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1. Define vertigo.
2. Describe the difference between vertigo and other sensations associated with dizziness.
3. Discuss the difference between peripheral and central vertigo.
4. Differentiate between the different etiologies of peripheral and central vertigo.
5. Discuss management of the patient with vertigo.
Lafe, a paramedic, and his EMT partner Steve are eating breakfast when their unit is dispatched to a residential address for a patient complaining of dizziness. Upon arrival, they are met at the front door by the patient's husband, who tells the crew that his wife “is not feeling well; she’s in the bathroom vomiting right now.” Lafe and Steve walk into the bedroom just as the patient, a 42-year-old female named Linda, crawls back into bed and lays back supine. She appears anxious and offers them a weak “hello.”
Lafe sits on a chair next to the bed and starts his exam while Steve takes Linda’s vital signs. Linda describes a two-day history of upper respiratory infection with some mild sputum production. She says, “I was feeling pretty good last night, but woke up today feeling dizzy and nauseous. When I got up to go to the bathroom, the dizziness was really bad and I felt like I was going to pass out.” She denies any chest discomfort or pain, back pain, abdominal pain or syncope. Lafe notes that her radial pulse is strong at about 80/min. Her skin is warm and slightly moist with good color and normal capillary refill. Linda’s breathing rate, tidal volume and effort appear normal. She tells Lafe she has a history of hypertension and non-insulin-dependent diabetes, for which she takes enalapril and glyburide, and has no allergies to medications. She also says both her father and mother died of heart attacks—her mother at 48 years old and her father at 54. “I’m not having a heart attack, am I?” Linda asks nervously as Steve places her on oxygen via nasal cannula at 2 lpm. Lafe starts running through the differential diagnosis for dizziness in his head, thinking, “AMI, hypertensive crisis, stroke, gastrointestinal bleed, hypoglycemia, hyperglycemia...”
There are few chief complaints that will elicit more sense of helplessness in the prehospital care provider than dizziness. Our diagnostic and clinical exam capabilities are limited in the prehospital environment, signs and symptoms are often vague and difficult for the patient to define, and the differential diagnosis is extensive. Behind this veil of uncertainty is the acknowledgement that dizziness can be the harbinger of many serious, potentially life-threatening conditions that initially appear benign; however, dizziness is a nonspecific term that is commonly confused with vertigo. The two are distinct clinical entities, but patients often use the terms synonymously. Arguably, most prehospital care providers are acutely aware of the potential causes of dizziness not caused by vertigo, as they are very often potentially life-threatening. We spend hours in training learning how to identify and manage patients with tachydysrhythmias, bradydysrhythmias, stroke and hypoglycemia, just a few possible etiologies of dizziness, but very little time is spent understanding vertigo.
It is estimated that 7.5 million patients with dizziness and possible vertigo are examined each year in ambulatory centers, making it one of the most common chief complaints in the emergency department. The lifetime prevalence of vertigo in adults ages 18 to 79 is 7.4%, with a clear increase in prevalence with age.1 One report indicated that dizziness and vertigo together accounted for 2.5% of all emergency department presentations during a 10-year period.2 While evaluation of a patient with a complaint of dizziness can present a challenge, understanding vertigo and its causes can help the prehospital care provider identify vertigo as the source of the patient’s complaint.
Dizziness is an imprecise complaint that can be used to describe vertigo, lightheadedness, near-syncope, and even syncope. It may also be used to describe gait instability, nausea, generalized weakness or anxiety. Vertigo (from the Latin verto, “to turn around”) is a specific type of dizziness in which the patient has the perception of movement when no movement exists. Terms such as spinning, whirling, falling or tilting may be used to describe the sensation, which is caused by a dysfunction of the vestibular system in the inner ear. The term “lightheaded” is often used to describe near-syncope, the feeling that one is about to faint or pass out. The patient may feel dizzy, but there is no feeling that they or their surroundings are moving. Syncope, the loss of consciousness, can be mistaken for dizziness if the patient is not aware that he did indeed lose consciousness. Patients will often recall the pre-syncopal period during which they were dizzy, but not their syncope. Disequilibrium refers to a perception of imbalance, unsteadiness, or a feeling of “floating” while walking. Even if a patient describes his symptoms as vertigo, it is important to ask questions in an effort to clarify his complaint, as many patients are not familiar with the exact meaning of medical terms and may have difficulty describing the sensations they are experiencing.
Causes of Dizziness and Vertigo
It is important for the prehospital care provider to be familiar with the possible etiologies of dizziness, which can range from relatively benign (vertigo) to life-threatening (cardiovascular) in origin. A recent study looked at whether ED patients with dizziness were diagnosed as having vertigo versus some other cause of their symptoms. It found that in most cases dizziness was not attributed to vertigo, but was often associated with cardiovascular or other potentially life-threatening medical causes that were classified as neurologic, cerebrovascular, metabolic, injuries and poisonings, psychiatric, digestive, genitourinary and infectious.3 As such, it is useful for the prehospital care provider to be familiar with the various etiologies of dizziness, especially the signs and symptoms suggestive of those that are life-threatening. Obtaining a thorough patient history and performing a clinical exam will not only allow ruling out more serious diagnoses, but will provide the best opportunity to identify vertigo as the cause. Once vertigo is strongly suspected, a systematic approach can differentiate the various types of vertigo from one another.
In humans (as well as most mammals), the vestibular system contributes to balance and our sense of spatial orientation and is housed within the bony labyrinth of the skull, making up the inner ear. The bony labyrinth can be subdivided into three parts: vestibule, semicircular canals and cochlea. The vestibule contains two structures, the saccule and the utricle, which help provide sensations of linear acceleration and gravity via the delicate relationship of calcium carbonate crystals (otoliths) attached to and pushing down on sensory hairs that can determine the head's position. When the head is in the normal, upright position, the otoliths push straight down on the sensory hairs via gravity. When the head is tilted to one side, the hairs are pushed down at an angle, bending the sensory hairs and telling the brain the head is not level. The vestibule and semicircular canals, which are continuous with one another and filled with endolymph liquid, together are termed the vestibular complex. Rotation of the head causes the endolymph to flow within the semicircular canals, stimulating receptors within the canals and leading to the sensation of movement. The cochlea contains receptors that provide the sense of hearing.
Information from the inner ear is carried to balance centers in the central nervous system (brain) by the vestibulocochlear nerve (cranial nerve eight). Vertigo can be classified as either peripheral (“otologic” or “vestibular”) or central, depending on which part of the vestibular system is triggering the patient’s symptoms. Peripheral vertigo is caused by disorders affecting the semicircular canals, otoliths and vestibulocochlear nerve, whereas central vertigo is caused by disorders affecting central nervous system structures, such as the brain stem and cerebellum. Common causes of peripheral and central vertigo are listed in Table 1.
Causes of Peripheral Vertigo
Causes of peripheral vertigo include benign paroxysmal positional vertigo (BPPV), Ménière's disease, labyrinthitis, ototoxicity and superior canal dehiscence syndrome. Hallmarks of peripheral vertigo are its sudden onset and provocation by changes in head position; most causes of central vertigo arise with a gradual onset.
Benign paroxysmal positional vertigo (BPPV)
BPPV is the most common cause of vertigo that occurs when otoliths are displaced from the utricle and saccule in the vestibule of the inner ear and migrate into the semicircular canals. When the head is moved, gravity displaces the otoliths floating within the semicircular canals, resulting in inappropriate flow of endolymph and a sensation of movement. The patient experiences vertigo with head movements such as tilting, looking upward or downward, or any other sudden head motion, as when lying down or rolling over in bed. BPPV can occur at any age, but the average onset is during the mid-50s. Women are twice as likely to be affected as men.5
Patients experiencing BPPV will describe an acute onset of vertigo, typically described as dizziness with a spinning or rotational component. There is often a slight delay from the precipitating movement to the onset of vertigo and the sensation will be fairly brief, usually lasting between a few seconds to minutes. Patients may experience nausea, but vomiting is uncommon. Symptoms of BPPV are usually worse in the morning, as the otoliths tend to clump together during sleep and exert a greater effect when the patient attempts to get out of bed. As the patient moves her head throughout the day and the otoliths disperse, symptoms become less severe and frequent. The clinical exam may reveal nystagmus, in which the eyes alternate between a relatively smooth deviation toward the affected ear with frequent beating or twitching movements in the opposite direction. Interestingly, frequent, repeated stimulation of vertigo leading to nystagmus will cause fatigue, lessening the severity of the resultant nystagmus with each episode.
Ménière’s disease occurs equally in men and women. The first attack usually occurs in patients aged 65 and older, but in rare instances begins during childhood.5 The pathophysiology of Ménière’s disease is poorly understood. It is thought to be the result of excessive endolymph in the vestibular complex, occurring secondary to trauma, allergies, genetic factors or viral infection.4 Increased pressure in the vestibular complex leads to vertigo and can also result in periods of tinnitus—ringing in the ears—that can lead to permanent hearing loss in the affected ear or ears. A patient may also describe a sensation of fullness or pressure in one or both ears. Episodes of vertigo secondary to Ménière’s disease typically last for hours, but rarely for more than a day, and are often accompanied by nausea, vomiting and diaphoresis. Clinically, patients experiencing an exacerbation of Ménière’s disease will appear in distress, may be vomiting, and may have an elevated heart rate, blood pressure and respirations, with pale skin secondary to sympathetic nervous system activation. The clinical exam will reveal nystagmus.
Labyrinthitis is an infection of the inner ear that can be of bacterial or viral origin. Signs and symptoms include tinnitus, fullness or pressure in the ear, otorrhea and hearing loss. The vertigo associated with labyrinthitis can be severe, lasting for 2–3 days, and may be followed by disequilibrium and imbalance lasting for days to weeks. Nystagmus may be present. The patient may have had recent ear surgery or be able to describe a recent or current upper respiratory infection, and may be febrile.
Any drug with the potential to cause toxic reactions to structures of the inner ear, including the cochlea, vestibule, semicircular canals and otoliths, is considered ototoxic. Many well-known and frequently prescribed classes of medications are ototoxic. They are listed in Table 2 with their respective signs and symptoms. Nystagmus is an uncommon finding in ototoxicity.
Superior canal dehiscence syndrome
Superior canal dehiscence syndrome, a rare condition of the inner ear, occurs when there is a complete absence or thinning of the part of the temporal bone that overlies the semicircular canal of the vestibular system. As such, a “window” is created from the cranial vault into the inner ear, allowing sound and pressure waves to enter and influence the semicircular canals. Loud sounds, or pressure changes from sneezing, result in the abnormal movement of endolymph and the sensation of vertigo. Patients will present with nystagmus and vertigo that typically worsens with loud sounds or sudden movements. Pulsatile tinnitus, a feeling of fullness in the affected ear, and headache are common. A patient may describe hearing bodily sounds, such as cervical spine or eye movement, or hearing their own voice (autophony).
Central Causes of Vertigo
Central vertigo occurs secondary to disorders that affect the brain stem or cerebellum. With most causes of central vertigo (vertibrobasilar insufficiency being the exception), changes in position do not provoke the sensation of vertigo.
Vertigo is a common symptom in patients with migraine headaches. Patients may describe episodes of constant vertigo, positional vertigo or dizziness. Vertigo may occur concurrently with the headache or independently. Some patients complain of vertigo lasting from several minutes to 2 hours, whereas others experience vertigo lasting longer than 24 hours.5 Patients with a migraine will typically describe the headache as unilateral, pulsatile and lasting from 4 to 72 hours. Other symptoms of migraine headache include photophobia (increased sensitivity to light), phonophobia (increased sensitivity to sound), nausea and vomiting.
Patients with multiple sclerosis can present with vertigo lasting from hours to days to weeks. The patient will usually describe a sensation of vertigo that is not particularly intense or debilitating, and often there is nystagmus that is more impressive than the vertigo described by the patient.
Mal de debarquement syndrome
Mal de debarquement (French for “disembarkation sickness”) syndrome is a rare disorder that usually occurs after a long flight, car trip, sea cruise or any other event that results in sustained motion. Patients will describe a persistent sensation of swaying or rocking, as if they were on a boat. Other symptoms include anxiety, dizziness, visual disturbances, headaches and confusion. Ear complaints such as tinnitus, fullness or pressure may also be described. The syndrome is most common in women in their 40s, and symptoms can last from months to years, with the average length of symptoms being about 3.5 years.6
Cerebellar hemorrhage and infarct
An intracerebellar hemorrhage can produce symptoms such as vertigo and ataxia (lack of muscle coordination). Patients often describe the vertigo as a perception of side-to-side or front-to-back motion. These patients will typically have unstable gait and poor hand-eye coordination in addition to the more traditional signs and symptoms consistent with stroke.
Brain tumors affecting the cerebellum, either directly from within or by increasing pressure on the tissue, can lead to gradual onset of vertigo that is often unrelenting in nature. Symptoms are generally more subtle and can be associated with motor and coordination difficulties.
Vertebrobasilar insufficiency (VBI) is a term used to describe a transient decrease of perfusion in the posterior circulation of the brain, which supplies blood to the cerebellum, medulla, pons and midbrain. This results in a transient ischemic attack (TIA). VBI affects men, usually in their 70s and 80s, twice as often as women.7 Symptoms of VBI can vary depending on which portions of the brain are experiencing decreased blood flow, but vertigo can occur if the brain stem is involved. Vertigo and other symptoms can last from minutes to hours, but commonly resolve within 24 hours. Unlike other causes of central vertigo, VBI may be provoked by turning the head, if doing so partially occludes the vertebral artery. Other signs and symptoms include dysarthria, diplopia, dysphagia, and even near-syncope or loss of consciousness if there is a sufficient loss of brain stem circulation.
Vertebral artery dissection
Like VBI, vertebral artery dissection can lead to decreased perfusion in the posterior circulation of the brain and can result in stroke. Mechanisms that can cause this injury include anything that can result in sudden and violent rotation or extension of the neck, such as high-velocity motor vehicle crashes, diving injuries, coughing, sneezing and chiropractic neck adjustments (although the likelihood is low).5 Signs and symptoms of vertebral artery dissection include vertigo, headache and unilateral Horner syndrome.
Breakout: Horner syndrome is a condition that occurs secondary to impaired sympathetic nervous system innervation to the face. Patients will present with unilateral ptosis (drooping eyelid), anhidrosis (decreased sweating), bloodshot conjunctiva and miosis (constricted pupil).
The Patient History: Delineating Vertigo from Nonvertiginous Dizziness
Obtaining a detailed history of the patient’s complaint is the key to differentiating vertigo from nonvertiginous dizziness. First, ask the patient to describe her symptoms, using words other than “dizzy.” Patients may use the term “dizzy” nonspecifically to describe sensations of weakness, unsteadiness, near-syncope, syncope and vertigo. Descriptions of whirling, spinning or motion while at rest are consistent with vertigo. Oftentimes, patients will describe being dizzy while lying in bed or turning over in their sleep. Specifically ask the patient if dizziness increases upon standing quickly, as this is suggestive of a cardiovascular origin that requires further evaluation.
Peripheral vertigo may cause distressing symptoms, but is seldom life-threatening. Episodes tend to .begin and resolve suddenly and can last from minutes to hours. Symptoms are fairly specific. Complaints such as ear pressure or fullness, tinnitus and hearing loss are common. Changes in position tend to provoke the sensation of vertigo, and lying still tends to relieve it. The patient is often without complaint between spells.
Disorders causing central vertigo may produce less distressing and more variable symptoms that have a slower onset than those due to peripheral vertigo. Central vertigo is often less severe than peripheral, and is often accompanied by other neurological complaints. With the exception of VBI, sudden head movements will typically not provoke the sensation of vertigo. Table 3 contains a summary of the differences observed between peripheral and central vertigo.
The treatment of vertigo is mostly supportive. As patients with peripheral vertigo may experience a worsening of symptoms with head movement, an effort should be made to place the patient in a position of comfort that will minimize such movements. Patients with severe nausea and vomiting may benefit from intravenous fluid and antiemetic medications such as ondansetron (Zofran) or prochlorperazine (Compazine). Diazepam, midazolam or other benzodiazepines may be helpful as a vestibular suppressant for patients with severe vertigo. If you suspect the vertigo has a cardiovascular origin, always err on the side of caution and perform a 12-lead ECG and orthostatic testing.
Assume that patients with signs and symptoms consistent with central vertigo are having a stroke until proven otherwise in the ED, and treat per established protocol. Administer oxygen, do cardiac monitoring, obtain peripheral IV access and consider transport to a stroke center.
“I’m not sure you are having a heart attack, but I want to ask you some more questions,” Lafe tells Linda. “Can you describe the sensation you are feeling without using the word ‘dizzy’?” Linda thinks about it and says, “I feel like the room is spinning, even though I’m lying still. It is getting a little better, though, as I’m lying here.” Lafe then asks about the onset of dizziness and nausea. “I awoke feeling fine, but the spinning started as soon as I rolled over to get out of bed and stood up. Then I felt like I was going to throw up. This went on for about an hour before I called you. I start to feel OK when I’m lying down, but it gets real bad when I try to get out of bed.”
“Do your ears hurt at all?” Lafe asks. “The right one doesn’t hurt, but it does feel like there’s some pressure in there,” Linda replies. Lafe smiles and says, “Believe it or not, this is pretty good news. It sounds like you may have an ear infection, most likely from that upper respiratory infection you had. An ear infection can cause vertigo—the sensation that you are spinning. I want to ask you some more questions and run a few tests to make sure it’s nothing more serious, but I think you are doing just great right now.”
1. Karatas M. Central vertigo and dizziness: Epidemiology, differential diagnosis, and common causes. Neurologist 14(6):355–364, 2008.
2. Kerber KA, Meurer WJ, West BT, Fendrick AM. Dizziness presentations in U.S. emergency departments, 1995–2004. Acad Emerg Med 15(8):744–750, Aug 2008.
3. Newman-Toker DE, Hsieh YH, et al. Spectrum of dizziness visits to US emergency departments: Cross-sectional analysis from a nationally representative sample. Mayo Clin Proc 83, pp. 765–775, 2008.
4. Wackym PA, Sando I. Molecular and cellular pathology of Ménière’s disease. Otolaryngol Clin North Am 30(6):947–960,1997.
5. Goldman B. Chapter 164: Vertigo and Dizziness. In: Tintinalli JE, Stapczynski JS, Cline DM, et al. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e.
6. Kutz JW. The dizzy patient. Med Clncs N Amer 94(5): Sep 2010.
Scott R. Snyder, BS, NREMT-P, is the EMS education manager for the San Francisco Paramedic Association in San Francisco, CA, where he is responsible for the original and continuing education of EMTs and paramedics. Scott has worked on numerous publications as an editor, contributing author and author, and enjoys presenting on both clinical and EMS educator topics. Contact him at firstname.lastname@example.org.
Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California San Francisco and a former New York City paramedic for 10 years. Contact him at email@example.com.
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also a flight paramedic for Ministry Spirit Medical Transportation in central Wisconsin and a lead instructor for Wilderness Medical Associates. Contact him at kcollopy@colgate