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› Refer a patient who reports that his dizziness is accompanied by hearing loss to an otolaryngologist for evaluation. C
› Use the HINTS (Head Impulse, Nystagmus, and Test of Skew) procedure to differentiate central from peripheral vertigo. A
› Use the Dix-Hallpike procedure to diagnose benign paroxysmal positional vertigo. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
With an estimated lifetime prevalence of 17% to 30%,1 dizziness is a relatively common clinical symptom, but the underlying cause can be difficult to diagnose. That’s because patients’ descriptions of dizziness are often imprecise, and this symptom is associated with a wide range of conditions. A careful history and physical examination are key to diagnosis, as is an understanding of the mechanisms of dizziness.
This article covers the range of diagnoses that should be considered when a patient presents with dizziness, and provides insight regarding features of the patient’s history that can better elucidate the specific etiology.
What do patients mean when they say, “I feel dizzy”?
“Dizziness” is a vague term, and patients who report dizziness should be asked to further describe the sensation. Patients may use the word dizziness in an attempt to describe many sensations, including faintness, giddiness, light-headedness, or unsteadiness.2 In 1972, Drachman and Hart proposed a classification system for dizziness that describes 4 categories—presyncope, vertigo, disequilibrium, and atypical (TABLE 1).3 These classifications are still commonly used today, and the discussion that follows describes potential causes of dizziness in each of these 4 categories. A stepwise approach for evaluating a patient who reports dizziness can be found in the ALGORITHM.3-6
Syncopal-related dizziness can have a cardiovascular cause
Presyncope is a feeling of impending loss of consciousness that’s sometimes accompanied by generalized muscle weakness and/or partial vision loss. Taking a careful history regarding the events surrounding the episode should distinguish this type of dizziness, and doing so is essential because most of the underlying pathogenesis involves the cardiovascular system and requires specific interventions.
Dysrhythmias can cause syncope and may or may not be accompanied by a feeling of palpitations. Diagnosis is made by electrocardiogram (EKG) followed by the use of a Holter monitor.
Vasovagal syncope is caused by a sudden slowing of the pulse that’s the result of stimulation of the vagal nerve. It can occur from direct stimulation of the nerve from palpation (or strangulation), or from an intense autonomic discharge, as when people are frightened or confronted with something upsetting (eg, the sight of blood.)
Orthostatic hypotension results from a change in body position in which either autonomic mechanisms cannot maintain venous tone, causing a sudden drop in blood pressure, or in which the heart cannot compensate by speeding up, as when a patient is taking a beta-adrenergic antagonist or has first-degree heart block. It can also result from hypovolemia.
Measuring the patient’s blood pressure in the recumbent, seated, and standing positions can verify the diagnosis if an episode occurred soon before the examination. This kind of dizziness can be treated by instructing the patient to rise slowly, or by making appropriate medication adjustments. If conservative measures fail, medications such as midodrine or droxidopa can be tried.7
Hypoglycemia, hypoxia, or hyperventilation can also precipitate syncopal symptoms. Taking a careful history to assess for the presence of seizure-related features such as tonic/clonic movements or loss of bowel and bladder control can be helpful in distinguishing this form of dizziness.
Vertigo can have a central or peripheral cause
Vertigo is dizziness that is characterized by the sensation of spinning. The presence of vertigo implies disease of the inner ear or central nervous system. The “wiring diagram” of the vestibulo-ocular reflex is fairly straightforward, but sorting out the symptoms that arise from lesions within the system can be a diagnostic challenge. Vertigo has classically been divided into causes that are central (originating in the central nervous system) or peripheral (originating in the peripheral nervous system).
The HINTS (Head Impulse, Nystagmus, and Test of Skew) protocol is a group of 3 tests that can be used to differentiate central from peripheral vertigo (TABLE 2).8,9 To perform the head impulse test, the examiner asks the patient to focus his gaze on a target and then rapidly turns the patient’s head to the side, watching the eyes for any corrective movements.10 When the eyes make a corrective saccade, the test is considered to be positive for a peripheral lesion.
Horizontal nystagmus is assessed by having the patient look in the direction of the fast phase of the nystagmus. If the nystagmus increases in intensity, then the test is considered positive for a peripheral lesion.
Vertigo can have many possible causes
Finally, the “test of skew” is performed by again having the patient fixate on the examiner’s nose. Each eye is tested by being covered, and then uncovered. If the uncovered eye has to move to refocus on the examiner’s nose, then the test is positive for a central lesion. A positive head impulse, positive horizontal nystagmus, and negative test of skew is 100% sensitive and 96% specific for a peripheral lesion.11
Benign paroxysmal positional vertigo (BPPV) is vertigo that is triggered by movement of the head. It occurs when otoconia that are normally embedded in gel in the utricle become dislodged and migrate into the 3 fluid-filled semicircular canals, where they interfere with the normal fluid movement these canals use to sense head motion, causing the inner ear to send false signals to the brain.12
Diagnosis is confirmed by performing the Dix-Hallpike maneuver to elicit nystagmus. The patient is moved from a seated to a supine position with her head turned 45 degrees to the right and held for 30 seconds. For a demonstration of the Dix-Hallpike maneuver, see https://youtu.be/8RYB2QlO1N4. The Dix-Hallpike maneuver is also the first step of a treatment for BBPV known as the Epley maneuver. (See “The Epley maneuver: A procedure for treating BPPV”.13,14)
Benign paroxysmal positional vertigo (BPPV) can be treated with the Epley maneuver. Like the Dix-Hallpike maneuver, the Epley maneuver isolates the posterior semicircular canal of the affected ear. However, it goes a step further to reposition otolithic debris away from the ampulla of the posterior canal, rolling it through the canal and depositing it in the utricle, where it will not stimulate nerve endings and produce symptoms.
For a demonstration of the Epley maneuver, see https://youtu.be/jBzID5nVQjk. A computer-controlled form of the Epley maneuver has been developed and can be as effective as the manual version of this procedure.13
In 38% of patients, BPPV spontaneously resolves. The Epley maneuver can improve this rate to 64% with a single treatment, and one additional maneuver improves the success rate to 83.3%.14 If this procedure doesn’t work the first time, there may be more sediment that didn’t have enough time to settle during the procedure. Therefore, the Epley maneuver can be repeated 3 times a day, and performed on subsequent days as needed.
Labyrinthitis—inflammation of the inner ear that can cause vertigo—is suggested by an acute, non-recurrent episode of dizziness that is often preceded by an upper respiratory infection. If the external canal is extremely painful and/or develops a vesicular rash, the patient might have herpes zoster of the geniculate ganglion (Ramsay Hunt syndrome type 2).
Vertigo can have many possible causes
Vestibular migraine and Meniere’s disease. When a patient who has a history of migraines experiences symptoms of vertigo, vestibular migraine should be suspected, and treatment should focus on migraine therapy rather than vestibular therapy.15
Symptoms of Meniere’s disease and vestibular migraine can overlap.16 The current definition of Meniere’s disease requires ≥2 definitive episodes of vertigo with hearing loss plus tinnitus and/or aural symptoms.17 Thirty percent of vertigo episodes in patients with Meniere's disease can be attributed to BPPV.18
Acoustic neuroma. In addition to vertigo, acoustic neuroma is often associated with gradual hearing loss, tinnitus, and facial numbness (from compression of cranial nerve V preoperatively) or facial weakness (from compression of cranial nerve VII postoperatively). Unilateral hearing loss should prompt evaluation with magnetic resonance imaging.
“Acoustic neuroma” is a misnomer. The lesion arises from the vestibular (not the acoustic) portion of the 8th cranial nerve, and isn’t a neuroma; it is a schwannoma.19 Although it actually arises peripherally within the vestibular canal, it typically expands centrally and compresses other nerves centrally, which can make the clinical diagnosis more challenging if one were using the classical schema of differentiating between peripheral and central causes of vertigo.
Age-related vestibular loss occurs when the aging process causes deterioration of most of the components of the vestibulo-ocular reflex, resulting in dizziness and vertigo. Usually, the cerebral override mechanisms can compensate for the degeneration.
Other causes of vertigo include cerebellar infarction (3% of patients with vertigo),20 sound-induced vertigo (Tullio phenomenon),21 obstructive sleep apnea,22 and systemic sclerosis.23 Diabetes can cause a reduction in vestibular sensitivity that is evidenced by an increased reliance on visual stimuli to resolve vestibulo-visual conflict.24
Disequilibrium
Disequilibrium is predominantly a loss of balance. Patients with disequilibrium have the feeling that they are about to fall, specifically without the sensation of spinning. They may appear to sway, and will reach out for something to support them. Disequilibrium can be a component of vertigo, or it may suggest a more specific diagnosis, such as ataxia, which is a lack of coordination when walking.
Atypical causes of dizziness
“Light-headedness” may have an element of euphoria or may be indistinguishable from the early part of a syncopal episode. Because other causes of light-headedness can be difficult to distinguish from presyncope, it is important to consider syncope in the differential diagnosis.
The differential of light-headedness can also include panic attack, early hyperventilation, and toxin exposure (such as diphenylarsinic acid,25 pregabalin,26 or paint thinner27).
CORRESPONDENCE
Shannon Paul Starr, MD, Louisiana State University Health Sciences Center, 200 W. Esplanade #412, Kenner, LA 70065; [email protected].
1. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a systematic review. Otol Neurotol. 2015;36:387-392.
2. Stedman TL. Stedman’s medical dictionary, illustrated. 24th ed. Baltimore, Md: William & Wilkins; 1982:419.
3. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology. 1972;22:323-334.
4. Angtuaco EJ, Wippold FJ II, Cornelius RS, et al; Expert Panel on Neurologic Imaging. ACR appropriateness criteria: hearing loss and/or vertigo. 2013. American College of Radiology Web site. Available at: http://www.acr.org/~/media/914834f9cfa74e6c803e8e9c6909cd7e.pdf. Accessed September 3, 2015.
5. Dros J, Maarsingh OR, van der Windt DA, et al. Profiling dizziness in older primary care patients: an empirical study. PLoS One. 2011;6:e16481.
6. Post RE, Dickerson LM. Dizziness: a diagnostic approach. Am Fam Physician. 2010;82:361-369.
7. Biaggioni I. New developments in the management of neurogenic orthostatic hypotension. Curr Cardiol Rep. 2014;16:542.
8. Batuecas-Caletrío Á, Yáñez-González R, Sánchez-Blanco C, et al. [Peripheral vertigo versus central vertigo. Application of the HINTS protocol]. Rev Neurol. 2014;59:349-353.
9. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40:3504-3510.
10. Barraclough K, Bronstein A. Vertigo. BMJ. 2009;339:b3493.
11. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20:986-996.
12. Vestibular Disorders Association. Benign Paroxysmal Positional Vertigo. Vestibular Disorders Association Web site. Available at: http://vestibular.org/understanding-vestibular-disorders/types-vestibular-disorders/benign-paroxysmal-positional-vertigo. Accessed September 1, 2015.
13. Shan X, Peng X, Wang E. Efficacy of computer-controlled repositioning procedure for benign paroxysmal positional vertigo. Laryngoscope. 2015;125:715-719.
14. Lee JD, Shim DB, Park HJ, et al. A multicenter randomized double-blind study: comparison of the Epley, Semont, and sham maneuvers for the treatment of posterior canal benign paroxysmal positional vertigo. Audiol Neurootol. 2014;19:336-341.
15. Stolte B, Holle D, Naegel S, et al. Vestibular migraine. Cephalalgia. 2015;35:262-270.
16. Lopez-Escamez JA, Dlugaiczyk J, Jacobs J, et al. Accompanying symptoms overlap during attacks in Menière’s disease and vestibular migraine. Front Neurol. 2014;5:265.
17. Beasley NJ, Jones NS. Menière’s disease: evolution of a definition. J Laryngol Otol. 1996;110:1107-1113.
18. Taura A, Funabiki K, Ohgita H, et al. One-third of vertiginous episodes during the follow-up period are caused by benign paroxysmal positional vertigo in patients with Meniere’s disease. Acta Otolaryngol. 2014;134:1140-1145.
19. Pineda A, Feder BH. Acoustic neuroma: a misnomer. Is Surg. 1967;33:40-43.
20. Seemungal BM. Neuro-otological emergencies. Curr Opin Neurol. 2007;20:32-39.
21. Harrison RV. On the biological plausibility of Wind Turbine Syndrome. Int J Environ Health Res. 2015;25:463-468.
22. Kayabasi S, Iriz A, Cayonu M, et al. Vestibular functions were found to be impaired in patients with moderate-tosevere obstructive sleep apnea. Laryngoscope. 2015;125:1244-1248.
23. Rabelo MB, Corona AP. Auditory and vestibular dysfunctions in systemic sclerosis: literature review. Codas. 2014;26:337-342.
24. Razzak RA, Bagust J, Docherty S, et al. Augmented asymmetrical visual field dependence in asymptomatic diabetics: evidence of subclinical asymmetrical bilateral vestibular dysfunction. J Diabetes Complications. 2015;29:68-72.
25. Ogata T, Nakamura Y, Endo G, et al. [Subjective symptoms and miscarriage after drinking well water exposed to diphenylarsinic acid]. Nihon Koshu Eisei Zasshi. 2014;61:556-564.
26. Qu C, Xie Y, Qin F, et al. Neuropsychiatric symptoms accompanying thrombocytopenia following pregabalin treatment for neuralgia: a case report. Int J Clin Pharm. 2014;36:1138-1140.
27. Rahimi HR, Agin K, Shadnia S, et al. Clinical and biochemical analysis of acute paint thinner intoxication in adults: a retrospective descriptive study. Toxicol Mech Methods. 2015;25:42-47.
› Refer a patient who reports that his dizziness is accompanied by hearing loss to an otolaryngologist for evaluation. C
› Use the HINTS (Head Impulse, Nystagmus, and Test of Skew) procedure to differentiate central from peripheral vertigo. A
› Use the Dix-Hallpike procedure to diagnose benign paroxysmal positional vertigo. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
With an estimated lifetime prevalence of 17% to 30%,1 dizziness is a relatively common clinical symptom, but the underlying cause can be difficult to diagnose. That’s because patients’ descriptions of dizziness are often imprecise, and this symptom is associated with a wide range of conditions. A careful history and physical examination are key to diagnosis, as is an understanding of the mechanisms of dizziness.
This article covers the range of diagnoses that should be considered when a patient presents with dizziness, and provides insight regarding features of the patient’s history that can better elucidate the specific etiology.
What do patients mean when they say, “I feel dizzy”?
“Dizziness” is a vague term, and patients who report dizziness should be asked to further describe the sensation. Patients may use the word dizziness in an attempt to describe many sensations, including faintness, giddiness, light-headedness, or unsteadiness.2 In 1972, Drachman and Hart proposed a classification system for dizziness that describes 4 categories—presyncope, vertigo, disequilibrium, and atypical (TABLE 1).3 These classifications are still commonly used today, and the discussion that follows describes potential causes of dizziness in each of these 4 categories. A stepwise approach for evaluating a patient who reports dizziness can be found in the ALGORITHM.3-6
Syncopal-related dizziness can have a cardiovascular cause
Presyncope is a feeling of impending loss of consciousness that’s sometimes accompanied by generalized muscle weakness and/or partial vision loss. Taking a careful history regarding the events surrounding the episode should distinguish this type of dizziness, and doing so is essential because most of the underlying pathogenesis involves the cardiovascular system and requires specific interventions.
Dysrhythmias can cause syncope and may or may not be accompanied by a feeling of palpitations. Diagnosis is made by electrocardiogram (EKG) followed by the use of a Holter monitor.
Vasovagal syncope is caused by a sudden slowing of the pulse that’s the result of stimulation of the vagal nerve. It can occur from direct stimulation of the nerve from palpation (or strangulation), or from an intense autonomic discharge, as when people are frightened or confronted with something upsetting (eg, the sight of blood.)
Orthostatic hypotension results from a change in body position in which either autonomic mechanisms cannot maintain venous tone, causing a sudden drop in blood pressure, or in which the heart cannot compensate by speeding up, as when a patient is taking a beta-adrenergic antagonist or has first-degree heart block. It can also result from hypovolemia.
Measuring the patient’s blood pressure in the recumbent, seated, and standing positions can verify the diagnosis if an episode occurred soon before the examination. This kind of dizziness can be treated by instructing the patient to rise slowly, or by making appropriate medication adjustments. If conservative measures fail, medications such as midodrine or droxidopa can be tried.7
Hypoglycemia, hypoxia, or hyperventilation can also precipitate syncopal symptoms. Taking a careful history to assess for the presence of seizure-related features such as tonic/clonic movements or loss of bowel and bladder control can be helpful in distinguishing this form of dizziness.
Vertigo can have a central or peripheral cause
Vertigo is dizziness that is characterized by the sensation of spinning. The presence of vertigo implies disease of the inner ear or central nervous system. The “wiring diagram” of the vestibulo-ocular reflex is fairly straightforward, but sorting out the symptoms that arise from lesions within the system can be a diagnostic challenge. Vertigo has classically been divided into causes that are central (originating in the central nervous system) or peripheral (originating in the peripheral nervous system).
The HINTS (Head Impulse, Nystagmus, and Test of Skew) protocol is a group of 3 tests that can be used to differentiate central from peripheral vertigo (TABLE 2).8,9 To perform the head impulse test, the examiner asks the patient to focus his gaze on a target and then rapidly turns the patient’s head to the side, watching the eyes for any corrective movements.10 When the eyes make a corrective saccade, the test is considered to be positive for a peripheral lesion.
Horizontal nystagmus is assessed by having the patient look in the direction of the fast phase of the nystagmus. If the nystagmus increases in intensity, then the test is considered positive for a peripheral lesion.
Vertigo can have many possible causes
Finally, the “test of skew” is performed by again having the patient fixate on the examiner’s nose. Each eye is tested by being covered, and then uncovered. If the uncovered eye has to move to refocus on the examiner’s nose, then the test is positive for a central lesion. A positive head impulse, positive horizontal nystagmus, and negative test of skew is 100% sensitive and 96% specific for a peripheral lesion.11
Benign paroxysmal positional vertigo (BPPV) is vertigo that is triggered by movement of the head. It occurs when otoconia that are normally embedded in gel in the utricle become dislodged and migrate into the 3 fluid-filled semicircular canals, where they interfere with the normal fluid movement these canals use to sense head motion, causing the inner ear to send false signals to the brain.12
Diagnosis is confirmed by performing the Dix-Hallpike maneuver to elicit nystagmus. The patient is moved from a seated to a supine position with her head turned 45 degrees to the right and held for 30 seconds. For a demonstration of the Dix-Hallpike maneuver, see https://youtu.be/8RYB2QlO1N4. The Dix-Hallpike maneuver is also the first step of a treatment for BBPV known as the Epley maneuver. (See “The Epley maneuver: A procedure for treating BPPV”.13,14)
Benign paroxysmal positional vertigo (BPPV) can be treated with the Epley maneuver. Like the Dix-Hallpike maneuver, the Epley maneuver isolates the posterior semicircular canal of the affected ear. However, it goes a step further to reposition otolithic debris away from the ampulla of the posterior canal, rolling it through the canal and depositing it in the utricle, where it will not stimulate nerve endings and produce symptoms.
For a demonstration of the Epley maneuver, see https://youtu.be/jBzID5nVQjk. A computer-controlled form of the Epley maneuver has been developed and can be as effective as the manual version of this procedure.13
In 38% of patients, BPPV spontaneously resolves. The Epley maneuver can improve this rate to 64% with a single treatment, and one additional maneuver improves the success rate to 83.3%.14 If this procedure doesn’t work the first time, there may be more sediment that didn’t have enough time to settle during the procedure. Therefore, the Epley maneuver can be repeated 3 times a day, and performed on subsequent days as needed.
Labyrinthitis—inflammation of the inner ear that can cause vertigo—is suggested by an acute, non-recurrent episode of dizziness that is often preceded by an upper respiratory infection. If the external canal is extremely painful and/or develops a vesicular rash, the patient might have herpes zoster of the geniculate ganglion (Ramsay Hunt syndrome type 2).
Vertigo can have many possible causes
Vestibular migraine and Meniere’s disease. When a patient who has a history of migraines experiences symptoms of vertigo, vestibular migraine should be suspected, and treatment should focus on migraine therapy rather than vestibular therapy.15
Symptoms of Meniere’s disease and vestibular migraine can overlap.16 The current definition of Meniere’s disease requires ≥2 definitive episodes of vertigo with hearing loss plus tinnitus and/or aural symptoms.17 Thirty percent of vertigo episodes in patients with Meniere's disease can be attributed to BPPV.18
Acoustic neuroma. In addition to vertigo, acoustic neuroma is often associated with gradual hearing loss, tinnitus, and facial numbness (from compression of cranial nerve V preoperatively) or facial weakness (from compression of cranial nerve VII postoperatively). Unilateral hearing loss should prompt evaluation with magnetic resonance imaging.
“Acoustic neuroma” is a misnomer. The lesion arises from the vestibular (not the acoustic) portion of the 8th cranial nerve, and isn’t a neuroma; it is a schwannoma.19 Although it actually arises peripherally within the vestibular canal, it typically expands centrally and compresses other nerves centrally, which can make the clinical diagnosis more challenging if one were using the classical schema of differentiating between peripheral and central causes of vertigo.
Age-related vestibular loss occurs when the aging process causes deterioration of most of the components of the vestibulo-ocular reflex, resulting in dizziness and vertigo. Usually, the cerebral override mechanisms can compensate for the degeneration.
Other causes of vertigo include cerebellar infarction (3% of patients with vertigo),20 sound-induced vertigo (Tullio phenomenon),21 obstructive sleep apnea,22 and systemic sclerosis.23 Diabetes can cause a reduction in vestibular sensitivity that is evidenced by an increased reliance on visual stimuli to resolve vestibulo-visual conflict.24
Disequilibrium
Disequilibrium is predominantly a loss of balance. Patients with disequilibrium have the feeling that they are about to fall, specifically without the sensation of spinning. They may appear to sway, and will reach out for something to support them. Disequilibrium can be a component of vertigo, or it may suggest a more specific diagnosis, such as ataxia, which is a lack of coordination when walking.
Atypical causes of dizziness
“Light-headedness” may have an element of euphoria or may be indistinguishable from the early part of a syncopal episode. Because other causes of light-headedness can be difficult to distinguish from presyncope, it is important to consider syncope in the differential diagnosis.
The differential of light-headedness can also include panic attack, early hyperventilation, and toxin exposure (such as diphenylarsinic acid,25 pregabalin,26 or paint thinner27).
CORRESPONDENCE
Shannon Paul Starr, MD, Louisiana State University Health Sciences Center, 200 W. Esplanade #412, Kenner, LA 70065; [email protected].
› Refer a patient who reports that his dizziness is accompanied by hearing loss to an otolaryngologist for evaluation. C
› Use the HINTS (Head Impulse, Nystagmus, and Test of Skew) procedure to differentiate central from peripheral vertigo. A
› Use the Dix-Hallpike procedure to diagnose benign paroxysmal positional vertigo. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
With an estimated lifetime prevalence of 17% to 30%,1 dizziness is a relatively common clinical symptom, but the underlying cause can be difficult to diagnose. That’s because patients’ descriptions of dizziness are often imprecise, and this symptom is associated with a wide range of conditions. A careful history and physical examination are key to diagnosis, as is an understanding of the mechanisms of dizziness.
This article covers the range of diagnoses that should be considered when a patient presents with dizziness, and provides insight regarding features of the patient’s history that can better elucidate the specific etiology.
What do patients mean when they say, “I feel dizzy”?
“Dizziness” is a vague term, and patients who report dizziness should be asked to further describe the sensation. Patients may use the word dizziness in an attempt to describe many sensations, including faintness, giddiness, light-headedness, or unsteadiness.2 In 1972, Drachman and Hart proposed a classification system for dizziness that describes 4 categories—presyncope, vertigo, disequilibrium, and atypical (TABLE 1).3 These classifications are still commonly used today, and the discussion that follows describes potential causes of dizziness in each of these 4 categories. A stepwise approach for evaluating a patient who reports dizziness can be found in the ALGORITHM.3-6
Syncopal-related dizziness can have a cardiovascular cause
Presyncope is a feeling of impending loss of consciousness that’s sometimes accompanied by generalized muscle weakness and/or partial vision loss. Taking a careful history regarding the events surrounding the episode should distinguish this type of dizziness, and doing so is essential because most of the underlying pathogenesis involves the cardiovascular system and requires specific interventions.
Dysrhythmias can cause syncope and may or may not be accompanied by a feeling of palpitations. Diagnosis is made by electrocardiogram (EKG) followed by the use of a Holter monitor.
Vasovagal syncope is caused by a sudden slowing of the pulse that’s the result of stimulation of the vagal nerve. It can occur from direct stimulation of the nerve from palpation (or strangulation), or from an intense autonomic discharge, as when people are frightened or confronted with something upsetting (eg, the sight of blood.)
Orthostatic hypotension results from a change in body position in which either autonomic mechanisms cannot maintain venous tone, causing a sudden drop in blood pressure, or in which the heart cannot compensate by speeding up, as when a patient is taking a beta-adrenergic antagonist or has first-degree heart block. It can also result from hypovolemia.
Measuring the patient’s blood pressure in the recumbent, seated, and standing positions can verify the diagnosis if an episode occurred soon before the examination. This kind of dizziness can be treated by instructing the patient to rise slowly, or by making appropriate medication adjustments. If conservative measures fail, medications such as midodrine or droxidopa can be tried.7
Hypoglycemia, hypoxia, or hyperventilation can also precipitate syncopal symptoms. Taking a careful history to assess for the presence of seizure-related features such as tonic/clonic movements or loss of bowel and bladder control can be helpful in distinguishing this form of dizziness.
Vertigo can have a central or peripheral cause
Vertigo is dizziness that is characterized by the sensation of spinning. The presence of vertigo implies disease of the inner ear or central nervous system. The “wiring diagram” of the vestibulo-ocular reflex is fairly straightforward, but sorting out the symptoms that arise from lesions within the system can be a diagnostic challenge. Vertigo has classically been divided into causes that are central (originating in the central nervous system) or peripheral (originating in the peripheral nervous system).
The HINTS (Head Impulse, Nystagmus, and Test of Skew) protocol is a group of 3 tests that can be used to differentiate central from peripheral vertigo (TABLE 2).8,9 To perform the head impulse test, the examiner asks the patient to focus his gaze on a target and then rapidly turns the patient’s head to the side, watching the eyes for any corrective movements.10 When the eyes make a corrective saccade, the test is considered to be positive for a peripheral lesion.
Horizontal nystagmus is assessed by having the patient look in the direction of the fast phase of the nystagmus. If the nystagmus increases in intensity, then the test is considered positive for a peripheral lesion.
Vertigo can have many possible causes
Finally, the “test of skew” is performed by again having the patient fixate on the examiner’s nose. Each eye is tested by being covered, and then uncovered. If the uncovered eye has to move to refocus on the examiner’s nose, then the test is positive for a central lesion. A positive head impulse, positive horizontal nystagmus, and negative test of skew is 100% sensitive and 96% specific for a peripheral lesion.11
Benign paroxysmal positional vertigo (BPPV) is vertigo that is triggered by movement of the head. It occurs when otoconia that are normally embedded in gel in the utricle become dislodged and migrate into the 3 fluid-filled semicircular canals, where they interfere with the normal fluid movement these canals use to sense head motion, causing the inner ear to send false signals to the brain.12
Diagnosis is confirmed by performing the Dix-Hallpike maneuver to elicit nystagmus. The patient is moved from a seated to a supine position with her head turned 45 degrees to the right and held for 30 seconds. For a demonstration of the Dix-Hallpike maneuver, see https://youtu.be/8RYB2QlO1N4. The Dix-Hallpike maneuver is also the first step of a treatment for BBPV known as the Epley maneuver. (See “The Epley maneuver: A procedure for treating BPPV”.13,14)
Benign paroxysmal positional vertigo (BPPV) can be treated with the Epley maneuver. Like the Dix-Hallpike maneuver, the Epley maneuver isolates the posterior semicircular canal of the affected ear. However, it goes a step further to reposition otolithic debris away from the ampulla of the posterior canal, rolling it through the canal and depositing it in the utricle, where it will not stimulate nerve endings and produce symptoms.
For a demonstration of the Epley maneuver, see https://youtu.be/jBzID5nVQjk. A computer-controlled form of the Epley maneuver has been developed and can be as effective as the manual version of this procedure.13
In 38% of patients, BPPV spontaneously resolves. The Epley maneuver can improve this rate to 64% with a single treatment, and one additional maneuver improves the success rate to 83.3%.14 If this procedure doesn’t work the first time, there may be more sediment that didn’t have enough time to settle during the procedure. Therefore, the Epley maneuver can be repeated 3 times a day, and performed on subsequent days as needed.
Labyrinthitis—inflammation of the inner ear that can cause vertigo—is suggested by an acute, non-recurrent episode of dizziness that is often preceded by an upper respiratory infection. If the external canal is extremely painful and/or develops a vesicular rash, the patient might have herpes zoster of the geniculate ganglion (Ramsay Hunt syndrome type 2).
Vertigo can have many possible causes
Vestibular migraine and Meniere’s disease. When a patient who has a history of migraines experiences symptoms of vertigo, vestibular migraine should be suspected, and treatment should focus on migraine therapy rather than vestibular therapy.15
Symptoms of Meniere’s disease and vestibular migraine can overlap.16 The current definition of Meniere’s disease requires ≥2 definitive episodes of vertigo with hearing loss plus tinnitus and/or aural symptoms.17 Thirty percent of vertigo episodes in patients with Meniere's disease can be attributed to BPPV.18
Acoustic neuroma. In addition to vertigo, acoustic neuroma is often associated with gradual hearing loss, tinnitus, and facial numbness (from compression of cranial nerve V preoperatively) or facial weakness (from compression of cranial nerve VII postoperatively). Unilateral hearing loss should prompt evaluation with magnetic resonance imaging.
“Acoustic neuroma” is a misnomer. The lesion arises from the vestibular (not the acoustic) portion of the 8th cranial nerve, and isn’t a neuroma; it is a schwannoma.19 Although it actually arises peripherally within the vestibular canal, it typically expands centrally and compresses other nerves centrally, which can make the clinical diagnosis more challenging if one were using the classical schema of differentiating between peripheral and central causes of vertigo.
Age-related vestibular loss occurs when the aging process causes deterioration of most of the components of the vestibulo-ocular reflex, resulting in dizziness and vertigo. Usually, the cerebral override mechanisms can compensate for the degeneration.
Other causes of vertigo include cerebellar infarction (3% of patients with vertigo),20 sound-induced vertigo (Tullio phenomenon),21 obstructive sleep apnea,22 and systemic sclerosis.23 Diabetes can cause a reduction in vestibular sensitivity that is evidenced by an increased reliance on visual stimuli to resolve vestibulo-visual conflict.24
Disequilibrium
Disequilibrium is predominantly a loss of balance. Patients with disequilibrium have the feeling that they are about to fall, specifically without the sensation of spinning. They may appear to sway, and will reach out for something to support them. Disequilibrium can be a component of vertigo, or it may suggest a more specific diagnosis, such as ataxia, which is a lack of coordination when walking.
Atypical causes of dizziness
“Light-headedness” may have an element of euphoria or may be indistinguishable from the early part of a syncopal episode. Because other causes of light-headedness can be difficult to distinguish from presyncope, it is important to consider syncope in the differential diagnosis.
The differential of light-headedness can also include panic attack, early hyperventilation, and toxin exposure (such as diphenylarsinic acid,25 pregabalin,26 or paint thinner27).
CORRESPONDENCE
Shannon Paul Starr, MD, Louisiana State University Health Sciences Center, 200 W. Esplanade #412, Kenner, LA 70065; [email protected].
1. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a systematic review. Otol Neurotol. 2015;36:387-392.
2. Stedman TL. Stedman’s medical dictionary, illustrated. 24th ed. Baltimore, Md: William & Wilkins; 1982:419.
3. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology. 1972;22:323-334.
4. Angtuaco EJ, Wippold FJ II, Cornelius RS, et al; Expert Panel on Neurologic Imaging. ACR appropriateness criteria: hearing loss and/or vertigo. 2013. American College of Radiology Web site. Available at: http://www.acr.org/~/media/914834f9cfa74e6c803e8e9c6909cd7e.pdf. Accessed September 3, 2015.
5. Dros J, Maarsingh OR, van der Windt DA, et al. Profiling dizziness in older primary care patients: an empirical study. PLoS One. 2011;6:e16481.
6. Post RE, Dickerson LM. Dizziness: a diagnostic approach. Am Fam Physician. 2010;82:361-369.
7. Biaggioni I. New developments in the management of neurogenic orthostatic hypotension. Curr Cardiol Rep. 2014;16:542.
8. Batuecas-Caletrío Á, Yáñez-González R, Sánchez-Blanco C, et al. [Peripheral vertigo versus central vertigo. Application of the HINTS protocol]. Rev Neurol. 2014;59:349-353.
9. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40:3504-3510.
10. Barraclough K, Bronstein A. Vertigo. BMJ. 2009;339:b3493.
11. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20:986-996.
12. Vestibular Disorders Association. Benign Paroxysmal Positional Vertigo. Vestibular Disorders Association Web site. Available at: http://vestibular.org/understanding-vestibular-disorders/types-vestibular-disorders/benign-paroxysmal-positional-vertigo. Accessed September 1, 2015.
13. Shan X, Peng X, Wang E. Efficacy of computer-controlled repositioning procedure for benign paroxysmal positional vertigo. Laryngoscope. 2015;125:715-719.
14. Lee JD, Shim DB, Park HJ, et al. A multicenter randomized double-blind study: comparison of the Epley, Semont, and sham maneuvers for the treatment of posterior canal benign paroxysmal positional vertigo. Audiol Neurootol. 2014;19:336-341.
15. Stolte B, Holle D, Naegel S, et al. Vestibular migraine. Cephalalgia. 2015;35:262-270.
16. Lopez-Escamez JA, Dlugaiczyk J, Jacobs J, et al. Accompanying symptoms overlap during attacks in Menière’s disease and vestibular migraine. Front Neurol. 2014;5:265.
17. Beasley NJ, Jones NS. Menière’s disease: evolution of a definition. J Laryngol Otol. 1996;110:1107-1113.
18. Taura A, Funabiki K, Ohgita H, et al. One-third of vertiginous episodes during the follow-up period are caused by benign paroxysmal positional vertigo in patients with Meniere’s disease. Acta Otolaryngol. 2014;134:1140-1145.
19. Pineda A, Feder BH. Acoustic neuroma: a misnomer. Is Surg. 1967;33:40-43.
20. Seemungal BM. Neuro-otological emergencies. Curr Opin Neurol. 2007;20:32-39.
21. Harrison RV. On the biological plausibility of Wind Turbine Syndrome. Int J Environ Health Res. 2015;25:463-468.
22. Kayabasi S, Iriz A, Cayonu M, et al. Vestibular functions were found to be impaired in patients with moderate-tosevere obstructive sleep apnea. Laryngoscope. 2015;125:1244-1248.
23. Rabelo MB, Corona AP. Auditory and vestibular dysfunctions in systemic sclerosis: literature review. Codas. 2014;26:337-342.
24. Razzak RA, Bagust J, Docherty S, et al. Augmented asymmetrical visual field dependence in asymptomatic diabetics: evidence of subclinical asymmetrical bilateral vestibular dysfunction. J Diabetes Complications. 2015;29:68-72.
25. Ogata T, Nakamura Y, Endo G, et al. [Subjective symptoms and miscarriage after drinking well water exposed to diphenylarsinic acid]. Nihon Koshu Eisei Zasshi. 2014;61:556-564.
26. Qu C, Xie Y, Qin F, et al. Neuropsychiatric symptoms accompanying thrombocytopenia following pregabalin treatment for neuralgia: a case report. Int J Clin Pharm. 2014;36:1138-1140.
27. Rahimi HR, Agin K, Shadnia S, et al. Clinical and biochemical analysis of acute paint thinner intoxication in adults: a retrospective descriptive study. Toxicol Mech Methods. 2015;25:42-47.
1. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a systematic review. Otol Neurotol. 2015;36:387-392.
2. Stedman TL. Stedman’s medical dictionary, illustrated. 24th ed. Baltimore, Md: William & Wilkins; 1982:419.
3. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology. 1972;22:323-334.
4. Angtuaco EJ, Wippold FJ II, Cornelius RS, et al; Expert Panel on Neurologic Imaging. ACR appropriateness criteria: hearing loss and/or vertigo. 2013. American College of Radiology Web site. Available at: http://www.acr.org/~/media/914834f9cfa74e6c803e8e9c6909cd7e.pdf. Accessed September 3, 2015.
5. Dros J, Maarsingh OR, van der Windt DA, et al. Profiling dizziness in older primary care patients: an empirical study. PLoS One. 2011;6:e16481.
6. Post RE, Dickerson LM. Dizziness: a diagnostic approach. Am Fam Physician. 2010;82:361-369.
7. Biaggioni I. New developments in the management of neurogenic orthostatic hypotension. Curr Cardiol Rep. 2014;16:542.
8. Batuecas-Caletrío Á, Yáñez-González R, Sánchez-Blanco C, et al. [Peripheral vertigo versus central vertigo. Application of the HINTS protocol]. Rev Neurol. 2014;59:349-353.
9. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40:3504-3510.
10. Barraclough K, Bronstein A. Vertigo. BMJ. 2009;339:b3493.
11. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20:986-996.
12. Vestibular Disorders Association. Benign Paroxysmal Positional Vertigo. Vestibular Disorders Association Web site. Available at: http://vestibular.org/understanding-vestibular-disorders/types-vestibular-disorders/benign-paroxysmal-positional-vertigo. Accessed September 1, 2015.
13. Shan X, Peng X, Wang E. Efficacy of computer-controlled repositioning procedure for benign paroxysmal positional vertigo. Laryngoscope. 2015;125:715-719.
14. Lee JD, Shim DB, Park HJ, et al. A multicenter randomized double-blind study: comparison of the Epley, Semont, and sham maneuvers for the treatment of posterior canal benign paroxysmal positional vertigo. Audiol Neurootol. 2014;19:336-341.
15. Stolte B, Holle D, Naegel S, et al. Vestibular migraine. Cephalalgia. 2015;35:262-270.
16. Lopez-Escamez JA, Dlugaiczyk J, Jacobs J, et al. Accompanying symptoms overlap during attacks in Menière’s disease and vestibular migraine. Front Neurol. 2014;5:265.
17. Beasley NJ, Jones NS. Menière’s disease: evolution of a definition. J Laryngol Otol. 1996;110:1107-1113.
18. Taura A, Funabiki K, Ohgita H, et al. One-third of vertiginous episodes during the follow-up period are caused by benign paroxysmal positional vertigo in patients with Meniere’s disease. Acta Otolaryngol. 2014;134:1140-1145.
19. Pineda A, Feder BH. Acoustic neuroma: a misnomer. Is Surg. 1967;33:40-43.
20. Seemungal BM. Neuro-otological emergencies. Curr Opin Neurol. 2007;20:32-39.
21. Harrison RV. On the biological plausibility of Wind Turbine Syndrome. Int J Environ Health Res. 2015;25:463-468.
22. Kayabasi S, Iriz A, Cayonu M, et al. Vestibular functions were found to be impaired in patients with moderate-tosevere obstructive sleep apnea. Laryngoscope. 2015;125:1244-1248.
23. Rabelo MB, Corona AP. Auditory and vestibular dysfunctions in systemic sclerosis: literature review. Codas. 2014;26:337-342.
24. Razzak RA, Bagust J, Docherty S, et al. Augmented asymmetrical visual field dependence in asymptomatic diabetics: evidence of subclinical asymmetrical bilateral vestibular dysfunction. J Diabetes Complications. 2015;29:68-72.
25. Ogata T, Nakamura Y, Endo G, et al. [Subjective symptoms and miscarriage after drinking well water exposed to diphenylarsinic acid]. Nihon Koshu Eisei Zasshi. 2014;61:556-564.
26. Qu C, Xie Y, Qin F, et al. Neuropsychiatric symptoms accompanying thrombocytopenia following pregabalin treatment for neuralgia: a case report. Int J Clin Pharm. 2014;36:1138-1140.
27. Rahimi HR, Agin K, Shadnia S, et al. Clinical and biochemical analysis of acute paint thinner intoxication in adults: a retrospective descriptive study. Toxicol Mech Methods. 2015;25:42-47.
