Approach to the Patient with Dizziness and Vertigo

Timothy C. Hain

Dizziness and vertigo are common symptoms. About 2.5% of all primary care visits are for dizziness and about 1 % are for vertigo. Dizziness and vertigo have diverse etiologies. Thus, a broadly based approach to the dizzy patient is necessary, at times requiring serious and life-threatening medical problems such as cardiac arrhythmia to be distinguished from the more common inner ear diseases and dizziness from unlocalizable sources.

I. ETIOLOGY

Vertigo can be categorized into four types: otologic, central, medical, and unlocalized (Table 16.1).

A. Otologic vertigo

is caused by dysfunction of the inner ear. It accounts for about onethird of all patients with vertigo. Table 16.1 lists entities that account for about 95% of all cases of otologic vertigo. The distribution of diagnoses varies greatly according to the referral base (e.g., neurology, otolaryngology, general medicine, and emergency room), but in all settings otologic vertigo comprises a substantial component.

1. Benign paroxysmal positional vertigo (BPPV) is the most common single type of otologic vertigo, accounting for roughly 20% of vertigo of all causes and 50% of all otologic cases. BPPV presents with brief vertigo provoked by changes in the orientation of the head to gravity. BPPV is caused by loose debris within the labyrinth.

2. Vestibular neuritis presents with vertigo, nausea, ataxia, and nystagmus. It is attributed to a viral infection of the vestibular nerve. Labyrinthitis presents with the same symptom complex, combined with tinnitus and/or hearing loss. Vestibular neuritis and labyrinthitis together account for about 15% of all otologic vertigo cases.

3. Ménière’s disease presents with intermittent vertigo accompanied by hearing complaints (see the so-called “hydrops” symptom complex in IV.A. 3). It accounts for about 15% of otologic vertigo cases.

4. Bilateral vestibular paresis presents with oscillopsia and ataxia, usually caused by loss of vestibular hair cells. The typical history is of treatment for several weeks with an intravenous or intraperitoneal ototoxic antibiotic (of which gentamicin is the most commonly used). Bilateral vestibular loss is uncommon.

5. The superior canal dehiscence (SCD) syndrome exemplifies several conditions in which there is an opening between the inner ear and a surrounding structure. They generally present with vertigo induced by sound (the Tullio’s phenomenon) or as ataxia provoked by activity or straining. The diagnosis of SCD has been rapidly increasing in recent years due to a combination of improved knowledge about the condition as well as greater use of a new diagnostic modality—vestibular evoked myogenic potentials (VEMP). In SCD, bone over the superior semicircular canal is absent. Similar symptoms are seen in perilymphatic fistula and cholesteatoma.

6. Tumors compressing the eighth cranial nerve, such as acoustic neuroma, present with asymmetric hearing loss combined with mild ataxia. Eighth nerve tumors are very uncommon in the vertiginous population (but are more common in the unilaterally hearing impaired).

B. Central vertigo

is caused by dysfunction of central structures that process sensory input from the inner ear. Central vertigo accounts for 2% to 50% of vertigo diagnoses, depending on the setting in which patients are seen. In a majority of cases, central vertigo is caused by migraine. Table 16.1 lists entities accounting for about 90% of central
vertigo diagnoses, the remainder being made up of individual unusual conditions (e.g., spinocerebellar degeneration).

TABLE 16.1 Etiologies of Vertigo

Otologic vertigo
	BPPV
	Vestibular neuritis and labyrinthitis
	Ménière’s disease
	Bilateral vestibular paresis or loss
	Superior Canal Dehiscence (SCD) and Perilymph Fistula (PLF)
	Tumors compressing the eighth cranial nerve
Central vertigo
	Migraine
	Stroke and TIA in vertebrobasilar arterial distribution
	Seizures
	MS
	Chiari malformation
Medical vertigo
	Postural hypotension
	Arrhythmia
	Cardiac
	Hypoglycemia and diabetes mellitus
	Medication effects
	Viral syndrome
Unlocalized vertigo syndromes
	Anxiety and panic
	Post-traumatic vertigo
	Hyperventilation
	Malingering
	Unknown

1. Basilar migraine ordinarily presents with vertigo and headache, but it can also present as isolated vertigo. Migraine causes about 75% of central vertigo cases. It is particularly common in women in their 30s.

2. Stroke and transient ischemic attack (TIA) involving the brainstem or cerebellum causes about one-third of all central dizziness cases. Pure vertigo can occasionally be the only symptom preceding a posterior fossa stroke; there are no reliable means of distinguishing a TIA affecting the vestibular nucleus or cerebellum from another process affecting the vestibular nerve or end organ.

3. Seizures present with vertigo combined with motor symptoms or confusion. About 5% of central vertigo is caused by seizures. Dizziness is a common symptom in persons with known epilepsy.

4. Multiple sclerosis (MS) combines vertigo with other central signs such as cerebellar dysfunction. MS is an uncommon source of vertigo. About 2 % of central vertigo cases are caused by MS. In persons with known MS, it is important not to attribute vertigo to MS without considering common peripheral causes that might be coincident, such as BPPV.

5. The Chiari malformation is a hindbrain malformation wherein the cerebellar tonsils herniate 5 mm or more below the foramen magnum. These patients complain of vertigo, ataxia, and occipital headaches, and often have downbeat nystagmus. Like SCD, symptoms may be precipitated by straining. MRI of the posterior fossa establishes the diagnosis. About 1% of cases of central vertigo are caused by the Chiari malformation.

6. Cervical vertigo is a controversial syndrome. Diagnosis is most often made after a whiplash injury where findings usually include vertigo, tinnitus, and neck pain. Examination usually demonstrates a nonspecific symptom complex including neck movement limited by pain and nausea or vertigo on neck positioning. Generally, there is no strong nystagmus even using video-recording methods. There are no definitive clinical or laboratory
tests for cervical vertigo. MRI of the cervical spine in these patients often shows cervical disks abutting but not compressing the cervical cord. Rare cases have been reported in whom vertigo can be traced to compression of a vertebral artery after neck rotation. Due to the lack of clarity in the diagnosis of cervical vertigo, its prevalence is unknown.

C. Medical vertigo

may be caused by altered blood pressure, low blood sugar, and/or metabolic derangements associated with medication or systemic infection. It is largely encountered in the emergency room, where it accounts for about 33% of all cases of dizziness. It is unusual in subspecialty settings (2% to 5%). Table 16.1 lists nearly all causes of dizziness reported in studies of vertigo as it presents to emergency rooms.

1. Postural hypotension often presents as giddiness, lightheadedness, or syncope. Dizziness occurs only while the patient is upright.

2. Cardiac arrhythmia presents with syncope or drop-attacks. Like those of postural hypotension, symptoms are characteristically present only when patients are upright.

3. Hypoglycemia and metabolic derangements associated with diabetes present with giddiness or lightheadedness. Hypoglycemia is often accompanied by autonomic symptoms such as palpitations, sweating, tremors, or pallor. Together they account for about 5% of the cases of dizziness in general medical settings.

4. Medication effects usually presents with giddiness or lightheadedness, but also can present with true vertigo. These diagnoses account for about 16% of the dizzy patients seen in the emergency setting, but are rare outside the emergency room. Medications commonly implicated include antihypertensive agents, especially α-1 adrenergic blockers such as terazosin, calcium channel blockers such as nifedipine, and sedatives. Benzodiazepines, such as alprazolam, can cause dizziness as part of the withdrawal syndrome. Alcohol intoxication can present as a transient positional nystagmus, cerebellar signs, and direction changing positional nystagmus.

5. Viral syndromes not involving the ear are the reported cause of dizziness in approximately 4% to 40% of all cases seen in the emergency room setting. Such syndromes include gastroenteritis and influenza-like illnesses.

D. Unlocalized vertigo

patients include those whose symptoms are attributed to psychiatric disorders, those whose symptoms are attributed to events without further definition (such as head trauma), and those with vertigo and dizziness of unknown origin. Common variants of unlocalized vertigo include psychogenic vertigo, hyperventilation syndrome, post-traumatic vertigo, and nonspecific dizziness. Between 15% and 50% of all patients with dizziness or vertigo fall into this category, depending both on referral base and diagnostic diligence.

1. Unknown (nonspecific dizziness). Diagnostic procedures are insensitive, and in dizziness evaluations it is usual to have as many as 50% of patients without any detectable abnormalities on careful clinical examination and thorough testing. Some authors wrongly define psychogenic vertigo as the complaints of patients falling into this category. About 75% of the unlocalized vertigo category consists of patients in whom there are no abnormalities on examination and testing.

2. Psychogenic. Patients with anxiety disorders, panic disorder, and post-traumatic stress disorder may complain of dizziness, ataxia, and autonomic symptoms. This is a common presentation. It is often impossible to determine whether or not anxiety is the sole cause or a reaction. In somatization disorder, symptoms may be present without anxiety.

3. Post-traumatic vertigo patients complain of vertigo following head injuries but frequently present no findings on examination or vestibular testing. BPPV is excluded by several negative Dix-Hallpike maneuvers using an adequately sensitive technique—e.g., video goggles. Post-traumatic vertigo is common.

4. Hyperventilation syndrome. These patients have vertigo after hyperventilation, without other findings or nystagmus. Hyperventilation-induced symptoms are commonly seen in well-documented structural abnormalities such as acoustic neuroma.

5. Multisensory disequilibrium of the elderly. Most elderly people have age-related multisensory impairment. Like the diagnosis of psychogenic vertigo, this diagnosis is often used in situations where examination is otherwise normal.

6. Malingering. Because vertigo can be intermittent and disabling, and frequently follows head injury, it may be claimed in an attempt to obtain compensation. Malingering is common only among patients who are being compensated for illness.

II. CLINICAL MANIFESTATIONS

A. Primary symptoms.

The primary symptoms listed in Table 16.2 are mainly the result of a disturbed sensorium.

1. Vertigo denotes a sensation of rotation—either of the person or of the world. It can be horizontal, vertical, or rotatory. It can be described as visual “blurring” or “jumping.” Horizontal vertigo is the most common type, usually resulting from dysfunction of the inner ear. Vertical vertigo is rarer. When transient, it is usually caused by BPPV. When constant, it is usually of central origin and accompanied by downbeat or upbeat nystagmus. Rotatory vertigo is the least frequent. When transient, rotatory vertigo is usually caused by BPPV. When chronic, it is always central and usually accompanied by rotatory nystagmus.

2. Impulsion denotes a sensation of translation, usually described as brief sensations of being pushed or tilted. Variants include rocking, floating, and perceived changes in the directions of up and down. Impulsion indicates dysfunction of the otolithic apparatus of the inner ear or central processing of otolithic signals. It is often a symptom of Ménière’s disease.

3. Oscillopsia is an illusory movement of the world evoked by head movement. Patients with bilateral vestibular loss are unable to see when their heads are in motion because of oscillopsia. Patients with unilateral vestibular loss often complain that “the world doesn’t keep up” when they rapidly rotate their heads laterally to the side of the bad ear.

4. Ataxia, unsteadiness of gait, is nearly universal in patients with otologic or central vertigo and is variably observed in patients with medical and unlocalized vertigo.

5. Hearing symptoms. Vertigo is often accompanied by tinnitus, hearing reduction or distortion, and aural fullness.

B. Secondary symptoms

include nausea, autonomic symptoms, fatigue, headache, and visual sensitivity. Visual sensitivity is also known as the “grocery store syndrome.” Patients complain of dizziness related to the types of patterned visual stimulation that occur when they view grocery store aisles, drive past picket fences or through bridges, or view large screen movies. The grocery store syndrome is a nonspecific common late symptom in patients with vertigo and is generally thought to be caused by a reweighting of sensory input related to balance (ear, eye, and body) resulting in greater dependence on vision.

C. Giddiness, wooziness, heavy-headedness, and lightheadedness.

These terms have no precise meanings in common usage. They are rarely used by patients with documented inner ear dysfunction but are frequently used by patients with vertigo related to medical problems.

TABLE 16.2 Symptoms in Patients with Dizziness and Vertigo

Primary symptoms
	Vertigo
	Impulsion and rocking
	Oscillopsia
	Ataxia
	Hearing symptoms
	Secondary symptoms
	Nausea, emesis, diarrhea
	Pallor, bradycardia
	Fatigue
	Headache
	Visual sensitivity
Nonspecific symptoms
	Giddiness
	Lightheadedness

III. EVALUATION

A. History.

The history must either be all-encompassing or follow a heuristic technique whereby questions are selected as the interview progresses. Here we outline the allencompassing approach.

1. Definition. Does the patient complain of vertigo (spinning), a secondary symptom (such as nausea), a nonspecific symptom (giddiness or lightheadedness), or something entirely different (e.g., confusion)?

2. Timing. Are symptoms constant or episodic? If episodic, how long do they last?

3. Triggering or exacerbating factors are listed in Table 16.3. All patients should be queried regarding these factors, either by going through them one by one, or by using an interview heuristic whereby one attempts to rule in or rule out a symptom complex (see IV).

4. Otologic history. Ask about hearing loss, tinnitus, and fullness. Positives are indications for an audiogram. Ask about the type of tinnitus—“roaring” tinnitus suggests Ménière’s disease.

5. Medication history. Numerous medications can induce dizziness, including ototoxic drugs, antiepileptic drugs, antihypertensives, and sedatives. All current medications, as well as previous exposure to ototoxic agents, should be considered as sources of dizziness.

6. Family history. Has anyone in the immediate family had similar symptoms? Is there a family history of migraines, seizures, Ménière’s disease, or early-onset hearing loss?

7. Review of systems should explore psychiatric problems (anxiety, depression, and panic), vascular risk factors, cancer, autoimmune disease, neurologic problems (migraine, stroke, TIA, seizures, and MS), otologic surgery, and general medical history (especially thyroid dysfunction, diabetes, Lyme’s disease, or syphilis).

8. Previous studies relevant to dizziness (see III.C) should be reviewed.

B. Physical examination.

The physical examination of the vertiginous patient is outlined in Table 16.4. It is ordered in such a way that procedures may be added on the basis of previous results. Because a full examination may be lengthy, it is most practical to expand or contract the examination dynamically. As an exception to the following procedure, if there is a history of positional vertigo, it is best to go immediately to the Dix-Hallpike test (see III.B.5.b).

1. General examination. Measure the blood pressure and pulse with the patient standing. Arrhythmia is noted, if present. If the standing blood pressure is low, check blood pressure with the patient lying flat. The heart, the carotid, and subclavian arteries are auscultated.

2. Balance is assessed via observation of gait (see Chapter 8), and the eyes-closed tandem Romberg’s test. The tandem Romberg’s test is extremely useful. Low-normal performance consists of the ability to stand heel-to-toe, with eyes closed, for 6 seconds. Young adults should be able to perform this test for 30 seconds, but performance declines with age.

TABLE 16.3 Triggering or Exacerbating Factors

Positional changes of head or body

Standing up

Rapid head movements

Walking in a dark room

Loud noises

Coughing, nose blowing, sneezing, or straining

Underwater diving, elevators, airplane travel

Exercise

Shopping malls, narrow or wide-open spaces, grocery stores

Foods (salt and monosodium glutamate)

Fasting

Alcohol

Menstrual periods

Boat or car travel

Anxiety or stress

It is helpful to develop a judgment of how much ataxia is appropriate for a given degree of ear injury. Patients with bilateral vestibular loss are moderately ataxic—they make heavy use of vision and are unsteady when their eyes are closed (with a narrow base). No patient with bilateral loss can stand in the eyes-closed tandem Romberg’s test for 6 seconds. Patients with an additional superimposed position sense deficit are unsteady with eyes open (with a narrow base). Patients with chronic unilateral vestibular loss show very little ataxia, and they are usually normal on the eyes-closed tandem Romberg’s test. The need to gauge ataxia does not come up in patients with recent unilateral vestibular imbalance because these patients have prominent nystagmus. Patients with cerebellar disorders, such as alcoholic cerebellar degeneration, have greater ataxia than is appropriate for their degree of nystagmus or vestibular paresis. Patients who are malingering also typically emphasize imbalance, which is the disabling aspect of their symptoms.

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