i. Dizziness is a highly nonspecific term used to describe an unusual sensation referable to head or gait unsteadiness. Lightheadedness and vertigo are common forms of dizziness.
ii. Lightheadedness is usually caused by an insufficient supply of oxygen, blood, or glucose to the brain. Lightheadedness can occur with hyperventilation, hypoglycemia, or immediately prior to a syncopal event.
iii. Vertigo, the topic of this chapter, is a false sensation of movement (most commonly described as “spinning”). The patient may describe the environment as moving while he or she remains stationary, or vice versa.
b. Clinical manifestations of vertigo
i. Nausea and vomiting
ii. Gait unsteadiness
iii. Worsens with head movement and improves with eye closure
c. Etiology. Vertigo most commonly results from a defect in the vestibular system and can occur anywhere along the pathway from the inner ear to the brainstem.
B. Types of Vertigo. While it is important to differentiate central vertigo (due to a lesion in the brainstem) from peripheral vertigo (due to a lesion in the peripheral vestibular system), it can be challenging to make this distinction.
a. Central vertigo is more often due to high-risk lesions (e.g., stroke) than peripheral vertigo.
i. Clinical manifestations of central vertigo
1. Central vertigo is usually accompanied by other brainstem or cerebellar signs (e.g., limb ataxia, true weakness, sensory changes, diplopia, dysarthria, dysphagia, headache). Nystagmus may be present and can take any form: horizontal, vertical, or multidirectional.
The presence of spontaneous vertical nystagmus almost always indicates a central etiology.
2. Central vertigo is usually not accompanied by tinnitus or hearing loss.
MNEMONIC: Causes of Central Vertigo (“MAIM”)
Acoustic neuroma or other cerebellopontine angle/brainstem tumor
Ischemia of the central nervous system (CNS)
Migraine (especially basilar) or medications (e.g., anticonvulsants or related medications that suppress neuronal activity)
b. Peripheral vertigo
i. Clinical manifestations of peripheral vertigo tend to cause more patient distress than those of central vertigo and are more often associated with nausea and vomiting. However, the episodes tend to be brief and short-lived because the CNS tends to adapt.
1. Tinnitus and hearing loss, if present, are relatively specific to peripheral vertigo.
2. Nystagmus, which is usually present, is most commonly unidirectional, horizontal, and worse when looking toward the unaffected ear. The fast component is toward the side of the unaffected ear. Unlike the nystagmus of central vertigo, the nystagmus of peripheral vertigo can be inhibited, if not eliminated, by visual fixation. Otherwise, the neurologic examination is normal while the patient is seated or lying down. One caveat is that in patients with severe peripheral vertigo, gait can be impaired in a nonspecific pattern due to the essential role of the vestibular system in maintaining balance.
ii. Causes of peripheral vertigo. Peripheral vertigo is usually a result of processes that involve the labyrinth (inner ear) or eighth cranial nerve. Causes can be remembered by the mnemonic “MVP”:
Common Causes of Peripheral Vertigo (“MVP”)
Ménière’s disease: episodic vertigo typically lasting hours, hearing loss, and tinnitus
Vestibular neuritis and labyrinthitis: acute, severe vertigo, nausea, and vomiting lasting days to weeks with a monophasic course, often in patients who have had a recent viral syndrome
Positional (BPPV): very brief (e.g., less than 1 minute) episodes of vertigo, usually brought on by head movement
C. Approach to the Patient
a. Patient history. Key elements include the duration of vertigo (episodic vs. continuous), associated symptoms (focal neurologic symptoms, hearing loss, tinnitus), provoking factors (head movement), and medications.
b. Physical examination. The examination should focus on the ears, eyes, and nervous system.
i. The presence or absence of an ear infection (e.g., otitis media or interna), nystagmus, and neurologic deficits should be ascertained.
ii. The Dix-Hallpike (or Nylen-Barany) test is important in the diagnosis of BPPV. The seated patient turns his or her head upward slightly and 45 degrees to one side and then quickly lays backward so that the head hangs over the edge of the table. The test is positive (and BPPV confirmed) if the patient develops upbeat rotatory nystagmus several seconds after the maneuver is performed. While a positive test typically reproduces the patient’s symptoms, the test is indeterminate if the patient develops symptoms but does not have typical pattern of nystagmus.
iii. The head impulse test (HIT) tests whether the patient’s vestibuloocular reflex (VOR) is intact and can be used to assess for vestibular neuritis. The patient is asked to fixate on the examiner’s nose while the examiner places one hand on each side of the patient’s head and—after verifying the patient can safely turn the head quickly—rapidly turns the head 30 degrees to one side. If the VOR is intact, the patient’s gaze will remain fixed on the examiner’s nose. If the VOR is impaired, the patient’s gaze will rotate with the head, and then a catch-up saccade will lead to refixation on the examiner’s nose. If a catch-up saccade is noted, that indicates an impaired VOR on the side that the head was turned toward and supports a diagnosis of vestibular neuritis.
iv. The presence of (1) any new abnormality on the neurologic examination, (2) a central pattern of nystagmus (or peripheral pattern with normal HIT), or (3) a skew deviation (vertical misalignment of the eyes) substantially increases the odds that stroke is the cause of vertigo.
c. Special tests should be ordered in the following situations:
i. If hearing loss or tinnitus is a major component, an audiogram is useful to evaluate for Ménière’s disease or acoustic neuroma.
ii. If an unexplained central cause is suspected, brain MRI can sometimes delineate a specific etiology.
CT of the head has a very low yield in vertiginous patients and should rarely be obtained. If a central cause of vertigo is suspected, order an MRI.
a. Central vertigo. Treatment depends on the cause. For patients with suspected stroke, see Chapter 86.
b. Peripheral vertigo. For acute peripheral vertigo of almost any cause, the patient can be prescribed antihistamines, anticholinergics, and/or benzodiazepines as symptomatic treatment, although there is limited efficacy. The patient should be cautioned regarding falls, especially if already at risk for this event.
i. Medications may prevent CNS adaptation to peripheral vertigo and, therefore, should not be used for an extended period.
ii. A mild exercise program can expedite the adaptation process.
iii. For BPPV, the Epley maneuver can be performed in the office and is curative in 60–90% of cases. Sometimes the maneuver needs to be repeated at a subsequent visit or by the patient at home. (See Fife et al. in the Reference list for instructions on how to properly perform the Epley maneuver.)
iv. For acute vestibular neuritis, methylprednisolone has been shown to improve extent of recovery at 12 months and is a treatment option.
Suggested Further Readings
Chimirri S, Aiello R, Mazzitello C, et al. Vertigo/dizziness as a drugs’ adverse reaction. J Pharmacol Pharmacother 2013;4:104–9.Find this resource:
Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2008;70:2067–74.Find this resource:
Kerber KA, Meurer WJ, Brown DL, et al. Stroke risk stratification in acute dizziness presentations: a prospective imaging-based study. Neurology 2015;85:1869–78.Find this resource:
Kim J-S, Zee DS. Benign paroxysmal positional vertigo. N Engl J Med 2014;370:1138–47.Find this resource: