Dizziness and Vertigo

Matthew L. Kircher

James A. Stankiewicz

Sam J. Marzo

When investigating the source of dizziness in a patient, it is useful to organize potential etiologies into four groups. The four major causes of dizziness and vertigo are peripheral vestibular, central vestibular, medical, and unlocalized. True vertigo, particularly rotatory vertigo, is often due to a peripheral vestibular (inner ear) disorder. Presyncope and loss of consciousness are not associated with vertigo of peripheral origin and should direct the examiner to investigate other, often cardiovascular or CNS causes. These are common clinical scenarios and illustrate the varied backgrounds from which a complaint of dizziness may arise, ranging from benign annoyance to signs of potentially life-threatening events.

Documentation of the impact of dizziness and vertigo on a patient’s quality of life is essential in formulating a treatment plan. Treatment options are driven by the severity of disease and limitation in activities of daily living. Disease impact will often differ between patients as what may be tolerable for a retired schoolteacher may not be tolerable for an airline pilot.

I. PERIPHERAL VESTIBULAR OR OTOLOGIC CAUSES OF VERTIGO

A. Benign paroxysmal positional vertigo.

1. Clinical features. Benign paroxysmal positional vertigo (BPPV) is characterized by brief vertigo associated with changes in head position. It is the most common cause of vertigo. It is typically the result of stimulation of the posterior semicircular canal by loose debris (calcium carbonate crystals) dislodged from the utricle. This dislodgement can result from trauma, labyrinthitis, or spontaneously. Typically the history is one of recurrent vertiginous episodes lasting not more than 1 minute and reproducible with repeated movement in the same direction. The Dix-Hallpike’s test (which is illustrated in Chapter 16) is commonly employed to diagnose BPPV and identify the affected labyrinth.

2. Treatment. Vestibular suppressant medications can lessen vertigo intensity but do not reduce the frequency of attacks. The mainstay of treatment is repositioning exercises to move the debris from the affected semicircular canal. Both office-based repositioning techniques and home exercises may be employed to accomplish this goal. Rarely, when positional vertigo is unresponsive to repositioning maneuvers, surgery may be considered.

Epley’s maneuver. It is a common technique used for canalith repositioning. It is most effectively used when the affected semicircular canal has been identified and can therefore be targeted (see Chapter 16).

Technique (Fig. 56.1).
- With the patient sitting upright, the head is turned 45° to the offending side, and the neck is extended 45°.
- From this upright position with the head turned, the patient is reclined supine with the head hung over the edge of the exam table; this position is held for 10 to 15 seconds.
- The head is then slowly rotated away from the offending side, through midline, to 45° to the opposite side, keeping the neck extended throughout.
- The body and head are turned to face downward opposite to the offending side.
- After 10 to 15 seconds, the patient is slowly lifted to a seated upright position keeping the head turned away from the offending side.
- The head is then slowly returned to midline.
Modified Semont maneuver.

Technique (described for right-sided BPPV) (Fig. 56.1).
- The patient sits upright on the edge of the bed with the head turned 45° to the left.
- The patient drops his/her head quickly to touch the right postauricular region to the bed and maintains this position for 30 seconds.
- The patient then rolls in a swift movement toward the left side, so that the trunk is lying supine and the head comes to rest on the left side of the forehead and maintains this position for 30 seconds.
- The patient sits up again.
  
  This maneuver should be performed three times daily and repeated until symptom free for 24 hours.
Surgery. Very rarely, repositioning techniques are ineffective, and in severe cases of refractory BPPV surgery may be offered. Surgical options, which can be performed by a neurotologist, include semicircular canal plugging and vestibular neuronectomy.

FIGURE 56.1 Self-treatment of BPPV. (From Radtke A, von Brevern M, Tiel-Wilck K, et al. Self-treatment of benign paroxysmal positional vertigo: Semont maneuver vs Epley procedure. Neurology. 2004;63:150-152, with permission.)

3. Results. When applied to patients with BPPV, canalith repositioning is successful in relieving symptoms in up to 90% of patients. The techniques can be performed and taught by a wide range of clinicians. In those patients with recurrent symptoms, teaching the patient repositioning techniques will allow self-treatment and continued symptomatic relief.

4. Special circumstances. When BPPV is bilateral, treatment begins with the side that has a more robust nystagmus on Dix-Hallpike’s testing. Patients with severe disease may need pretreatment with 5 to 10 mg of diazepam 30 minutes prior to repositioning.

B. Vestibular neuronitis and labyrinthitis.

1. Clinical features. Vestibular neuronitis and labyrinthitis are often discussed together because of their similar presenting features. Both involve vertigo that can last for hours to days, often severe enough to induce nausea and vomiting. Labyrinthitis is associated with sensorineural hearing loss (SNHL), whereas vestibular neuronitis is not. These are typically self-limited conditions that are attributed to a viral infection. After the acute phase, vestibular equilibrium gradually returns over the course of several weeks in most patients.

2. Treatment. Using a combination of vestibular suppression, anti-inflammatory agents, antiemetics, and vestibular rehabilitation, treatment aims to reduce the severity and duration of acute symptomatology while allowing for vestibular recovery.

Vestibular suppression. Vestibular suppressants are generally grouped into three categories: benzodiazepines, antihistamines, and anticholinergics (Table 56.1). Benzodiazepines work via gamma-aminobutyric acid (GABA) potentiation and subsequent inhibition of vestibular stimulation. Anticholinergics and antihistamines work to suppress vestibular input. These medications are generally well-tolerated in low doses, although it is important to realize that a high level of vestibular suppression may reduce central compensation, and thus they are best used in a limited fashion. Antiemetics are a fourth category of pharmacotherapy, often used concurrently with vestibulosuppressants to target frequently associated nausea.
- Antihistamines. Antihistamines, notably those of the histamine-1 antagonist group, are commonly used in the management of peripheral vertigo. They are believed to exert a vestibulosuppressant effect via a central anticholinergic mechanism. Meclizine is most commonly used, starting at small doses (12.5 to 25 mg two to three times daily) and titrating to effect. Its effect is limited with adequate suppression typically lasting only 1 to 2 months. Promethazine is another antihistamine that also has antiemetic properties.
- Anticholinergics. Scopolamine is an anticholinergic medication commonly used in the prevention of motion sickness. It is not as valuable in the management of acquired vestibulopathy, but may be effective in the prophylaxis of motion sickness.
- Benzodiazepines. They are a class of psychoactive drugs that work via central inhibitory GABA potentiation resulting in anxiolysis, sedation, and in some cases amnestic, anticonvulsant, and muscle relaxation effects. Lorazepam and diazepam are frequently used for their ability to prevent and mitigate attacks of dizziness and vertigo from a variety of etiologies. Diazepam at a low dose (5 to 10 mg) acts as a vestibulosuppressant and can be used for acute or chronic otologic dizziness. Care must be taken when utilizing benzodiazepines because of their increased potential for dependence and subsequent withdrawal symptoms on cessation of therapy.
- Antiemetics (Table 56.2). Antiemetics are used to relieve nausea and vomiting associated with vertigo. Prochlorperazine is a phenothiazine that exerts a strong antiemetic effect but also carries the risk of extra pyramidal side effects. Metoclopramide is a dopamine receptor antagonist and serotonin receptor antagonist/agonist with antiemetic and prokinetic properties. Ondansetron provides antiemesis via serotonin 5-HT₃ receptor antagonism.
Corticosteroids/antivirals/antibiotics. Corticosteroids may be effective in treating associated hearing loss with labyrinthitis. Although most cases of labyrinthitis are believed to arise from viral infection, the addition of antiviral therapy to corticosteroids has not been shown to offer additional benefit. Antibiotics are of value in cases of bacterial or suppurative labyrinthitis; however, the decision to use antibiotics should be dictated by objective signs of infection.
Vestibular rehabilitation. It refers to physical therapy aimed at enhancing recovery from peripheral vestibulopathy. The exercises range from simple head-turning to increasingly more complex postural and ambulation challenges with and without head movement. Simple walking is a form of vestibular rehabilitation that can be recommended to patients with limited disequilibrium. The earlier vestibular rehabilitation takes place, the better the outcome, and patients should be titrated off vestibular suppressants to optimize vestibular challenge and recovery.

TABLE 56.1 Common Oral Medications for Treatment of Vertigo

Medication	Class	Dose
Clonazepam	Benzodiazepine	0.25-0.5 mg q8h
Diazepam	Benzodiazepine	5-10 mg q12h
Lorazepam	Benzodiazepine	1-2 mg q8h
Dimenhydrinate	Antihistamine	50-100 mg q4h-q6h not to exceed 400 mg daily
Diphenhydramine	Antihistamine	25-50 mg q4h-q6h not to exceed 300 mg daily
Meclizine	Antihistamine	12.5-50 mg q4h-q6h
Scopolamine	Anticholinergic	0.5 mg patch q72h

3. Results. Although there is some support for steroid use and vestibular rehabilitation enhancing vestibular recovery, randomized control trials are lacking. Fortunately, over 90% of patients with vestibular neuronitis or labyrinthitis will return to their presymptomatic baseline.

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