal positional vertigo; CNS = central nervous system; URI = upper respiratory infection. | ||
Evaluation of Dizziness and Vertigo
History
History of present illness should cover the sensations felt; an open-ended question is best (eg, “Different people use the word ‘dizziness’ differently. Can you please describe as thoroughly as you can what you feel?”). Brief, specific questioning as to whether the feeling is faintness, light-headedness, loss of balance, or vertiginous may bring some clarity, but persistent efforts to categorize a patient’s sensations are unnecessary. Other elements are more valuable and clear-cut:
Severity of initial episode
Severity and characteristics of subsequent episodes
Symptoms continuous or episodic
If episodic, frequency and duration
Triggers and relievers (ie, triggered by head/body position change)
Associated aural symptoms (eg, hearing loss, ear fullness, tinnitus)
Severity and related disability
Is the patient having a single, sudden, acute event, or has dizziness been chronic and recurrent? Was the first episode the most severe (vestibular crisis)? How long do episodes last, and what seems to trigger and worsen them? The patient should be asked specifically about movement of the head, arising, being in anxious or stressful situations, and menses. Important associated symptoms include headache, hearing loss, tinnitus, nausea and vomiting, impaired vision, focal weakness, and difficulty walking. The severity of impact on the patient’s life should be estimated: Has the patient fallen? Is the patient reluctant to drive or leave the house? Has the patient missed work days?
Review of systems should seek symptoms of causative disorders, including symptoms of upper respiratory infection (inner ear disorders); chest pain, palpitations, or both (heart disease); dyspnea (lung disease); dark stools (anemia caused by gastrointestinal blood loss); and weight change or heat or cold intolerance (thyroid disease).
Past medical history should note presence of recent head trauma (usually obvious by history), migraine, diabetes, heart or lung disease, and drug and alcohol abuse. In addition to identifying all current drugs, drug history should assess recent changes in drugs, doses, or both.
Physical examination
Examination begins with a review of vital signs, including presence of fever, rapid or irregular pulse, and supine and standing blood pressure, noting any drop in blood pressure on standing up (orthostatic hypotension) and whether standing provokes symptoms. If standing does provoke symptoms, postural symptoms should be distinguished from those triggered by head movement by returning the patient supine until symptoms dissipate and then rotating the head.
The otologic and neurologic examinations are fundamental. Specifically, with the patient supine, the eyes are checked for presence, direction, and duration of spontaneous nystagmus. Direction and duration of nystagmus and development of vertigo are noted.
A gross bedside hearing test is done, the ear canal is inspected for discharge and foreign body, and the tympanic membrane is checked for signs of infection or perforation.
Cerebellar function is tested by assessing gait and doing a finger-nose test and the Romberg test (see How to Assess Sensation). The Fukuda stepping test (marching in place with eyes closed, previously known as the Unterberger test) may be done by specialists to help detect a unilateral vestibular lesion. The remainder of the neurologic examination is done, including testing the rest of the cranial nerves. Use of the HINTS exam (Head Impulse, Nystagmus, Test of Skew exam) to differentiate central from peripheral causes of acute vestibular syndrome is under investigation.
Red flags
The following findings are of particular concern:
Head or neck pain
Ataxia
Loss of consciousness
Focal neurologic deficit
Severe, continuous symptoms for > 1 hour
Interpretation of findings
Traditionally, differential diagnosis has been based on the exact nature of the chief complaint (ie, distinguishing dizziness from light-headedness from vertigo). However, the inconsistency of patients’ descriptions and the poor specificity of symptoms make this unreliable. A better approach places more weight on the onset and timing of symptoms, the triggers, and associated symptoms and findings, particularly otologic and neurologic ones.
Some constellations of findings are highly suggestive (see table Some Causes of Dizziness and Vertigo), particularly those that help differentiate peripheral from central vestibular disorders.
Peripheral: Ear symptoms (eg, tinnitus, fullness, hearing loss) usually indicate a peripheral disorder. They are typically associated with vertigo and not generalized dizziness (unless caused by uncompensated peripheral vestibular weakness). Symptoms are usually paroxysmal, severe, and episodic; continuous dizziness is rarely due to peripheral vertigo. Loss of consciousness is not associated with dizziness due to peripheral vestibular pathology.
Central: Ear symptoms are rarely present, but gait/balance disturbance is common. Nystagmus is not inhibited by visual fixation.
Testing
Patients with a sudden, ongoing attack should have pulse oximetry and fingerstick glucose test. Women should have a pregnancy test. Most clinicians also do an ECG. Other tests are done based on findings (see table Some Causes of Dizziness and Vertigo), but generally gadolinium-enhanced MRI is indicated for patients with acute symptoms who have headache, neurologic abnormalities, or any other findings suggestive of a central nervous system etiology.
Patients with chronic symptoms of central vestibular pathology should have gadolinium-enhanced MRI to look for evidence of stroke, multiple sclerosis, or other central nervous system lesions.
Patients for whom results of bedside tests of hearing and vestibular function are abnormal or equivocal should undergo formal testing with audiometry and electronystagmography.
ECG, Holter monitoring for heart rhythm abnormalities, echocardiography, and exercise stress testing may be done to evaluate heart function.
Laboratory tests are rarely helpful, except for patients with chronic vertigo and bilateral hearing loss, for whom syphilis serology is indicated.
Treatment of Dizziness and Vertigo
Treatment of dizziness and vertigo is directed at the cause, including stopping, reducing, or switching any causative drugs.
If a vestibular disorder is present and thought to be secondary to active Meniere disease or vestibular neuronitis or labyrinthitis, the most effective vestibular nerve suppressants are oral antihistamine/anticholinergic drugs (eg, meclizine 25 to 50 mg 3 times a day) or diazepam (2 to 5 mg orally every 6 to 8 hours, with higher doses given under supervision for severe vertigo). All of these drugs can cause drowsiness, thereby limiting their use for certain patients. Nausea can be treated with prochlorperazine 10 mg IM four times a day or 25 mg rectally twice a day. Vertigo associated withbenign paroxysmal positional vertigo is treated with the Epley maneuver (otolith repositioning) done by an experienced practitioner. Meniere disease is best managed by an otolaryngologist with training in management of this chronic disorder, but initial management consists of a low-salt diet and a potassium-sparing diuretic.
Patients with persistent or recurrent vertigo secondary to unilateral vestibular weakness (such as secondary to vestibular neuronitis) usually benefit from vestibular rehabilitation therapy done by an experienced physical therapist. Most patients compensate well, although some, especially older patients, have more difficulty. Physical therapy can also provide important safety information for older patients or particularly disabled patients.
Geriatrics Essentials: Dizziness and Vertigo
As people age, organs involved in balance function less well. For example, seeing in dim light becomes more difficult, inner ear structures deteriorate, proprioception becomes less sensitive, and mechanisms that control blood pressure become less responsive (eg, to postural changes, postprandial demands). Older people also are more likely to have cardiac or cerebrovascular disorders that can contribute to dizziness. They also are more likely to be taking drugs that can cause dizziness, including those for hypertension, angina, heart failure, seizures, and anxiety, as well as certain antibiotics, antihistamines, and sleep aids. Thus, dizziness in older patients usually has more than one cause.
Although unpleasant at any age, the consequences of dizziness and vertigo are a particular problem for older patients. Patients with frailty are at significant risk of falling with consequent fractures; their fear of moving and falling often significantly decreases their ability to do daily activities.
In addition to treatment of specific causes, older patients with dizziness or vertigo may benefit from physical therapy and exercises to strengthen muscles and help maintain independent ambulation as long as possible.
Key Points
Vague or inconsistently described symptoms may still be associated with a serious condition.
Cerebrovascular disease and drug effects should be sought, particularly in older patients.
Peripheral vestibular system disorders should be differentiated from central vestibular system disorders.
Immediate neuroimaging should be done when symptoms are accompanied by headache, focal neurologic abnormalities, or both.
